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74 Cards in this Set

  • Front
  • Back

somatic and autonomic which is conscious and which is unconsciousess

somatic - consc


auto - unconsc

structure of afferent neuron

-single long dendrite


-short axon


-smooth rounded cell body



-the dendrite is strucurally and functionally similar to axon

4 receptors of somatosensory

-chemo


-thermo


-photo


-mechano

visceral afferent

incoming afferent pathway from organs (viscera)


-mostly subconscious but pain receptors can make u become aware

somatic sensations vs special senses

somatic - somaesthetic, proprioception



special - hearing, smelling, seeing, taste, equilibrium

perceptions dont replicate reality

- different receptors result in diff perceptions, other species with diff receptors perceiev different

somatosensory vs specal senses receptors

somato - ex. free nerve endings consist of neuron with exposed receptor



special - ex.turn mechanical stimulation into neural by synapsing on a sensory neuron

trasduction

mechanical or chemical stimulation converted into electrical signal thru changes in ion permeability at controlled ion channels

4 properties allwoing CNS to differentiate between incoming stimuli

modality, location, intensity, duration

modality

the type of receptor, sent to cerebral cortex

generator potential

same as receptor potential but ending of an afferent neuron

photoreceptors are hyperpolarized upon stimulation

yes

duration

graded potential last longer with stronger stimulus

seperate receptor

chemicals will travel to afferent and open ion channels for action potential

magnitude

greater stimulus, more frequent action potential

adaptation

stimuli can diminish extent of depolarization despite sustained stimulus strength

tonic receptors

dont or hardly adapt


- imprt in situations where valuable to maintain info about stimulus


-ex.


-muscle stretch, and joint proprioceptors


-constantly need infor to monitor

phasic receptors

rapidly adapting


- no longer responds to maintained stimulus but when stimulus removed receptor slightly depolarizes and is called off response



-useful to signal change in stimulus


-ex.tactile (touch) receptors in skin signalling pressure


- not consciouss continually of wearing clothes but when some new comes on u become accustomed, when taking offf u aware of removal because of off response

order sensory neurons

order of neurons from afferent receptor up to brain

labelled lines

since stimulus seems same to brain, labelled lines relay specific, location, and type etc

phantom pain

pain percieved as orginating from somewhere but it is just the neural pathway this would take being falsely stimulated



-person feels foot pain but leg was amputated, free nerve endings falsely doin it doe



-brain attempt at remapping when limb severed could lead to signal of pain misinterpretation

receptive field

each neuron hs region of skin surface of receptors it responds too, small field = more receptors = more senstiive (greater acuity and discriminative ability)

lateral inhibition

-pencial prick on finger, region around the point feels slight stimulation, lateral inhibition blocks these from sending action potentials so brain can pinpoint exact spot

mechanoreceptors (5)

pressure,strech, vibration, acceleration sound

receptor location

sent to corresponding somatosensory cortex pathway

pacnian corpuscles

-touch and deep pressure


-detect moderately rough/rougher surfaces


-very sensitive to vibration


-350 per fingy - 800 in palm


-phasic tactile mechanoreceptor


-onion like connective tissue layers at end of myelinated axon


-to adapt, as stimuli continues pressure energy dissapates as layers slip like onion

meissners corpuscles

phasic tactile myelinated mechanoreceptors


- nerve endings in skin - light touch


-encapsulated nerve endings surrounded by connective tissue capsule


-fingers lips nipples, light touch, low frequency vibration threshold

merkels discs

most senstive mechanoreceptor


- slowly adapting type 1 myelinted


-superficial layers of skin and mucosa


-clustered beneath ridgs of fingertips making up fingerprint


-mammary glands


-merkels nerve endings are clustered into specialized epethelial structues called touch domes or hair discs

ruffini corpuscles

-myelinated, encapsulated, slow adapting nerve endings found in deep layers of skin & joints


- tied into collagen matrix


-respond to stretch & torque


-register mechanical deformation within joints and continuous pressure

free nerve endings

skin,hair roots, eyes, other tissues


- myelin/unmyelinated


- most abundant skin receptors


- touch & pressure & temp & nociception


- tickling an itching (unmyelinated slow fibres)


neurotransmitters used by effector neurons (2)

acetylcholine & norepinephrine

where do sympathtic nerve fibres originate

thoracic & lumbar regions of spinal cord

some preganglionic fibres pass thru ganglion chain w/o synapsing instead they end later in sympathetic colateral ganglia (halfway between CNA and effector) and post ganglionics take from here

euuss

where do parasympathtic preganglioncs originate from

braina nd sacral ares , very long cause terminate at terminal ganglia which are close to effector

what neurotransmitters do pre/post ganglioncs mau for sympa/parasympa

both pres release acetylcholine



sympa - noradrenaline (adrenergic fibres)



