Term
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Definition
molecules that bind to specific cell memb receptor proteins
EXAMPLES OF LIGANDS: Hormones Neurotransmitters (for nervous cells) Cell recognition molecules (neighboring cells responding to each other) |
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Definition
** Cells use surface proteins to communicate **
“Chemical” Communication - Autocrine & Paracrine: local signaling (near neighbors), synapse - Endocrine signaling: distant targets; diffuses through vascular system
“Electrical” Communication - Gap junctions: local (in heart or muscle) - Ion Channels: allow charge to move across memb - Nervous syst: very fast, very targeted (discreet and localized), distant target |
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Definition
MOTOR- start in CNS and extend out to the PNS, has a synapse that makes change in musc. Can cause or stop contraction
SENSORY- starts a signal in the periphery and relays toward the CNS (brain) (EX: heat on skin)
ASSOCIATION- run from one type of neuron to another. Can go in all directions and can connect motor + sensory, goes from lrg networks of interneurons speaking to eachother through electrical signals to dictate properties of though, behavior, etc. |
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Definition
lipid-rich, n: on-conductive lipid/protein compound that surrounds the axons of some neurons in a patterns of nodes (non myelinated) and internodes (myelinated); better facilitates rapid conduction of electrical impulses by saltatory conduction |
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Definition
no obvious axon but has lots of dendrites. Mat also do secrting Some Cns neurons |
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Definition
2 distinct processses from cell body some special senses |
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Definition
dendrite and axon continuous (most sensory neurons) |
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Definition
1 axon, 2+ dendrites (motor neurons + CNS neurons) |
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Definition
Pancinian corpuscles photoreceptors Golgi tendon organs taste and smell receptors Meissener’s corpuscles
More specifically, Pacinian Corpuscles wil pick up mechanical signals so when the membrane gets distorted, ion channels open and things start moving based on press differences. Confirmation can also be changed by thermal and osmotic press changes.
Usually mechanically gated ion channels |
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Definition
* Support: metabolic and structural * Like nurse for neurons b/c they have high E demands * Development, migration neurons * Uptake of some neurotransmitters (GABA, glutamate) * Damage control after injury: phagocytosis * Rid of cellular debri from dead cells * Control cerebral blood flow * Blood-brain barrier
10x as many as there are neurons |
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Definition
oligodendrocytes schwann cells astrocytes microglia |
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Definition
a structural/ anatomical feat of vascular elements of the CNS which restricts solute passing between blood and nervous tissue;
Passage Restricts: Lrg molecules cannot pass easily molecules w/ high electric charge poorly lipid-soluble molecules
BBB is maintained by: Astrocytic processes enveloping the capillaries A complete capillary endothelium (tight junc and ne fenestrations)
Importance: Limits pathogen/toxin entry to CNS limit s drug delivery to CNS Sometimes a limiting factor in therapy w. drugs that cannot easily pass through BBB |
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Term
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Definition
SIMPLE DIFFUSION (PASSIVE) PRIMARY ACTIVE TRANSPORT SECONDARY ACTIVE TRANSPORT |
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Term
Passive diffusion through ion channels |
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Definition
These ions are diffusing down a gradient based on [ ] differences and charge→ a lot on outside will make them want to move in to reach equal [ ] |
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Term
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Definition
movement of substances (ions, molecules) against their [ ] gradient Consumes metabolic E (usually ATP) Usually mediated by an enz EX: Na+/K+ ATPase, Na+/H+ ATPase Highly active in cels that need to move ions (neurons, kidney, muscle, intestine) or which require a charge on the memb |
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Term
secondary active transport |
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Definition
Rely on primary active transport (ex: Na+/K+ ) to produce ion [ ] gradietns Cotransporters use “stored” energy to move other molecules (ex: amino acids, glucose) against [ ] gradients Indirect consumption of ATP They rely on the E consumption of 1 active transport mechanisms Usually done by symporter or antiporter proteins EX: co-transporters, counter-transporters something sneaking in w/ Na usually kinds of things that get transported are glucose, amino acids, an-ions (negative charged)** |
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Term
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Definition
flux of K+ (or any ion, provided the memb is selectively permeable to that ion) across the memb is determined by the [ ] gradients AND the electrical potential, creating a electrochemical balance/ electrochemical gradient
The only ios that make a difference to charge on membrane are the ones that can move across it.
