Term
| What distinguishes paraplegia and quadriplegia in terms of where the injury occured? |
|
Definition
Paraplegia- lower body. lower portion of lumbar system of spinal cord.
quadriplegia-4 both legs arms and fingers. Caused by upper spinal cord injury but futher up near neck area |
|
|
Term
| What is the most common cause of hemiplegia? |
|
Definition
| Stroke. damage to the brain. |
|
|
Term
| Which neurons die off in patients with amyotrophic lateral scelrosis (ALS; lou gehrig's disease) |
|
Definition
| kills motor neurons in lower SC, brainstem, uppoer motor neurons in motor cortex. almost always fatal. |
|
|
Term
| What are the main symptoms of ALS? |
|
Definition
| Weakness, paralysis in hands, feet, limbs, slurred speech, decreased swallowing, breathing, some PTS - death of non motor neurons - decreased memory, cog. |
|
|
Term
| Which neurons die off in patients with parkinson's disease, and how does this affect other neurons? |
|
Definition
| death of neurons in substantia nigra, so decreased DA(dopamine) input to caudate nucleaus and putamen. |
|
|
Term
| What are the main symptoms of parkinson's disease? |
|
Definition
| resting tremor(1 or both hands), muscle rigidty, akinesea,decreased posture/balance, shuffling gait, decreased memory, "frontal lobe" cog problems |
|
|
Term
| Describe one medication and one neurosurgical treatment that can be beneficial to parkinson's patients |
|
Definition
Sinemet, DA agonists, anti-oxidants (free radical scavangers)
Damage globus pallidus (restore balance in basal ganglia)
Thalamus - period high frequency eletrical stimulation - "pacemaker" |
|
|
Term
| Which neurons die off in patients with huntington's disease? |
|
Definition
| death of neurons in caudate nucleus, putamen |
|
|
Term
| What are the main symptoms of huntington's? |
|
Definition
| chorea, restlessness, akinesia, reduced memory, cog- “frontal lobe” problems |
|
|
Term
| How does huntington's differ from parkinson's disease and ALS in terms of it's most common age of onset? |
|
Definition
50% getting it?????????
30s 40s 50s
why 50/50 has bad dominant gene on one chromsome, and has good chrosome, so it's a crap shoot?????? |
|
|
Term
| what causes huntington's disease? |
|
Definition
| dominant gene on chromosome 4 CAG |
|
|
Term
| what is endogenous circadian rhythm, and what brain area is most curcially involved? |
|
Definition
| sleep/wake, body temp, light helps reset clocks; suprachiasmatic nucleus (hypothalamus) |
|
|
Term
| What is melatonin, where does it come from, and what does it do? |
|
Definition
increases sleepiness
pineal gland (input from retina)
To fall asleep |
|
|
Term
| Describe how EEG activity is different, in the 5 stages of sleep |
|
Definition
1. Theta waves – 3.5- 7.5 Hz
2. Theta and sleep spindles, K complexes
3. Delta waves (<3.5 Hz) -20-50%) (deep slow wave sleepiness)
4. >50% delta (deep slow wave sleepiness
REM sleep- beta, alpha, theta, dreaming 80 |
|
|
Term
| besides being low freq, how are the EEG waves in slow wave sleep different from the waves in other stages? |
|
Definition
| Bigger waves. Higher amplitude.signifying fewer neurons are active. neurons taht are firing, firing together. your body slows down. |
|
|
Term
| Describe motor activity during REM sleep and the physiological reason for this. |
|
Definition
motor neurons inhibited (by pons, medulla)
eYE MOVEMENTS-OXYGEN FOR CORNEAS? |
|
|
Term
| Describe how a typical person would cycle through the sleep stages in a night's sleep, and the general pattern of deep sleep versus REM sleep during the night. |
|
Definition
few minutes in all stages, then fair amount of time in 4. then cycle back to REM sleep, woke up here have dream. cycle back down. cycle back up to REM, then woke up. fell back to sleep. second half of night. less tendency to go back to stage 4 sleep. then long REM period. woke up again. then go to REM period. then 2, wake up.