parasympa - acetylcholine (cholnergic fibres)

postganglionic varicosities

many swellings that release neurotransmitter over large area of innervated organ



-allows autonomics to influence whole organs

times of sympathetic dominance

- fight or flight


- digestion and urination arent essential functions at this time so they are inhibited

times of parasympathetis dominance

-quiet restful circumstances


- digestion/urination


-no need for heart beat rapid in tranquil setting

advantages of dual autonomic innervation

- accelerator and brake system in automobile


-antagonistic, one can slow while other fires

tonic control

one autonomic system controls

exceptions to dual innervation

most innervated blood vessels - sympathetic


most sweat glands - sympathetic


salivary glands - both, not at same time

adrenal medulla

modified sympathetic ganglion that doesnt give rise to postganglionic fibres


- on stimulation from preganglionic it secretes hormones into blood


-nor/epinephrine and reinforce sympathetic activity

cholinergic receptors (2)

nitotinic and muscarininc

nicotinic receptors

activated by nicotine


- postganglionic cell bodies in all autonomic ganglia


-binding of actylclne opens cation channels in postganglionic cell (Na and K)

muscarinic receptors

effector cell membranes (parasympathetic)


- bind with actyclne released from para post ganglionic, 5 subtypes all linked to G proteins for 2nd messenger systems

adrenergenic receptors (5)

a1,a2,b1,b2,b3



- 2nd messenger G proteins

b2 receptors

- epinephrine


-cAMP


-inhibitory


- respiratory airway dilation

b1 reeptors

nor/epinephrine


- cAMP


- heart


- excitatory response, increased rate and force of cardiac contraction

a1 receptors

norepinephrine


-Ca2+ 2nd messenger


-excitatory response


-most sympathetic target tissues

a2 receptors

norepinephrine


-inhibits cyclic AMP production


-inhibitory response to effector organ


-decreased smooth muscle contraction in digestive tract

b3 receptors

rare but found in adipose tissue, stimulates adipose to break down along with a2

agonists

drugs that bind to same receptor as neurotransmitter and mimics

antagonists

drugs that bind w/receptor and block neurotransmitter response



- can use to block out para or sympa use of NT but keep other free of inhibition

medulla most responsible for?

autonomic output -centres for cardio, respiratory and digestive are here

hypothalamus integrates what 3 systems

autonomic somatic and endocrine for emotional response

some autonomic reflexes (urination, defecation, erection) are integrated mostly where

spinal cord

emotional expresson nd characteristics are integrated by what?

pre-frontal associatoon cortex and responses can take place thru hypothalmic-medullary pathways

cell bodies of motor neurons supplying muscles of head located where?

brain stem

motor neuron axon terminals release_______

acetychlone

can motor neurons stimulate an dinhibt muscle cells

only stimulate, inhibition must block synaptic input to dendrites and cell body

poliovirus

destroys cell bodies of motor neurons - paralysis of affected neurons

ALS

pathological changes in neurofilaments that


-block axonal transport of crucial materials


-accumulation of toxic levels glutamate


- mitochondiral dysfunction - reduced energy


-aggreation of misfolded proteins

End-plate potential (EPP)

- graded potential similar to EPSP but much larger


- more NT released from terminal button than presynaptic knob


- motor end plate has bigger surface area for greater density of receptors


-more ion channels open


-creates the larger depolarization

where does neuromuscular juction hit muscle fibre and how is whole muscle contracted thru action potential

middle and spreads both ways allowing contraction

higher centres involved in ANS

- spinal cord


- medulla


- hypothalamus


- pre-frontal associatio cortex

higher centres involved in SNS

- spinal cord


- motor cortex


- basal ganglia


- cerebellum


- brain stem

where is site of action potential initiation of afferent neuron

first excitbale portion of membrane adjacent to receptor

AChE

destroys acetylcholine in synaptic cleft and parts can be reuptaken by synaptic vesicles

black widow spider venom

explosive release of ACh at all cholinergic sites causimng prolonged depolarizaton which keeps diaphragm contracted and stopping the in and out of breathng and death

botulinim toxin

blocking release of ACh from button


- causes botulism (form of food poisoning) which prevents muscles from responding to nerve impulses


- death due to respiratory failure because diaphragm cant contract


- one of most lethal poisons

curare

reversibly binds to ACh receptors on motor end plate


- paralysis ensues, inability to contract diaphrgam causes death

OP's

binds to AChE so acetylcholine isn't destoryed


-death cause diaphragm cant repolarize and get phresh air

myasthenia gravis

autoimmune body produces antibodies against own ACh receptors, not enough receptors to bind to causing weakness

treatment of myasthenia gravis

drug neostigmine inhibits AChE giving chance for ACh to find receptor, instead of OP which irreversiblly bind to AChE