Ex: Electrical potential diff moves K into cell while conc gradient moves K out |
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Term
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Definition
the charge on the memb that is dictated by ions that can pass through (EX: K+ happens b/c of leaky ion channels)
K = neurons Cl= skeletal musc |
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Definition
if cell interior becomes less - ° electrochem gradient will drive K+ out ° charge will decrease (become mire -) If cell interior becomes more - °electrochem grafient woll pull K in ° charge will rise (become less -) |
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Term
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Definition
Memb can rach ~-55mV b/c of many reasons: most common change is when an AP hits a synapse and there is a synapse at the surface of this cell→ hits neurotransmitter → trying to bind to ligand channel→ which lets a bunch of ions in (usually Na) |
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Term
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Definition
Rmp K(neuron) = -91mv (-70--90) Rmp CL (musc) = -88 mv Potential Na= +65-75mv Threshold for depolarizrom. =-55mv |
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Definition
This means that the AP does not occur at the myelinated regions (internodes) along axons. ONLY occur at nodes. As a result, the charge diffuses rapidly along the inner surface of the memb and “refreshes/ strengthens” by stimulating a new round of opening of voltage gated Na+ at each node This happens more rapidly than in non-myelinated fibers. This is called Saltatory Conduction Nodes of raniver is where the voltage gated ion channels are localized and will jump across myelin (saltatory conduction) |
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Definition
the chemical signal at synapses The axon terminus synthesizes NT and stores them in vesicles 1 type if neuron usually makes 1 class/family of NT
Different ones for PNS and CNS |
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Term
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Definition
Acetylcholine (ACh) and Norepinephrine (NE) are the primary NTs found |
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Definition
AMINO ACIDS GABA, glycine, glutamate
ACETYLCHOLINE (ACh)
AMINES Serotonin, dopamine, norepinephrine, epinephrine
NEUROPEPTIDES Oxytocin, vasopressin, neuropeptide Y |
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Term
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Definition
Ligand-gated ion channels EX: nicotinic AChR G-protein receptors EX: muscarinic AChR → Ligand binds to receptor and bound w/ G protein allows it to open up (coupled) Many others Most lead to changes (+ or -) in the RMP of the post-synap memb |
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Term
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Definition
Ionotropic (binds directly to ligand)
Ligand gated ion channels (R is an ion channel) EX: AMPA, NMDA, Nicotinic ACh R
NEED TO KNOW FOR TEST |
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Definition
Metbotropic ( associated w/ other types of neurotransmitters as well but is coupled w/ G. proteins) G-protein coupled R acts through G-protein to activate enz/ion channel
EX: mGluRs, Muscarinic ACh R
NEED TO KNIW FOR TEST |
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Term
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Definition
1. Stimulation of post synap memb leads to opening of ligand-gated Na+ or Ca+ channels
2. Promotes Excitation of memb EX: depolarization
3. Charges become less - and favors formation of an AP Called an EXCITATORY POST-SYNAP POTENTIAL (EPSP)
EX: Nicotinic AChR at neuromusc junc |
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Term
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Definition
1. Stim of post-synap memb opens K+ or Cl- channels Causes hyperpolarization
2. Charge becomes more -. This means that the potential is low and neuron is less prone to firing
3. May prevent the formation of AP Called INHIBITORY POST_SYNAP POTENTIAL (IPSP)
EX: GABA receptors in CNS- ligand gated Cl- channels |
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Term
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Definition
** EPSPs and IPSP add up (summate) over space (spatial summation ) and time (temporal summation) and influence the memb potential on the neuron surface (particalluary the axon hillock- a structure where the charges migrate) ** |
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Definition
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WHAT HAPPENS AFTER A POST-SYNAP RESPONSE IS GENERATED |
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Definition
depends on NT and type of neuron** 1) ACh is broken down into acetic acid and choline by acetylcholinesterase → Choline is taken up by presynaptic neuron and used Have lots of drugs an toxins that interfere with this enz. Can give an inhibitory to prevent acetylcholine so itll block the effect of excess acetylcholine
2) Most Amine NT (ex: NE, dopamine, serotonin) are taken up by pre-synap neuron (REUPTAKE) and reused. Some is broken down by specific enz in axon terminus REUPTAKE- some can get taken up by synaptic bulb. If you block reuptake, can have more activity at synapse. Can use this in drug making.
3) Some diffuses away from synapse (ex: GABA, etc) to be metabolized by astrocytes etc |
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Term
Dtugs/toxins that act at synapses |
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Definition
*Organophosphates * sarin *Curare * atropine *strychnine * tensilon * Neostigmine * etc
Need to know for test |
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Term
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Definition
Block the release of NT EX: Botulism, tetanus toxins
Block re-uptake of NT EX: SSRI, SBARI
Block receptor EX: atropine
Block metabolism Sarin, organophosphates, tensilon NEED TO KMOW FOR TEST |
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Term
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Definition
CERVICAL → C-7 THORACIC→ T-13 LUMBAR→ L-7 SACRAL→ S-3 COCCYGEAL→ ~1-20 |
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Term
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Definition
Have evolved modified structure to support skull and allow enhanced movement compared to the rest of the vertebral column
No intervertebral disc between C1 and the skull NOR between C1 and C2 Allows for more range of motion |
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Term
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Definition
a set of 3 tissue membranes surrounding brain and spinal cord; provide protection, support for blood vessels, and containment of CSF |
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Term
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Definition
1) DURA MATER Outermost layer, strongest
2) ARACHNOID MATER Thin, spider web-like membranes between pia and dura; separator for fluids running through diff departments
3) PIA MATER Bound tightly to surface of brain and spinal cord, most blood vessels present in this layer |
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Term
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Definition
EPIDURAL- external to the dura, anesthetics injected here
SUBDURAL SPACE- serous fluid
SUBARACHNOID- between the pia and arachnoid, filled w/ CSF |
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Term
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Definition
The region of the spinal cord from which the spinal nerves originate EX: C6 segment is the source of C6 spinal nerves |
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Term
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Definition
DERMATOME- the area of skin innervated by the sensory fibers from an individual spinal nerve/ spinal segment; all exit in a very defined region
MYOTOME- the muscles innervated by the motor fibers from an individual spinal nerve/segment **both innervate diff regions of body**
Keep in mind sensory VS motor |
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Term
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Definition