First ½ night -more deep sleep (stage 3-4)
last ½ of night – more REM sleep. |
|
|
Term
| What distinguishes the sleep stage make up of infant's sleep |
|
Definition
| lots of sleep – greater % of REM sleep |
|
|
Term
| What brain areas and NTs promote wakefulness and alertness? |
|
Definition
(pons and mixbrain)Glutamate
(basal forebreain waking - related neurons) Ach ramping up brain.
Hypothalamus --orexin (excitatory waking related)
NE
Adenosine inhibits- builds up during day -> basal forebrain waking - related neurons |
|
|
Term
| Which brain areas and NTs promote sleep? |
|
Definition
GABA inhibitory (hypothalamus-> sleep related neurons --gaba--> thalamus cortex)
Melatonin
5-HT (seratonin) |
|
|
Term
| When are PGO waves produced, and which brain areas produce them? What are some other brain areas that are active during this sleep stage? |
|
Definition
Produced during REM sleep; Pons, lateral geniculate, occipital cortex;
increased activity in inferior temporal lobe(visual areas) inferior parietal lobe, amygdala decreased activity(low) - prefrontal cortex |
|
|
Term
| Which NT promotes REM sleep? |
|
Definition
Ach promotes REM
5-HT interrupts REM |
|
|
Term
| wHAT FUNCTIONS MIGHT SLOW-WAVE SLEEP AND rem SLEEP SERVE? |
|
Definition
| decreased overall activity (many neurons" resting" -can replenish NTs), but activity is synchronized – may help str some memories |
|
|
Term
| In persons who are deprived of sleep, when they do sleep how does it differ from a normal night's sleep? |
|
Definition
| when sleep occurs, increased stage 4 and REM |
|
|
Term
| What are some approaches to treating people with insomnia? |
|
Definition
| treat their symptoms. treat the pain, stress, or anxiety disorders. get to root cause. |
|
|
Term
| What is sleep apnea, and why is it harmful? |
|
Definition
| Temporarily stops breathing, then gasp for air. increased risk in obese men. |
|
|
Term
| Describe two symptoms of narcolepsy. Which NT has been implicated in this disorder? |
|
Definition
Sudden attacks of sleepiness during the night. attack muscles. sleep paralysis.
Orexin |
|
|
Term
| Why is our body temp kept at a fairly high set point? |
|
Definition
| muscles more efficient, easier to warm body up than cool it down. |
|
|
Term
| Which brain area is more crucial in regulating body temp? how does it do this (where does it receive input from, and where does it send output to)? |
|
Definition
posterior hypothalamus
receive input from temperature receptors in the skin and spinal cord
seek shelter |
|
|
Term
| Distinguish between what causes osmotic thirst and hypovolmeic thirst. |
|
Definition
Osmotic thirst -ingest solutions like Na- causes water to leave cells-- osmosis
Hypovolemic thirst-caused by loss of body fluids from bleeding, sweating, vomiting, diarrheat, menstruation |
|
|
Term
| Which brain area near the third ventricle is activated in osmotic thirst? how does this happen? where do neurons in this area send output and what are the effects of this output? |
|
Definition
| OVLT; neurons detect their own H2O leaving; axons go to lateral preoptic (hypothalamus) thirst and drinking |
|
|
Term
| Which structure releases antidiuretic hormonoe, and what effect does this hormone have? |
|
Definition
| Kidneys causes kidneys to excrete less H2O into urine. |
|
|
Term
| Which hormones are involved in hypovolmeic thirst? |
|
Definition
| Increased angiotensisn ii |
|
|
Term
| What does the process of transduction involve? (generally speaking) |
|
Definition
| change in receptor's potential likelihood of firing AP. If changing eletrical potential, changing that receptor AP. |
|
|
Term
| Give examples of how the process of reception, transduction, and coding operate in the visual or auditory systems. |
|
Definition
|
|
Term
| Describe the functions of various muscles in the eye (in the iris, attached to the sclera, and lens). |
|
Definition
. Sclera- white part of eye. (Not involved in vision, no light passing through. Important, lots of muscles attached to sclera. ) eye movements, cornea, iris-muscles control size of pupil, lens, virteous humor, retina, fovea, blind
Lens- behind pupil and iris. Light passes through. Muscle fibers attached to lens. Important because so it can change shape how far away the object is. |
|
|
Term
| What is the fovea and why is it important? |
|
Definition
| Region of retina recepters are densely packed especially cones. acute vision. They connect to a single bipolar cell which turn connects to a single ganglion cell which has an axon to the brain. |
|
|
Term
| Why is there a blind spot (in the retina, and in our vision)? |
|
Definition
| Any large energy hit in that region is not responding to the light energy. That eye is not seeing what's that producing htat light. |
|
|
Term
| Distinguish between the types of visual stimuli the rods and cones best to |
|
Definition
Receptors Rods Cones
Number More Less (cones provide 90% of all input that's processed in the brain.)
