top

towards the head

below

towards the feet

impulses from peripheral receptors to spinal cord

going towards (spinal column)

relay signals from spinal cord and CNS to periphery

going away (from spine)

think exit or efflux

relay info b/n periphery and the CNS

cONSISTS OF: cell body or soma

dendrites

nerve fiber or axon

3 Na out

2 K in

resting potential is negative (-90mV)

threshold potential

afferent nerve fiber

myelin

innervate skeletal muscle

proprioception

afferent nerve fiber

myelin

tactile sensory receptors (Messner's corpuscles, hair receptors, pacinian corpuscles)

touch, pressure, proprioception

afferent nerve fiber

myelin

muscle spindle motor neuron (tone)

fine tuning (where a-alpha is more large movements)

afferent nerve fiber

myelin

FAST pain, touch tempature

nerve fiber

B

afferent nerve fiber

myelin

preganglionic autonomic fibers

nerve fiber

C

NO MYELIN

SLOW pain, touch, tempature, postganglionic sympathetic ANS fibers

insulator

prevents flow of ions across nerve membranes

interuption of myelin

ions can flow freely b/n nerve fibers and extracellular fluid here

action potentials are conducted from node to node

JUMPING

succesive excitation of nodes of ranvier by impulse that jumps b/n sucessive nodes

increases velocity of nerve transmission

conserves energy bc only nerves of ranvier depolarize

depolarization only @ nodes little energy is needed for reestablishing Na/K conc differences

chemical mediators that are released into synaptic cleft in response of action potential at nerve ending

release of all NTs is voltgage dependent

requires CA and energy

excitary/inhibitory

mainly EXCITATORY NT in CNS

widely distrubutes but concentrated at

-hippocampus

-outer layer of cerebral cortex

-substantia gelatinosa

CA ion dpendent process

terminated by high affinity NA dependent uptake

Iontropic glutamate receptors: ligand-gated channels (mostly NA)

undergo confirmational change to open receptors

Metabotropic glutamate receptors: transmembrane receptors linked to guanine (G) proteins

triggers second messnger

major INHIBOTORY Nt in CNS

as many as 1/3 of all synapses are GABA

2 molecules of GABA bind to the receptor, CL channel opens---becomes hyperpolarized (more resistant to neuronal excitation)

EXCITATORY (CNS and ANS)

INHIBITORY (ANS)

Nicotinic receptors: ligand gated ion channels (like NMJ)

Muscarinic receptors: Gprotein

INHIBITORY

50% of catecholamines

high conc in basal ganglia

may act on dopamine-sensitive adenylate cyclase

INHIBITORY (CNS)

EXCITATORY (ANS)

large amts in reticular activating system and hypothalamus

INHIBITORY (CNS)

EXCITATORY (ANS)

present in reticular activating system

INHIBITORY NT in spinal cord

increases Cl conductance

Endorphins

(and enkephalins)

EXCITATORY

secreted in thalamus, hypothalamus, brainstem and spinal cord

excitatory nt for descending pathways that inhibit transmission of pain

INHIBITORY

high conc in brain, profound effects on mood and behavior

INHIBITORY

high conc in hypothalamus, reticular activating system

cAMP may serve as 2nd mess

0.3-0.5 ms

time to release NT, diffusion of NT, binding/acting NT

decrease in # of discharges by postsynaptic membrane

act as a protective mechanism (seizure)

exhaustion of NT stores in synaptic vesicles

Increased responsiveness after rest preceded by repetitive stim

increased release of NT due to enhanced perm to CA

short-term memory ?

increased excitability

hyperventalation can cause seizure w ph 8

DK acidosis

with a ph 7 decrease in neuronal acitivity--coma

Seperates frontal (primary motor area)

Parietal (primary somesthetic area)

motor: location of pyramidal or betz cells

premotor: controls motor cortex

prefrontal: selection of behavior patterns

contralteral side of body

somatosensory=somesthetic cortex

contralateral side of body

say words

infaract here severe aphasia

make sense w/speech

infaract here complete word salad

mostly regulate INHIBITORY motor impulses

NT: dopamine (-), GABA (-)

balance of agonist and antagonist muscles

know bc huntingtons (chorea) and Parkinsons (rigidity)

know bc with these diesases there is lose of inhibition which shows muscular side effects

on top of brainstem, relay system

all sensory info (except olfactory) must go through thalamus then to cortex

cingulate gyri functions w limbic system

emotions and behaviors associated w emotions

brainstem

midbrain

tectum, tegmentum, cerebral peduncles

(auditory and visual info relay)

descending cortical motor tracts

control movement

(substantia nigra)

brainstem

ponds and medulla

maintains ALL unconcious activity

regulation of BP, breathing, equilibrium, feeding reflexes

brainstem

reticular activating system

all through medulla, pons, midbrain

excitatory and inhibitory effects

determines overall level of CNS activity

wakefulness, sleep, attention

turns on cortex

small lesion here results in coma

cordination of fine skeletal muscle activities

ex: posture, equilibrium, typing, running

spinocerebellar pathways are the fastest in the body

w/o could still move but very uncordinated, unbalanced

"drunk test" test cerebellum

dura

|

arachnoid

|

pia (connected to brain)

spinal cord meninges (membrane)

start at the cord

pia

|

arachnoid

|

dura