Cervical are the # of vert + 1 All other vertebrae spinal nerve equal each other
Spinal nerves exit the vertebral canal via intervertebral foramen cranial to the vert after which they are named between C1 and C7
Then, C8 exits caudual to the 7th cervical vert Then, all subsequent spinal nerves exit caudal to the the vert after which they are named T1-T13, L1-L7, S1-S3 |
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Term
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Definition
he spinal cord ends cranial to the end of the vert column w/ the terminal spinal segments found clustered in a short stretch of the spinal canal in the area of L4-L6 vert The spinal nerves from the terminal segments course caudally and form- CAUDA EQUINA → occupy the cancel caudal to L6 This happens b/c the caudal spinal segments of spinal cord are smaller than the cranial |
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Term
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Definition
CERVICAL (CERVICOTHORACIC) ENLRGMENT- spinal seg that supply nerves to forelimbs (Segments C6, C7, C8, T1, T2) Forlimb reflexes and LMNs
LUMBOSACRAL ENLRGMENT- spinal segments that supply nerves to the hindlimbs (segments L4, L5, L6, L7, S1, S2) Hjndlimb reflexes and LMNs
** these elrgments are present b/c there are more neurons therefore more nerves innervating limbs → important for controlling fine musc movements ** Get injuries in these areas and has big problems b/c that where a lot of nerves are innervating |
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Term
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Definition
primarily composed of neuron cell bodies; divided into horns
DIVISIONS DORSAL HORN- sensory neurons 2° VENTRAL HORN- motor neurons 1° LATERAL HORN- autonomic neurons (in thoracic and first few lumbar and sacral segments only |
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Term
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Definition
Primarily composed of axons. tract (clusters of axons w/ all the same func/info); divided into white matter columns (or funiculi) which contain individual tracts (axons carrying specific type of info- sensory or motor)
DIVISIONS DORSAL COLUMNS- sensory tracts LATERAL COLUMN- mix sensory and motor tracts VENTRAL COLUMN- mix of sensory and motor tracts |
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Term
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Definition
DORSAL ROOT- where axons from sensory neuron enter the spinal cord so the first neurons that they usually synapse upon, called a 2° neuron, are the first neurons encountered VENTRAL ROOT- where axons of motor neurons exit the spinal cord, and the nerve cell bodies where these axons originate are physically close to this root
Dorsal root going in spinal cord and ventral going out and fuse together → mix Ventral root is always motor → any info going out Dorsal root is always sensory → any info going in |
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Term
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Definition
Each carries a specific “type” of sensory or motor info ASCENDING carries sensory info to the brain DESCEDNING carries motor info from the brain |
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Term
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Definition
Spinal cord is segmentally supplied by branches that arise from… Vertebral artery (in cervical and anterior thoracic regions) Intercostal artery (in thoracic region) Aorta (in lumbar region)
These feed into … NEED TO KNOW THESE NAMES The ventral spinal artery (follow the ventral surf of cord) Paired dorsolateral spinal arteries (run along base of dorsal roots of spinal nerves) radial branches split off and supply the core of the spinal cord[image]062e81783204|center} |
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Term
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Definition
local phenomena that do not require input from high senders → Happens entirely in spine at a single spinal segment. Going to involve at least 1 (+ often more) synapses |
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Term
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Definition
simple neuronal circuit in which a sensory neuron enters the CNS and, ater one or more synapses, leads to an AP in a motor neuron and a detectable response in an effector organ (ie a musc)
BUT higher senders can modulate a reflex. |
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Term
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Definition
(voluntary responses/proprioceptors) start and end in the PNS. BUT the synapses are in the CNS. the arc enters and exits locally). In other words, they Always go into the CNS but always come out locally w/out having to go in the brain
KEEP IN MIND: paired spinal nerves enter and exit the spinal cord at each spinal level, and reflexes can occur on each side at each level (as well as the brain)
Spinal reflexes are present on both sides of the animal and occur along the length of the spinal cord. Their presence reflects the activity in the PNS and/or in the CNS at the level they enter and leave the spinal cord. |
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Term
Components of a reflex arc |
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Definition
1) Sensory receptor 2) Sensory neuron 3) Interneuron (not always present, but could also have 1 or more in between ) -Reflex withdrawal in dog (pinch toes anad see if they react) involves an interneuron 4) Motor neuron 5) effector organ |
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Term
CLASSIFICATION OF REFLEX ARC |
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Definition
EFFECTOR DIVISION- Does it involve skeletal or smooth musc? SOMATIC- skeletal musc AUTONOMIC- smooth musc
INTEGRATION SITE- where in the CNS are the neurons and synapses involved? SPINAL CORD- spinal reflexes BRAIN- cranial nerve reflexes
# OF SYNAPSES/NEURONS- How many neurons are in the pathway? MONOSYNAPTIC POLYSYNAPTIC |
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Term
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Definition
MONOSYNAPTIC IPSILATERAL Myostatic (stretch) reflex: tap each patellar tendon and watch rapid extension of the knee (patellar knee–jerk reflex Muscle stretch simulated musc spindle somewhere on the outside→ sensory neuron synapses w/ motor neuron in spinal cord → motor signal goes to same musc for reflex
MULTISYNAPTIC IPSILATERAL Flexor reflex (withdrawal reflex): pinch toe and observe flexion of leg Response to pain in limb → flexors in the same limb contract Hardest to asses clinically in context of deep pain Looking to see if they withdraw their leg and respond w/ other things like growling/biting
MULTISYNAPTIC CONTRALATERAL Crossed-extensor reflex: pinch toe (like flexor reflex) and observe extension in opposite leg Response to pain in limb → extensors in opposite limb contract and extend leg Part of normal integrated gait pattern (since they walk on 4 limbs) EX: SPINAL WALK- example of multisynap, contralateral neuron issue (and exaggerated reflex ==> CNS issue). cant achieve normal gait but still has reflexes; support back end w/ towel so as each leg touches the ground and contracts. They have alternating flexion and contraction but cant figure out there legs |
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Term
UNDERSTANDING SIMPLE MONOSYNAPTIC REFLEX |
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Definition
MUSC SPINDLE ORGAN (INTRAFUSAL FIBER)- a type of mechanoreceptor. Fires when musc stretched. Stope when musc shortens. “Senses” musc length and sends that signal to CNS
Primary sensory neuron is first sensation that goes into spinal cord Alpha motor neuron causes musc contraction Secondary sensory neurons and gamma motor neuron will reset the intrafusal fiber tension. |
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Term
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Definition
responsible for proprioception, fine touch/press and vibration; this tract is very sensitive (location based stimuli) have L+R dorsal column; ONLY carry that information, so never motor info here If you cut this out, animal will not know where limb is in space but can still move it.