Location Through out retina Most concentrated in or near fovea. Far away vision, rods
Dim light Sensitive Insensitive (rods responsible for night
Detail Not too good Good
Color Insensitive Sensitive |
|
|
Term
| What is the main input to, and out from, the ganglion cells in the retina? |
|
Definition
detail?
start with rods and cones, (horizontal)communicate with bipolar, then ganglion. Axons of ganglion cells come to gether to form big optic nerve. |
|
|
Term
| What and where are photopigments and how are they affected by light energy? |
|
Definition
| Photopigments- 2 parts, opsin (vision) and retinal- vitamin a – rods: 1 type – cones: 3 types of opsin) (each single cone has 1 of the 3) |
|
|
Term
| How are the electrical potentials of rods and cones, and bipolar cells affected when light is present? |
|
Definition
Dark- //
Bent attached. (op)----(ret)// when in bent, stays attached to opsin. Key chemical: cyclic GMP. Holds Na+ gates open. Receptors (rods) depolarized.-> bipolar cell not active.(-> Inhibitory).
Light-
(op)----ret
Retinal straightens detaches.
Enzyme activated (inside rod or cone) Cylic GMP decreases, Na+ gates close.
Receptors hyperpolarized not going to AP
Inhibition decreases. Bipolar increase |
|
|
Term
| What is the main pathway of axons traveling from the retina back to the primary visual cortex? |
|
Definition
|
|
Term
| What brains tructures other than the thalamus and visual cortex receive visual input? |
|
Definition
|
|
Term
| What and where are optic radiations? |
|
Definition
| axons that spread out into white matter; later geniculate nucleus |
|
|
Term
| How would damage to the right optic tract affect vision in two eyes? |
|
Definition
| Left eye will be fine. Right eye: should be wiped out. |
|
|
Term
| How would damage to the left lateral geniculate nucleus affect vision? |
|
Definition
| Won't be able to see well in both eyes on the left visual field side. |
|
|
Term
| HOw would damage to the optic radiations in the right temporal lobe affect vision? |
|
Definition
| carries info of upper portion of visual field: blindness of left upper quadrant of both eyes. |
|
|
Term
| What type of cell does the trichromatic theory of color vision apply to, and what is the physiological mechanism? |
|
Definition
| cones- 3 opsins: describes what's going on at level of cones of the retina. Each cone has one of the three types of opsin. Best at absorbing different wave length of light. |
|
|
Term
| What type of cell does the opponent process theory of color vision apply to, and what is the physiological mechanism? |
|
Definition
| Bipolar cells; perceives color on a continuum from red to gree, another form yellow to blue, and another from white to black. |
|
|
Term
| What is color constancy, and what part of the cortex is involved? |
|
Definition
| still recognize different colors despite change in lighting (green tinted light bulb) neurons; V4 cortex |
|
|
Term
| What is the most common form of color blindness (color vision deficiency) and why is it much more common in males than in females? |
|
Definition
| Can't see red from green because their long and medium wave cones have the same photopigment instead of different ones. The gene causing deficiency is the X chromosome. |
|
|
Term
| What distinguishes parvocellular ganglion cells from magnocellular ganglion cells (and parvocellular and magnocellular cells in the LGN)? |
|
Definition
Parvo-most input from cones (through bipolar cells) color, detail.
