a&p II final

presynaptic neuron

sends signal

postsynaptic neuron

receives a signal

electrical signal receive @ axon terminal then

opens ca2+ channels

how are nts released

exocytosis d/t ca2+

higher frequency =

bigger nt release + electrical signal

when nt bings to postsynaptic receptors…

membrane potential changes

major symptom of too much botox

chronic migraine

first step of termination nt response

enzyme degrades nt

second step of nt response

presynaptic neuron “reuptakes” nt

third step of nt response

nt dilutes/diffuses out of synaptic cleff

nitric oxide

diffuses across membranes (postsynaptic neuron to presynaptic neuron)

glutamate

excitatory (depolarized)

gaba

inhibitory (hyperpolarization)

ach

binds to 4 different ach receptors

neuromuscular junctions

excitatory

cardiac muscle

inhibitory

neuromuscular junction + cardiac muscle

can change how the body reacts

channel linked receptors (ionotropic)

direct action = open an ion channel

rapid response, localized, brief

g protein-linked nt receptors (metabotropic)

indirect action = via second messenger

slow response, prolonged, complex

facilitated zone

stim from other sources can induce ap

discharge zone

linked to presynaptic input > does not fire

divergence

one neuron amplifies a signal to multiple neurons

ex: reaching multiple brain regions at once

convergence

multiple neurons giving information to one neuron

ex: brain combing touch, pain, and temp input

reverberating

neurons repeating

ex: breathing, heart rate

parallel processing

inputs into different pathways (simultaneously)

important in higher mental function > problem solving and connecting parts

mechanoreceptors

mechanical pressures - nerve impulse

thermoreceptors

temperature

chemoreceptors

chemicals in solution

nociceptors

pain damaging stimuli

ganglia (dorsal root ganglia)

with “afferent” nerve fibers

cell bodies from sensory neurons

reflex arcs

reflexes occur over specific neural pathways

receptor (reflex arc)

site of stimulation

sensory neuron (reflex arc)

transmits “afferent” impulse to cns

cns integration center (reflex arc)

single or multiple synapses in cns

motor neuron (reflex arc)

transmits efference impulse from integration center to effector

effector (reflex arc)

muscle/gland responding to “efference” impulse

intrafusal muscle fibers

primary noncontractile

extrafusal fibers

functional fibers

primary type IA

center of spindle

secondary type II

ends of spindle (contractile)

how is primary type IA activated

by both rate and amount of stretch

how is secondary type II activated

only by degree of stretch

muscle spindles

muscle length + stretch

far ends of muscle spindles are contractile so they are supplied by

gamma efferent fibers

external force to lengthen muscles

weight bearing or by contracting antagonistic muscles

“external stretch”

activating gamma motor neuron

(brain) stims distal ends of fiber to contract

“internal stretch”

alpha motor neurons

contract to resist muscle stretch

reflexive muscle contraction of extrafusal fibers =

resist further stretch

reciprocal inhibition

when quad flexes = hamstring relaxes

less stretch =

less spindle ap

muscle stretch =

spindle stretch

gamma motor neuron

tells muscle spindles to stay slightly stretched

gives brain into about muscle condition

somatic ns

skeletal muscle

autonomic ns

cardiac muscle + smooth muscle + glands (involuntary)

motor neurons in somatic ns

cell bodies in cns (no ganglia)

axons go to spinal cord to muscles

motor neurons in autonomic ns

two neuron chain w/ ganglia

1st neuron in auto. ns

in cns

2nd neuron in auto. ns

outside cns

preganglionic axon

from cns to ganglion

postganglionic axon

from ganglion to target organ

nts in somatic ns

ach

is somatic ns excitatory or inhibitory

always excitatory

is auto. ns excitatory or inhibitory

both but receptor dependent

nts in auto. ns

ach (parasympathetic) or norepinephrine (sympathetic)

sympathetic ns nt pathway

ach > ganglion/adrenal medulla > norepinephrine

parasympathetic ns nt pathway

ach > ganglion > ach (ach releases ach)

parasympathetic ns

functional during non stressful times

lowers bp, cardiac + respiratory rate

sympathetic ns

functional during excitement, stress, or under threat

increase in hr, resp, high sweating

ach

released by cholinergic fibers

norepinephrine

released by adrenergic

nicotinic receptors

on skeletal muscles and all ganglionic neurons

is nicotinic receptors stimulatory or inhibitory

always stimulatory

muscarinic receptors

on all parasympathetic and some sympathetic target organs

is muscarinic receptors inhibitory or stimulatory

both stim/inhibit but depends on target organ

alpha adrenergic

stimulatory

beta adrenergic

inhibitory

there are different subtypes of adrenergic receptors =

can do different things

beta blockers

binds to and blocks beta 1 receptors

tx for myasthenia gravis

blocking acetylcholinesterase

how does blocking acetylcholinesterase help with tx

acetylcholinesterase doesnt break down ach = allows ach to bind to receptors

sympathetic tone

controls by sns; usually partially constricted

blood vessels can dilate/constricted based off needed blood flow

what regulates autonomic ns

brain stem

hypothalamus role in auto. ns

limbic lobe can activate sns if in danger

biofeedback training

monitors physiological functions for pain tx, stress management, headache

what causes htn

overactive sympathetic vasoconstriction

htn tx

adrenergic receptor blockers

glomeruli complex structures can convey similar info =

similar smells = same glomerulus

granule cells

inhibits odor

smell adaption

brain learns to ignore constant smells = strong/important smells keep sending signals

what is color

objects that reflect/absorb light

what happens to eyes when objects are close

lens accommodate

constriction of pupils

eyes turn inward

rod cells

connects cell body by “outer fiber”

what’s in the outer segment

rod cells and cone cells

photopigments

changes shape when light is absorbed

rods

activated by dim light (gives us night vision)

cone

activated by bright light

what happens to opsin in light

dissociates from retinal

what happens to opsin in dark

connects with retinal

somatogenic pain

direct injury to physical tissue