Proprioception travels in dorsal column |
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Term
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Definition
sensory afferent Carry info to brain
- dorsal root gang house the nerve cell bodies - fivers always enter the dorsal root - crossover - carries CP and UCP fibers |
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Term
Spinal tracts that carry CP info |
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Definition
aka general somatic afferent tracts 1) spinothalamic tract 2) dorsal column 3) nonspecific, multisynaptic pathways |
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Term
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Definition
AKA: ventrolat/ anterolat tract LOCATIIN: Ventrolat areas of spinal cord white matter FUNC: Carry pain and T sensation CHARACTER: Small to modrte diam fibers with low levels of myelination -relativeky resistant to injury |
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Term
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Definition
AKA: fasciculus cutaneous and fasiculus gracilis LOCATION: most dorsal aspects of spinal cord. 2 subsets 1) fas. Cut. (Lat) = forelimbs, cranial T6 2) fas.grac. (medial)= hind limbs, caudal T6
FUNC: Carry CP info (where limbs are). Kinesthesia and fine touch CHARACTER: -lrg super myelin fibers °high susc to injury °conduct info quick °demyelin = liss of func - single long fiber from periphery to brain Mas then mult synapses on brajn. Fivers do crossover |
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Term
Non specific, multisynap paths |
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Definition
Take a complicated path to brain but conduct info very slowly (low myelunayion)
Tracts ascend in the white matter throughout the spinal cord and terminate as part of the RAS (reticular activating system) in the brain |
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Term
Spinal tracts that carry UCP info |
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Definition
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Term
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Definition
Spine to cerebellum Used by interneurons in the cerebellum to modify the activity of motor neurons These fibers never cross over (decussate) Instead, they ascend on the ipsilateral side of the spinal cord and enter the cerebellum via the caudal cerebellar peduncle Heavy myeslation and located in spinal cord So very susceptible to injury |
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Term
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Definition
somatic musc movement
-travel in wm so all That leave spinal cord will synapse at 1 LMN - 3 major descending and 2 minor paths ° 2-3 neurons in series that start at the brain and end on LMN |
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Term
major and minor descending tracts |
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Definition
MAJOR Rubrospinal tract (driver) Reticulospjnal tract (modifier) Vestibulospinal tract (modifier)
MINOR corticospinal tract Tectospinal tract |
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Term
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Definition
- red nuc roidbrain - travel through w in a series of neurons, synaoses on LMN - devussates jn midbrain - voluntary mkvement |
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Term
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Definition
-retic form (in medulla) to Spink cord -moatly ipsilat -involuntary move
FUNC: -balance and posture -contain inhibitory neurons to prevent excessive response to stimuli |
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Term
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Definition
* vestibular nuc to s Pinal cord * entirely ipsilateral * involuntary
FUNC: -synergy of musc movements, equillinrium, balance -comtaim inhibitory neurons tpnprevemt excessive response to stim |
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Term
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Definition
UPPER MOTOR NEURONS Initiate musc contraction and movement after synapsing on LMN LOWER MOTOR NEURONS Leave the spinal concord at each level to innervate musc
Damage to motor tract wil lcause weakness or paralysis/ paresis Know that animal has moderately sever spinal cord injury |
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Term
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Definition
Func: Initiate musc contraction and movement after synapsing on LMN
Refers to: All neurons in a motor tract except the final neuron which leaves the spinal cord and directly innervates a muscle fiber
Location: Entirely in the CNS (brain and spinal cord) Are in tracts They NEVER leave the spinal cord only synapse |
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Term
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Definition
Func: Leave the spinal cord at each level to innervate musc
Refers to: The final neuron in a motor pathway, which exits the spinal cord and travels via the ventral root to a target musc. Key part of reflex arcs
Location: Start in the CNS, and terminate in the PNS |
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Term
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Definition
UMN can only be injured if spinal cord is injured °If you damage the spinal cord, that is the only way to do damge to UMN (b/c they are independent entities (reflex archs are entirely local
LMN can be injured if - spinal cord is injured OR - the peripheral n in which they travel is injured
