vibration of the basilar membrane causes slideing of steriocillia against the tectorial membrane.

when the steriocillia move towards the largest steriocillium, K channels open

the influx of K depolarizes the hair cell, resulting in eventual increase in Ca influx, and release of glutiamate to the auditory (cochlear) nerve

paravertibral ganglia (sympathetic trunk) lie next to the vertibral column (one per side

prevertibral chain forms one plexus in front of the aorta.

reuptakes NE back to the presynaptic neuron. 

inhibited by cocaine, tricyclic antidepresents. 

after uptake, NE is metabolized by MAO which becomes deaminated derivatives

a pump that is NOT sensative to cocaine

brings NE back to postsynaptic neuron.

after uptake into the postsynaptic neuron, NE is metabolized by COMT which becomes normetanepherine

at what temperature is thermoregulation lost?

increase secretion of thyroid and epinepherine

vasoconstriction

vasodilation

decreased muscle tone and activity

less thyroid hormone and epinepherine

decrease apetite.

what signals satiety?

the ventromedial (bottommiddle hypothalamus).  lesions cause hyperphagia (fullness)

but there is no receptor for calories consumed.

Leptin: counteracts neuropeptide Y.  (low leptin = fat, high leptin = no effect)

PYY: might hold the key, still being researched

Inhibitory neurotransmitter

Diazepam enhances GABA (relaxes muscles)

inhibits spinal reflexes

strychnine/tetanus mess with glycene

excitatory transmitter plays roles in seizures/neurodegenerative disseases

researched

felbamate ( antiepileptic drug) blocks NMDA receptor of GLUTamate

natural product (Pavulon)

competative neuromuscular blockers of ACH

causes paralysis without loss of consciousness

"depolarizing neuromuscular blocker"

1.) stimulates cholinergic receptors

2.) desensitization of the receptors

causes paralysis without loss of consciousness

prevent hydrolysis of AC

low: raise muscle tone/spasms

High: paralysis

disease of # & sensitivity of cholinergic receptors on muscle, results in muscle weakness.

Neostigmine & Pyridostigmine (ACE inhibs) treats by raising AC

inhibits ACE at motor end plate

symptoms:

1.) muscle spasm

2.) paralysis due to depolarization of neuromuscular blocade b/c high AC

Benzodiazepams

(EG) Diazepam

acts at spine/brain to enhance GABA

when Benzodiazepines bind to separate sites on GABAa, more Cl influx = stronger hyperpolarization occurs

treats muscle spasms

(acts at CNS to effect PNS)

an analog of GABA acts at GABAb to inhib release of excitatory transmitters (Glut/Aspartate).  treats spasms from MS/spine injuries

(acts at CNS to effect PNS)

inhibits CA from Sarcoplasmic Reticulum.

treats spasticity, and best for treating malignant hyperthermia

also treats neuroleptic malignant syndrome

Convulsant (rat poison)

acts as antagonist at glycene receptors at CNS

countered by Diazepam

released by Clostridium Tetani

prevents release of Glycine from Renshaw cells in spine

causes tetanus/convulsions

treatment: diazepam/antimicrobial

innervates the extrafusal muscle fibers that generate force

cell body located in ventral horn, get comands from descending pathways and spinal reflex circuits.

innervates intrafusal muscle fibers. 

cell body located in ventral horn of spine

stretch receptors

nuclear chain fiber: monitors muscle stretch

nuclear bad fibers: monitors stretch rate.

muscle spindles wrap around intrafusal fibers

(rubber band)

Golgi Tendon Organs at tendons of muscles monitor.

the tendon organ has axcess to antagonist muscle.  if its too heavy, golgi organ inhibits the muscle and activates the antagonist.

emotional dissorder

Posative symptoms: halucinations

Negative symptoms: sad

treatment: thorazine/haldol/clozapine

mechanism: high dopamine inhibits control of limbic

low Seratonin/NE

lithium for bipolar

MAO inhibitors

Tricyclics (prozac)

1.)light

2.) cis retinal to trans retinal, no longer can inhibit opsin, retinal pops off

3.) opsin binds to transducin (G protein), activates phosphodiesterase

4.) phosphodiesterase hydrolizes CGMP (low CGMP in light, high in dark)

5.) less cation channels open, so less depolarization

6.) hyperpolarization occurs

7.) CA channels close so less neurotransmitter

(photoreceptors dont fire AP)

interneurob between photoreceptor and ganglion cells fires GP

ganglion first place to fire AP

axon of ganglia - optic nerve

Cholinergic

ALL preganglionic release it

only sympathetic sweat releases it postganglionic

ALL parasympathetic release it post ganglionic

(adrenergic)

all sympathetic post ganglionic release it (exept sweat)

(hormone)

only released from adrenal madulla after sympathetic

eye dilation

cardiovascular constriction

constrict GI sphincter

decrease smooth muscle contraction

increase blood glucose

decrease insuline release

(parasymnpathetic only) located on target organs

shrinking of pupil lower heart rate widening of heart blood vessels closing of airways increase watery saliva increase smoothe muscle movement increase digestive enzymes insuline release from pancreas store glycogen in liver INCREASE SWEAT shrink bladder for urination

(excitatory for muscle and autonomic)

at motor end plate of muscle voluntary control of muscle

anesthesiologists play with this

on ganglia

(sympathetic and parasympathetic)

adrenal medula

antagonists of this block transmission.

no initiative

cant imagine consequences

not able to adapt

hard keeping hand stable at rest

cant initiate upper and lower limb

rigid arm

visual info goes to the lateral geniculate nucleus in the thalamus

the primary visual cortex is devided into cell layers oriented differently to respond to directions,movement,color