Magno- most input from rods- moving stimuli, overall shape, brightness
(also parvo (get input from parvo cellular ganglions) and magno cells (get input from magnocellular ganglion.) |
|
|
Term
| Describe the main components of the three visual pathways (for perception of motion, color and brightness, and detail/form)? |
|
Definition
Movement- Magno cells in retina/thalamus- V1 (first destination in cortex, that process visual information)- V2 (infront of V1 primary visual cortex do more processing of information that come from magnocellular system. Then send axon forward and communicate with neurons in middle part of temporal lobe)- middle temporal- motion parietal – where things are, maps of world – use to guide movement.
Motion blindness- can't see smooth movement.
Color and brightness- color->parvo. Brigthness-> magno..(achromatopsia)...Parvo/magno- V1(different neurons than visual pathway)- V2- V4( some neurons involved in color constancy)- posterior temporal area.
If damage in second pathway called achromatopsia- color/vision. Defeicit of color vision.
Detail/form -mostly Parvo – V1-V2-V4- inferior temporal lobe- what things are
Damage- visual object agnosia- lack of knowledge of visual objects
Prosopagnosia (faces) – right hemisphere.
Part -----whole
left hem.....right hem.. |
|
|
Term
|
Definition
| damage in the cortex, V4. color/vision. Defeicit of color vision. |
|
|
Term
| What is visual object agnosia and prosopagnosia, and what parts of the brain are likely to be damaged in patients with these disorders? |
|
Definition
Agnosia- lack of knowledge of visual objects/animals. recognize by other senses (damage to temporal cortex/shape path)
Prosopagnosia- (faces) – right hemisphere. Third visual pathway. (damage to inferior temporal cortex/right hemi) |
|
|
Term
| Distinguish between the left and right hemispheres' abilities to process visual parts/details versus visual wholes. |
|
Definition
Left hemisphere of the brain can perceive parts.
right hemisphere of the brain can perceive whole.
Damage in the left hemisphere can draw wholes.
Damage in the right hemisphere can draw parts. |
|
|
Term
| What is neglect, and what area of the brain is most often damaged in patiens with this disorder? |
|
Definition
ignore left side of space (visual), also left auditory, tactile stimuli, left side of own body damage- right inferior parietal.
(right hemisphere) |
|
|
Term
| Give an example of a critical period in some aspect of the development of vision. |
|
Definition
Early in life when individual needs visual experience in order for visual system to develop normally.
Also critical periods for developing depth perception (need input from both eyes), motion perception, pattern perception (horizontal, vertical, diagonal, complex patterns). |
|
|
Term
| What can be helpful in some children with amblyopia (lazy eye)? |
|
Definition
| Humans- amblyopia (lazy eye) put patch over good eye. Lazy eye can get worse and worse. |
|
|
Term
| Which characteristics of soundwaves are loudness and pitch related to? |
|
Definition
Loudness -amplitude of sound wave – decibles.
Pitch -freq of sound wave – hertz – cycles per second (hz) |
|
|
Term
| Why are the hammer, anvil, and stirrup needed? |
|
Definition
| When sound waves strike the tympanic membraine they cause it to vibrate that convert the sound waves into stronger vibrations in the cochlea. |
|
|
Term
| Describe the structure of the cochlea, and what happens when soundwave energy is transfered into it. |
|
Definition
| A snale like structure displace the hair cells along the basilar membrane in the cochlea. |
|
|
Term
| What are the receptors in the auditory system, and how are they affected by soundwave energy? |
|
Definition
| Hair cells; displace the hair cells. |
|
|
Term
| Where do axons from cochlea go to (in the brain)? |
|
Definition
| Medulla (cochlear nucleus) |
|
|
Term
| What is the pathway of auditory info from medulla up to the primary auditory cortex? |
|
Definition
| Cochlear Nucleus (medulla)--most crosses over to...->superior olive (medulla) → inferior colliculus(sudden loud sound, look towards it)-> thalamus medial geniculate nucleus. |
|
|
Term
| What is one function of the inferior colliculus (hint: involves responding to an auditory stimulus)? |
|
Definition
| Look towards a sudden loud sound |
|
|
Term
| What is the primary auditory cortex, and how are its neurons organized in terms of the type of auditory info they respond to? |
|
Definition
| MGN->Primary auditory cortex- tonotopic maps different neurons respond to different frequencies. ?????? |
|
|
Term
| What mechanisms operate in the cochlea to code for the pitch and loudness of low, med, and high freq soundwaves? |
|
Definition
Low freq- ipolar neurons produce Aps at same frequency (rate of firing).