° Reflex arc works thorugh LMN so if reflex is not working than you know LMN is affected ° the arc enters and exits locally). In other words, they Always go into the CNS but always come out locally w/out having to go in the brain |
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Term
Sensory tracts and motor neurons |
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Definition
Reflex sensroy neurons synapse on same LMN (directly- monosynaptic, or polysnyaptic)
All motor neurons are in the ventral root, not dorsal |
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Term
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Definition
feedback mech that influence the way a motor tract does its job can be very complicated
The cerebellum and vestibular apparatus provide both excitatory and inhibitory APs through the vestibulospinal and reticulospinal pathways that adjust posture and balance subconsciously that modifies the primary motor impulse in the rubrospinal and corticospinal tracts |
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Term
hindlimb VS forlimb probs |
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Definition
If problem is in front leg C6-T2 is region theres a prob Bc of cervicothoracic emlrgment
If problem is in hindlimbs L4-S2 is prob Bc of lumbisacral enlrgment |
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Term
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Definition
When proprioceptive tracts are damged you see ataxia sign of cp defecits
CP deficits are sensory signs so does not have to do w/ UMN or LMN. motor does not involve proprioception
Proprioception can be local, like in radial n avulsion. BUT can also be more generalized like ataxia (ataxia is a CNS sign indicated by loss of proprioception; ataxia does not apply to PNS issues) |
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Term
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Definition
C6-T2 → Brachial Plexus L4 - S2 → Lumbosacral Plexus |
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Term
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Definition
The spinal nerves from 2-4 different (but adjacent) spinal levels give rise to specific peripheral nerves °radial nerve → composed of C7, C8, T1 °Sciatic nerve → composed of L6, L7, S1
A single spinal segment may provide axons for more than one peripheral nerve EX: subscapular and median nerves have roots in C8 |
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Term
nerves to note (brachial plex) |
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Definition
suprascapular C5,6,7 Subscapular C6, 7 Musculocutaneous C6, 7,8 Axillary C6, 7, 8 Radial C7, C8, T1,2 Median C8, T1,2 Uknar C8, T1,2 |
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Term
nerves to.note lumbosacral plex |
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Definition
femoral L4,5,6 Obturator L4,5,6 Cranial gluteal L6,7,S1 Caudal gluteal L7, S1,2 Sciatic L6,7, S1,2 Pedundal S1,2,3 |
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Term
How do we distinguish between UMN vs LMN damage? |
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Definition
1) Evaluate tone in the musc of the affected limb?
2) Evaluate the reflexes- Rember: LMN are a key part of reflex arc |
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Term
Evaluate tone in the musc of the affected limb? |
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Definition
LMN damage leads to: -decreased tone (flaccid paresis/paralysis); recent injury -Neurologic atrophy (after a week or so)
UMN damage leads to: -Increased tone (spstic paresis/paralysis) *UMN damge tract can be inhibitory so have level of hyperactivity in that musc and will have enhanced reflexes but animal cant voluntraily move muscle but still responds to reflex test (Spastic paralysis) -Disuse atrophy develops over a long time period as the animal no longer uses the limb effectively *These musc will not waste away as quickly but will occur over time
Keep in mind that TONE is a reflex (defined as the static state of a musc)
Loss of tone (flaccid) = neurogenic atrophy increased tone (spastic) = disuse atrophy |
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Term
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Definition
Rember: LMN are a key part of reflex arc
LMN damage leads to -Diminished reflex EX: Loss of reflexes to forelimbs = LMN sign of damage to forelimbs but NOT hindlimbs
UMN damage leads to -exaggerated reflex *Loss of inhibitory inputs by UMN in descending tracts
Damage on green circuit will be a LMN sign and diminished reflexes Damage on blue circuit will be a UMN sign and see exaggerated reflexes |
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Term
ALGORITHM FROM LOCALIZING A LESION IN SPINAL CORD VS PNS |
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Definition
1) Does the animal have a neurologic lesion? 2) What limb(s) are affected? 3) Is there ataxia 4) What reflexes are decreased 5) Consider again what limbs are affected? 6) Consider #4 and #5 together? |
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Term
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Definition
1 limb → likely a peripheral nerve issue -Radial n, schiatic n, tibial n -Will have loss of tone, reflexes in one limb -Cant tell at this point whether it is sensory or motor *If you are only showing proprioceptive signs, you cant really see motor signs -can usually give more time w/ periph n issues
2-4 limbs (bilaterally) → likely in the spinal cord/ CNS |
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Term
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Definition
Does the animal know where its limb(s) are in space? What limbs are affected?