Med freq--combo of Aps from diff bipolar neurons add up to freq
high freq-high freqs peak close to base (near stirrup) lower freqs- closer to end (apex) loudness – rate of firing of neurons at point where peak of wave hit. |
|
|
Term
| How do we localize where a sudden-onset sound came from? |
|
Definition
| diff in time of arrival L and R ear. |
|
|
Term
| How do we localize where a high-freq continous sound is coming from? |
|
Definition
Place theory- Where on the basilar membrane does the peak of the traveling wave hit? Very high freqs peak close to base (near stirrup) lower freqs- closer to end (apex) loudness – rate of firing of neurons at point where peak of wave hit.
difference in loudness at 2 ears sound at side biggest difference. |
|
|
Term
| Which structures in the inner ear are the vestibular organs, and what kind of info do they provide to our brains? |
|
Definition
saccule, utricle and three semicircular canals.
Saccule- translates head movements
utricle- stimulate cillia
canals- Hair (cell) → Bipolar (cells) –(Vc nerve)--> Vestibular (sometimes go to spinal cord) (nucleus medulla) → midbrain, pons (eye movement) cerebellum posture and balance |
|
|
Term
| Which brain structure receivews vestibular input from the inner ear, and where does it send output? |
|
Definition
Hair cell
Hair (cell) → Bipolar (cells) –(Vc nerve)--> Vestibular (sometimes go to spinal cord) (nucleus medulla) → midbrain, pons (eye movement) cerebellum posture and balance |
|
|
Term
| What types of receptors respond to pain and temperature (in the skin)? |
|
Definition
|
|
Term
| Where are kinesthetic receptors, and what kind of info do they provide? |
|
Definition
Muscles and tendons
– position and movement of body parts. |
|
|
Term
|
Definition
| skin area connected to a single sensory nerve. |
|
|
Term
| What distinguishes the two somatosensory pathways, in terms of the types of info they convey; and what are the main components of these two pathways? |
|
Definition
1. light touch, pressure, kinesthesia.
2. Pain and temperature.
light- receptors → dorsal root ganglion (cluster of neurons outside of CNS)(DRG)--(SC dorsol columns—medulla crossing-->medulla dorsal column nuclei->thalamus-> primary somatosensory cortex (parietal lobe) -body maps
Pain- (neurons)Receptors (located in skin)-> DRG(stops just outside of spinal cord)dorsal root ganglion—substance P (glutamate) -->SC gray matter (dorsal horn)---UP SC towards to dorsal crossing-->thalamus(2)-->(what did it touch,body position, where body the painful stimulus occured) somatosensory cortex-->cingulate gyrus (middle of brain, on top of corpus callosum) |
|
|
Term
| Where is the primary somatosensory cortex, and in what sense does this cortex contain a number of different "body maps"? |
|
Definition
| Parietal lobe; along each stripe of somatosensory cortex, diff subareas respond to diff areas of the body. |
|
|
Term
| How might the cingulate gyrus contribute to our experience of pain? |
|
Definition
| omatosensory cortex-->cingulate gyrus (part of the limbic system, emotional processing.) if loved ones shocked, somatosensory is dormat, but cingulate gyrus was active. |
|
|
Term
| Which new NT are released in response to intensely painful stimuli? |
|
Definition
|
|
Term
| What is the gate theory of pain, and what is the physiological mech involved (hint: involves the periacqueductal gray area) |
|
Definition
Gate theory- pain signals from body entering through “gate” in SC, but signals coming down from brain can narrow the gate – less pain signal gets through and goes up to brain.
Pga (2) → Spinal cord- inhibits sub P release (less substance P= less signal)
PGA->Medula l^ |
|
|
Term
| Describe three types of situations in which endorphins are released? |
|
Definition
Pain (inescapable)
Antipation of pain
Naloxone (blocks endorphine receptors and blocks effects of endorphine)
Inhibits further pain |
|
|
Term
| What are the main types of taste receptors? why might we have developed these particular types of receptors? |
|
Definition
Clockwise...