If ataxia is present → lesion is likely in the spinal cord Shows that proprioceptive tracts are damged |
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Term
What reflexes are decreased? |
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Definition
If reflexes in the forelimb are decreased → lesion is in the spinal cord at the cervicothoracic enlargement -Also tracts that pass through the area to the hindlimmb will be affected (usually CNS dz) -This is only if severe enough to damage the n
If hindlimb reflexes are decreased → lesion is in the lumbosacral enlargement
If there is no decrease in reflexes in the limbs → the lesion is between C1-C5 or T3-L3 |
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Term
Consider again what limbs are affected? |
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Definition
Hind limbs only affected → lesion must be caudal to T2 -This is where the last spinal nn for the forelimb enter/ exit -This means the lesion does not affect the motor or sensory fibers above that level and forelimbs appear normal
Forelimbs and hindlimbs affected → lesion must be above T2 b/c it is affecting the sensory and motor tract pathways in ALL legs -NOTE: the severity of signs don't need to be the same in all the limbs. It is whether or not they show signs |
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Term
Consider #4 and #5 together. |
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Definition
If hind limbs ONLY are affected + hindlimb reflexes → lesion is L4-S2
If hindlimbs only affected and NO decreased reflexes → lesion is T3-L3
If forelimbs and hindlimbs affected + forelimb reflexes are decreased → lesion is C6- T2
If hindlimb and forelimb are affected and NO decreased reflexes → C1-C5 |
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Term
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Definition
Ataxia
Proprioceptive decrease in all 4 limbs -Tracts are affected
MAY see paresis/paralysis -If motor tracts affected
Decreased pain -If pain tracts affected
Normal to increased reflexes in all 4 limbs -UMN affected, reflex arcs/LMN for limbs not affected) |
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Term
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Definition
Ataxia
Proprioceptive decrease in all 4 limbs -Effects on tracts, LMN, reflex arcs
MAY see paresis/parayiss -If motor tracts or LMN affected
Decreased pain -If pain tracts affected
Decreased reflexes in formelimbs -LMN affected
Normal to increased reflexes in hindlimbs -UMN affected |
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Ataxia
Proprioceptive decrease in hindlimbs ONLY -Effects on tracts
paresis/paralysis -If motor tracts affected
Decreased pain -If pain tracts affected
Normal reflexes in forelimbs
Normal to inc reflexes in hindlimbs -UMN affected |
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Ataxia
Proprioceptive decrease in hindlimbs only -Effects on tracts, LMN reflex arcs
MAY see paresis/paralysis -If motor tracts or LMN affected
Decreased pain -If pain fibers/tracts affected
Decreased reflexes in hind limbs ONLY -LMN and reflex arcs affected.
Normal reflexes in forelimbs |
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These apply to CNS ONLY: Animals will lose Proprioceptive Motor Pain **tells us severity ** For PNS, usually mild signs bc their susceptibility to injury is lower that in the CNS |
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multinucleated musc cell; each fiber has one neuromusc junc (NMJ) |
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1) Na influx 2) Depolarization 3) Release of Ca2+ -Through voltage gated Ca channels 4) Interaction of actin/ myosin 5) Shortening of sarcomere 6) Na+ channels close and Na+ pumped out 7) Repolarization 8) Ca2+ channels close and Ca2+ pumped into SR 9) Sarcomere relaxes -Once Ca gone |
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made of contractile proteins, actin/myosin arranged in a regular pattern between Z-lines (attachment plates) |
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the area between 2 z-lines; region of myofiber that undergoes a contractile event; the minimal func unit but is the area from Z line to zline (disks) |
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super rich in mitochondria since contraction requires a lot of E. wrap around e. Myofibril at Z-disc; rich in Ca + SR and deliver Ca+ from outside cell, |
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containing Ca2+; stretches between T-tubules along surface of the myofibril; SR deliver Ca from inside cell |
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T-tubules→ deliver Ca+ from outside cell SR → deliver Ca from inside cell |
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THIN FILAMENTS *ACTIN- thin filaments; anchored at Z-line Thin is attached to Z disc and disrupted in the middle *TROPONIN *TROPOMYOSIN
THICK FILAMENTS *MYOSIN- thick filaments; located between actin Thick is attached to titan filament and continuous (not split in middle) |
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*Thin filament *F-actin (filamentous) consists of chains of G-actin (globular) *Has binding sites for myosin (hidden by tropomyosin head) -Prevents interaction *Troponin has high affinity for Ca2+ -Troponin molecules are bound to e. Tropomyosin strand -When Ca is available troponin woll associate w/ it *Troponin and tropomyosin act like inhibitors |
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* Contractile protein that is a homodimer HOMODIMER- 2 molecules coil together to form a tail region w/ 2 head groups
*Head groups are hinged moves back and forth to stick to/release on actin filaments. The heads stick out all the way around.
*Many myosin molecules combine to form thick filament |
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EXCITATION- CONTRACTION COUPLING |
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probably best to draw it out |
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*Sources of E used by musc cells for long and short term contraction *Uses oxidative phosphorylation and glycogenolysis to remake ATP |
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*creatine uses ATP and CK (enz) --> creatine phosphate + ADP -Processes can also be reversed to form ATP. -Therefore, creatine phosphate is an E reserve for musc contraction
* Creatine phosphate allows glycolytic enz to cont making ATP, keeps ATP production maximal Having ADP will keep pathways active in making ATP but hide the phosphate in creatine phosphate
*When at rest, you are going to move towards the right Minimally active so storing E in phosphate bond on creatine phosphate At rest, should have highest [ ] of creatine phosphate *During exercise, CK converts back to ATP and creatine Atp will then be used by myosin in musc contraction |
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FAST TWITCH AKA CONTRACTION COMPONENTS METAB |
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white
short, fast
Larger in size More extensive SR
Anaerobic metab CK |
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SLOW TWITCH AKA CONTRACTION COMPONENTS METAB |
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red
long, slow
Smaller in size Less extensive SR
Aerobic metab glycogen |
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** Once contraction event is over, you need to get rid of Ca. causes musc to relax **
Ca ATPases (pumps) reset the intracellular Ca level by moving Ca out of the cell/ back into SR -E using pumps to pump Ca out of cell or into SR.(he doesn’t care if we know names of channels, but will eventually need to know them for cardio)
*Cell surf pump = plasma memb Ca ATPase (PMCA) *SR pump = sarcoplasmic/endoplasmic reticulum ATPase (SERCA) |
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Frontal Parietal Temporal Occipital Ethmoid (penetrated by olfactory n) Maxilla (upper jaw) Mandible Nasal |
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DOLICHOCEPHALIC: long and narrow Afghans and Greyhounds PROB: smaller eye sockets → have ocular abnormalities
MESATICEPHALIC: intermediate length and width
BRACHYCEPHALIC: shorter nasal compartment, alterations in sinuses/cranial shape Lhasa apso, pugs, bulldog PROB:small nares + long soft palette → resp issues |
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single passageway where the spinal cord enters the skull and becomes the brain. Medulla ends and spinal cord begins |
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certain feat of the ear are found |
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# of teeth, names, and position
Maxillary Side on each side 3 incisors 1 canine 4 premolars (adult) -3 deciduous (juvenile) 2 molars
Mandibular Side On each side 3 incisors 1 canine 4 premolars (adult) -3 deciduous (juvenile) 3 molars
NEED TO KNOW FOR EXAM |
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Rads are not good for looking at brain bc thick skull gets in the way VD/DV can potentially see a mass inside the skull |
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dura mater (closer to skull) *periosteal layer *meningeal layer
arachnoid mater
Pia mater (closer to brain) |
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Periosteal layer (outermost) Meningeal layer |
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reabsorbs CSF that circulates in the subarachnoid space
found in abundance in Falx cerebri and Tentorium cerebelli |
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2 major folds exist in the meninges around the brain |
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composed of dura mater and arachnoid
FALX CEREBRI -In the longitudinal fissure between the cerebral hemispheres -Extends into the space between the L and R cerebral hemisph
TENTORIUM CEREBELLI -In the transverse fissure separating cerebellum from cerebrum -Like a tent over the top of the cerebellum
can find abundance of aracnoid grans |
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The NS is 3 interconnected cyst: |
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1) CNS Brain Spinal cord Located inside skull and vertebral column, covered by meninges
2) PNS Peripheral n Cranial n
3) ANS (autonomic NS) |
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localizing a brain lesion |
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For brain lesions, tend to look for specific signs and try to localize to 3 func regions
1) thalmcortex 2) brainstem 3) cerebellum |
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signs of thalamocortex lesions |
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Sz Behavior changes Motor probs Circling in one direction
b/c cortex + thalamus have many integrated/overlapping func, neuro lesions/injuries in these areas can have similar presentations. |
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divisions of thalamocortex |
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cortex thalamus hypothalamus pineal gland |
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*Most anterior region, usually associated w/ advanced func *Derived from telencephalon (ancestral region) *Three divisions/subdivisions:
1)Cerebral cortex Gray matter is external (folding pattern of telencephalon during development put gray matter on outside and formed several diff lobes)
2)Rhinencephalon Anterior and ventral t cerebral cortex Olfactory portion of brain and limbic syst (emotional responses)
3) Basal nuclei (ganglia) Collection of Nerve cell bodies in NS |
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gyri (gyrus = outward fold) AND Sulci (sulcus = inward fold) |
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cerebral cortex divisions |
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*2 hemispheres on e. Side Via longitudinal fissure R hemisph receives info from L side of body (vice versa) due to decussation
*5 lobes piriform/olfactory lobe internally folded: medial to temporal bone Also have frontal, temporal, parietal, and occipital lobes |
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Frontal: caudal → sensory, rostral → behavior, learning, voluntary movement
Pariteal: sensory and association
Temporal: audition, equilibrium, association
Occipital: visual cortex, association
piriform /olfacotry: olfactory, learning, emotion, memory |
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cerebral cortex white matter tracts |
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White matter of the cerebral cortex contains axons covered w/myelin (oligodendrocytes) Tracts that connect neurons w/in same hemisphere via association fibers EX: Corona Radiata
Tracts that connect cortex to brainstem via projection fibers EX: optic radiations
Tracts that connect hemisphere together via commissural fibers EX: Corpus Callosum |
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regions of rhinencephalon |
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OLFACTORY PORTION Olfactory n (CN1) Olfactory bulb Olfactory peduncles Entorhinal cortex (piriform lobe)
LIMBIC SYST Amygdala Septum Hippocampus |
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inside skull where olfactory n first interact w/ and where preliminary processing event soccur |
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relay collected info into cortex |
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Connected to the cortex (cingulate gyrus), thalamus, and hypothal
Control emotions/behavior
Well described in primates, not so well understood in domestic animals |
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Subcortical collection of gray matter FUNC: modulate voluntary movement signals from cortex |
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composed of 4 nuclei, important in motor func NEED TO KNOW NAMES Caudate nucleus Putamen Globus pallidus Claustrum |
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Derived from diencephalon
Composed of several bilateral nuclei (groups of neurons) -Lateral geniculate nuclei: vision -Medial geniculate nuclei: audition
Receives all sensory info (except olfaction) and projects to specific area of the cortex -Clinically linked w/ cerebral cortex
Gets feedback from cortex and basal nuclei
Some motor func: cranial part of red nucleus (origin of rubrospinal tract) |
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Derived from diencephalon Receives and sends connection to thalamus, limbic cyst, ANS Grouped into several nuclei w/ specific func |