Sour sweet salty bitter (back)
To detect dangerous chemicals. sweet mean it's good and nutritious |
|
|
Term
| What is a feature of taste receptors that distinguishes them from visual and auditory receptors. |
|
Definition
| taste buds (papillae) skin cells |
|
|
Term
| What part of the brain receives taste input from the tounge? |
|
Definition
| Oribital prefrontal cortex |
|
|
Term
| How could a food's taste influence appetite and eating (neuroanatomically) |
|
Definition
| eceptors(from tounge) --3 cranial nerves-->solitary nucleus (medulla) → pons ->hypothalamus (hunger-feeding. Pons-> thalamus-> somatosensory (sense of touch) cortex. Pons-> gustatory-> orbital prefrontal cortex |
|
|
Term
| Name two regions of cortex that receive taste input |
|
Definition
| Somatosensory cortex and primary taste cortex |
|
|
Term
| Where are olfactory receptors located and how are they activated? |
|
Definition
Olfactory cells which line the olfactory epithelium area in the rear of the nasal air passages.
When an odor attaches to the receptor |
|
|
Term
| What fact about olfactory receptors (as a whol) distinguishes them from the receptors in other sensory systems? |
|
Definition
| Unlike other sensory information, olfactory information does not go to the midbrain or thalamus. Instead, it passes directly to the cerebral cortex by the olfactory bulbs. |
|
|
Term
| What brain areas receive olfactory input? |
|
Definition
| receptors (olfactory)-> olfactory bulb –olf tract → pyriform cortex → hypothalamus. Pyriform cortex → orbital prefrontal cortex |
|
|
Term
| Where are lower motor neurons located, and how do they influence muscle fibers? |
|
Definition
|
|
Term
| What causes a muscle fiber to contract? |
|
Definition
| Calcium to be released from storage sites |
|
|
Term
| Distinguish between the types of movements controlled by the lateral, ventromedial, and corticobulbar motor systems. |
|
Definition
Lateral sys-independent movements of fingers, hands, arms, toes, feet, legs. Controlls in a very precise way. Typing on keyboard-lateral system
Motor cortex-(upper motor neurons controlling, fingers, hands etc)=--medulla cross over--->SC ventral horn-->muscles. Medulla cross over-> lateral corticospinal tract.
Rubrospinal tract- red nucleus (tegmentum)-> SC
Ventromedial system- whole body movements- neck shoulders, trunk, hips
Ventro corticospinal tract-
Motor cortex (neck etc)- medulla only some cross---> SC-->muscles
Vestibulospinal tract- vestibular nucleus (medulla) → SC
Tectospinal tract Visual--> Tectum. Auditory → tectum----> SC
Corticobulbar system- movements of the head area, mouth, and face.
Motor cortex (face, lips, tongue, throat)---> cranial nerve nuclei (medulla, pons)---> mouth, face, etc.
Additional structures/areas in motor system – premotor cortex and supplementary motor area- selections and initations of motor program- movement sequences → primary motor cortex PET scan studies – imagine movement |
|
|
Term
| Which pathway would be most involved in standing up and sitting down? |
|
Definition
|
|
Term
| What path way would be most involved in talking? |
|
Definition
|
|
Term
| What pathway would be most involved in typing? |
|
Definition
|
|
Term
| Where does the lateral corticospinal tract begin and end? why is it called "lateral" |
|
Definition
Begins in primary cortex to the spinal cord.
Lateral tract controls muscles in the lateral parts of the body; hands and feet |
|
|
Term
| Why do upper motor neurons in the lateral system mainly control movements on the opposite side of the body? |
|
Definition
| displaces the ipsilateral control |
|
|
Term
| Describe the pathways of the three main tracts in the ventromedial system |
|
Definition
Ventro corticospinal tract-
Motor cortex (neck etc)- medulla only some cross---> SC-->muscles
Vestibulospinal tract- vestibular nucleus (medulla) → SC
Tectospinal tract Visual--> Tectum. Auditory → tectum----> SC |
|
|
Term
| Which part of the brain (other than the cortex) does the corticobulbar system involve? |
|
Definition
| cranial nerve nuclei (medulla, pons)---> mouth, face, etc. |
|
|
Term
| What are the two areas of frontal lobe cortex that communicate with 3 motor systems, and what functions do they contribute to? |
|
Definition
| premotor cortex and supplementary motor area- selections and initations of motor program- movement sequences → primary motor cortex PET scan studies – imagine movement |
|
|
Term
| Describe the main inputs and outputs of the cerebellum, and indicate where the inputs entere the cerebellum, and where the outputs leave from. |
|
Definition
Inputs (kinesthetic) SC
premotor cortex and supplementary motor area- selections and initations of motor program- movement sequences → primary motor cortex PET scan studies – imagine movement
Oututs thalamus( → cortex), vestibular and red nucleus.
cerebellar cortex –axons white matter--> deep nucleus –axons--> thalamus, etc. |
|
|
Term
| Where are Purkinje cells located, how are they organized, and how do they influence other neurons in the cerebellum? |
|
Definition
Cerebral cortex.
flat (two dimensional) cells in sequential planes, parallel to one another. APs in paralel fibers excite Purk cellsafter another. each cell then transmits inhibitory messenge to cells in the nuclei of the cerebellum -> deep nucleus. |
|
|
Term
| Why does the finger-to-nose test require the contribute of the cerebellum? |
|
Definition
| Trouble with initial rappid movement |
|
|
Term
| Describe the types of timing functions the cerebellum contributes to. |
|
Definition
timing of muscle contractions, ballistic movement – finger-to-nose test.
Eye movements- saccades (ballistic eye movements.
Use visual feedback to guide and control movement- line tracing
help maintain posture and balance
other timing funcitons – rhythmic finger tapping, estimating short time intervals |
|
|
Term
| Which areas of the cortex provide much input to the basal ganglia (caudate nucleus and putamen)? |
|
Definition
|
|
Term
| How does the substantia nigra influence the functioning of the caudate nucleus and putamen? |
|
Definition
| Sends dopamine releasing axons to the caudate and putamen; can be a cause to parkinsons |
|
|
Term
| How do the basal ganglia indirectly influence the functioning of neurons in the frontal cortex? |
|
Definition
| planning sequences of behavior for certain aspects of memory and emotianal experiences. |
|
|
Term
| What is akinesia, and what could cause it? |
|
Definition
Decrease self initiated movement
damage to excitatory circuits |
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Term
| How could basal ganglia dysfunction or damage cause tics or tremors? |
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Definition
| Death of neurons in substantia nigra; loss of control speech, movement, and posture. |
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Term
| Unlike the three main motor systems, the cerebellum and basal ganglia do NOT send output directly to the____ |
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Definition
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Term
| Which glands secrete aldosterone, and what are the effects of this hormone? |
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Definition
| Adrenal glands; kidneys to excrete less Na into urine. |
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Term
| What is conditioned taste aversion, and which brain areas contribute to this phenomnenon? |
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Definition
eat new food → get sick → avoid in the future
Brain structures – solitary nucleus and amygdala |
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Term
| How do glucose and insulin levels influence hunger? |
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Definition
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Term
| Describe one physiological mechanism involving the stomach that reduces hunger |
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Definition
| stretch receptors (hypothalamus, somatosensory cortex) |
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Term
| Provide two examples of the effects of damaging different parts of the hypothalamus on eating and weight gain/loss. |
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Definition
Multiple nuclei in the hypothalamus: arcuate, paraventricular( damage → overeating, weight gain), lateral (damaging → undereating, weightloss)
outputs from lateral hypothalamus: prefrontal cortex (food-seeking plans/ behaviors), nucleus accumbens (reinforcement circuit), solitary nucleus (influences taste/flavor exp), autonomic NS |
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Term
| Where are neuropeptide Y and leptin, and how are they related to hunger? |
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Definition
NT Neuropeptie Y(visceral adipose tissue )- tends to increase appetite, increase hunger., ghrelin- (increase hunger) ; CCK, GABA (decrease hunger)
Hormones: leptin (fat cells), insulin: both decrease hunger. |
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