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Heart rate Bp Body temp Water balance Food intake Circadian rhythms Emotions |
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ways the endocrine syst works w/ the NS (hypothalamus) |
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1) NEUROHYPOPHYSIS 2) ADENOHYPOPHYSIS
controls the endocrine secretions of these processes |
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Direct secretion into bs as opposed to synap cleft -Direct secretion into bs and act as hormones
Secrets: neuropeps → oxytocin, vaasopressin (antidieuretic) |
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Release of peptide releasing hormones causes release of pituitary hormones from adenohypophysis
Several diff nuclei in hypothal w/ long axons that extend to pituitary gland and when stim by AP, cause release of 2ndary hormones into bs |
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hormones and their acts on adenohypohysis |
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THYROTROPIN RELEASING HORM (TRH) stimulates secretion of TSH (thyroid stim horm)
CORTICOTROPIN RELEASING HORM (CRH) stim secret of adenocorticotropin (ACTH)
gonatroproin releasing horm (GnRH) stim secretion of FSH and LH
PROLACTIN RELESE HORM stim secretion of prolactin
GROWTH HORM RElEASING HORM (GHRH) stim sec of growth horm (GH) |
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dorsal to thal but not associated w/ hypothal
regulate day/night cyc through melatonin release - serotonin + light stim = melatonin |
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includes pons, medulla oblongata, midbrain
these strutures are: - anatomically continuoous - have many related func (basic control of life supporting activities) -associated w reticular formation |
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*derived from mesenceph *2 portions:
1) SENSORY PORTION → Colliculi Receive visual and auditory signals Visual = rostral reflexes Auditory = caudal reflexes Mediate movement of the head in response to light and sound
2) MOTOR PORTION Contraction of iris musc/pupils: oculomotor n (CN III) Movement of the eye: oculomotor and trochlear n (CN IV) Also abducens n (CN VI) from medulla Gait (caudal part of red nucleus- origin of rubrospinal tract) *remember: thalamus has the cranial part |
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Gives rise to trigeminal n (CN V) -Facial sensation -Masticatory musc move
Tracts in the pons Communicates w/ cerebellum (regulation of movement)
Some nuclei that participate in resp control Centers for integration/control of micturition |
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Unconscious vs conscious propeioception |
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UNCONSCIOUS • path runs to cerebellum • allows involuntary movement • defected tracts cause ataxia • EX: can walk w/o thinking about which joints to flex/extend
CONSCIOUS • paths run to thalamus and cerebrum(cortex) • voluntary movement • defected tracts cause CP deficits • EX: sensing position of limb |
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*derived from myelenceph *very complex region: controls most basic func of life -has cardiovasc and resp involvement so daamge here can cause death *contain nuc of CN 6 and 12 *ascending ras syst --> maintain state of concoiuosness
*relays SENSORY info from sc -temp, pain, tactile, prop *relays MOTOR info from from cortex and bs |
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*complex network of neurons *present in all parts of brainstem (medulla, pons, midbrain, +thalamus) *recieve sensory info from entire NS and projects to cortex via synapses in thalamus *lies at the pinnacle of ARAS |
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reticular formation function |
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*involved in st of arousal/heightened st of consciousness (reason why ts hard to fall asleep if too much goping on)
*locomotion and musc tone (where reticulospial tract originates)
*true pain (retic form is at distal end of poorly defined tracts/spinreticular. active when animal experiences pain)
*reflex processing: v, swallowing, sneezing
*linked to ANS: micturition, defecation, resp, and HR modulation (resp and cardio vasc control) |
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ascending reticular activating syst
send continuous flow of impulses to cerebral cortex: when the impulses pass a certain frequency animal becomes awake (awakening); responsible for level of arousal |
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To differentiate them: the reticular formation is the network, and the ARAS is the series of impulses sent there |
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LESION OF ARAS (brainstem) |
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Lethargy Obtundation Stupor Coma |
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RESP : Specific nuclei in medulla and ponsa re integrated w/ e.other to control inspiration, expiration, breath holding in response to changes in psychological demand
CARDIOVASC: *Part of the ANS
*Cardiac accelerator center (sympathetic) -Inc heart rate (chronotrope +) AND -Contraction strength (inotrope +)
*Cardiac inhibitory center (parasymp) through vagal n -Chronotrope and inotrope
*Vasomotor center: regulated bp -Gets info from baroreceptors -Carotid sinus (CN IX) -Aortic arch (CN X) |
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AKA Flocconodular lobe part of cerebellum that integrated w/ vestibular syst |
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Composed of:: 2 lateral hemispheres A medial vermis
*Latin: “little brain”
*Compares intended movement (info from cortex) to actual musc activity (spinal cord) --> corrects disparities and smoothens movement -uses 3 peduncles (anterior/rostral, medial, caudal)
*tight integration w/ vestibular syst (important for balance)
*we know it picks up lots of info b/c spinocerebellar tracts end here (CP)
*w/o cerebellar output, animal can still walk, just very uncoordinated/ not smooth |
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1) Proprioceptive/Spinal ataxia Spinal cord or brainstem injury to UCP wm tracts -absence of head involvement -sway/wobbliness -abnormal limb stance/gait -circumduction, abduction/adduction/ crossing when animal walks
2) Vestibular ataxia Damage to vestibular syst (ex: brainstem or inner ear) -easiest to recognize (head tilt to side of lesion) -leaning, falling, rolling, cometimes circling, strabismus, nystag
3) Cerebellar ataxia Cerebellum injury/lesions Seeing abnormalities in gait due to a sensory defect -dysmetria (cant control rate/range of steps) -hypermetria (exaggerated step, can often see in prolonged flexion/protraction of limb) -head/body tremors -wide pelvic limb stance -often do not display paresis/CP deficits (UMN intact) --> may help distinguish between spinal ataxia and cerebellar |
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*BAR probably not a brainstem problem. *If showing depression, signs are probably in brain *Brain prob and cranial nerve issues => head tilt, nystagmus, loss of tone
Signs in spinal cord --> ataxia |
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