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Human Body_TP > PNS Physiology > Flashcards

PNS Physiology Flashcards

1
Q

how is the PNS divided?

A

autonomic and somatic

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2
Q

cellular origins of PNS

A

-neural crest cells give rise to entire PNS during embryogenesis
-neural tube —> forms the spinal cord and neural crest cells arise from the dorsal region of the neural tube

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3
Q

why are the neural crest cells called transient stem cells?

A

only present during development and they can differentiate into different types of cells

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4
Q

neural crest fate

A

-melanocytes
-glia Schwann cells
-dorsal root ganglion neurons
-sympathetic neurons

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5
Q

what molecules are involved in neural crest cells fate?

A

-cascade of transcription factors like neurogenins (NgI) —> determine cell fate so if you knock this out, the neuronal cell cannot be differentiated or express it in the muscle cell it can turn into a neuron
-once cell fate is determined, need neuron to survive with a set of genes called neurotrophins and receptors
-need them to extend their exons to target regions —> need axon guidance molecules like netrins, which are attractive or repulsive
-once axon arrives they need glutamate receptors to refine the targets

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6
Q

autonomic nervous system

A

-controls visceral functions like heart rate, digestion, salivation, perspiration, dilation of pupil, urination, and sexual arousal
-essential for maintaining homeostasis
-divided into parasympathetic and sympathetic divisions
-functions largely under the level of consciousness

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7
Q

autonomic nervous system

A

-axons innervate cardiac muscle and smooth muscles as well as glands to regulate basic functions
-relays visceral sensory info to the CNS by inducing the release of hormones mediating energy, metabolism, and cardiovascular functions
-major neurotransmitters are acetylcholine and epinephrine

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8
Q

sympathetic nervous system

A

-2 neuron network- one neuron (sympathetic pre-ganglion neuron) is located in the thoracic or lumbar segments of the spinal cord with the cell body in the spinal cord
-the axons extend out and synapse with post-ganglionic neurons, cell bodies aggregate to form ganglions
-post-ganglionic neurons extend axons to different organs
-connect spinal cord/CNS through ganglion to tissues

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9
Q

parasympathetic nervous system

A

-2 neuron network- pre-ganglionic neuron resides either close to brain/brainstem or lateral horns of the spinal cord
-pre-ganglionic neurons extend their axons outside the CNS and synapse with parasympathetic ganglions that are located near organs

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10
Q

differences in functions between the sympathetic and parasympathetic nervous systems

A

sympathetic:
-most active in time of stress —> fight/flight so dilate pupils, inhibits salivation, relaxes bronchii to breathe more, and shut down digestion
parasympathetic:
-rest and digest to conserve the body’s energy

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11
Q

enteric nervous system

A

-unlike the parasympathetic and sympathetic nervous systems, it is made up of 2 plexuses along wall of GI tract
-2 networks of neurons embedded: submucuous plexus that is close to the lumen of tract and myenteric plexus
-contain local sensory neurons which detect changes in tension of gut and chemical environment
-called second brain since it has a network of neurons in gut that control GI movement

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12
Q

somatosensory system

A

-responsible for receiving stimuli from external and internal environments
-under conscious control
-DRG and trigeminal ganglions —> initiate and mediate somatosensation
-processes info like touch, temperature, and pressure
-main neurotransmitter is glutamate

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13
Q

sensory neurons

A

-cell bodies of primary sensory neurons are in the dorsal root ganglion (DRG)
-31 pairs of DRGs along spinal cord and each ganglion innervate to certain regions of the body
-primary sensory neuron is the first neuron to detect sensation
-2 axons: pseudounipolar so from the cell body it extends a small stump out where one goes to the peripheral and the other axon goes to the CNS to detect sensory info and send it to the spinal cord

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14
Q

comparison of somatic vs autonomic organization

A

-for autonomic, you have two neurons with pre-ganglionic cell bodies in the CNS, extend axons to autonomic ganglions, and synapse with post-ganglionic neurons and their axons go to the peripheral target
-for sensory, DRG/trigeminal only have one axon that extends to the peripheral target and CNS —> DRG controls sensory info for body and back of head then the trigeminal sends axons to face

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15
Q

peripheral projections

A

-each DRG sends axons to certain segments of the body called dermatomes which are an area of skin innervated by a DRG
-map dermatome by recording nerves and seeing where they innervate
-adjacent dermatomes overlap —> each dorsal root sends axon to skin that can branch out and at the boundary there is overlap by the axons

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16
Q

skin somatosensory nerve endings

A

-very different nerve skin innervation patterns
-meissner’s, pacinian, merkel, and ruffini’s corpuscles with different endings that are innervated by nerves

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17
Q

stimuli and nerve skin endings

A

-end organ can allow nerve to sense different types of sensation especially touch or mechanical sensors
-if nerve associated with merkel/ruffini is stimulated, slow adapting (nerve fires AP during duration of indentation on skin)
-if nerve associated with meissner/pacinian, rapidly adapting (fire different patterns and they only fire when the AP is on and off)
-combination of slowly/rapidly adapting can feel quality and quantity of touch
-large group of nerve endings without association that send axons to skin —> sense pain and temperature

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18
Q

central projections

A

-spinal cord is the first relay point of somatic sensory info
-axons come into the spinal cord, DRG axons go out to different regions
-dorsal side of spinal cord has dorsal horn and ventral side has ventral horn
-dorsal horn controls pain, temperature, touch, and itch
-ventral horn controls muscles and movement

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19
Q

how is sensory info detected and relayed?

A

primary sensory neurons in DRG —> spinal cord neuron called secondary neuron —> thalamus —> cortex

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20
Q

what do secondary neurons do?

A

their axons cross the midline to go to the other side of the spinal cord to thalamus then cortex

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21
Q

anterolateral system

A

-processes pain and temperature
-spinal cord —> through DRG, which synapses with secondary neurons —> cross midline and ascend to thalamus and the axons of the thalamus go to the cortex

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22
Q

dorsal column-medial lemniscal system

A

-processes touch and vibration
-spinal cord —> DRG synapses with secondary neurons —> ascends closer to the midline

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23
Q

how is sensory info mapped in the primary sensory cortex?

A

-somatotopically- adjacent areas in the body are represented by adjacent areas in the cortex
-the representation of the perioral region is disproportionately large in humans
-sensory homunculus

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24
Q

barrel cortex

A

-part of somatosensory cortex in rodents
-sensory info from whiskers is represented here
-discrete areas of layer IV form anatomically distinguishable structures
-found barrel structures where one single barrel contains ~2500 neurons arranged in ring-like structure and processes tactile input from single whisker
-# of barrels = # of whiskers on contralateral side and arranged pattern corresponding to topology of whiskers
-another strain of mice had extra ring of barrels and showed extra row of whiskers

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25
Q

whisker pattern

A

-pattern maintained throughout central pathways of trigeminal system
-allows organism to know what type of sensory info is received and where on face this info is being sensed

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26
Q

referred pain

A

-when people have a heart attack, they feel the pain in their left arm or chest
-people think convergency of 2 DRG neurons into the same projection neurons in the dorsal horn
-internal organ has issue and the person may feel it in their skin —> one DRG may innervate the heart and another sends to skin and it sends axon to the same spinal cord neuron

27
Q

primary sensory neurons in the DRG

A

-heterogeneous
-different sizes to send axons to different locations

28
Q

nociceptive neurons

A

-cells detecting noxious stimuli capable of causing tissue injury
-if stimuli is severe enough to cause damage you activate neuron

29
Q

two components of pain

A

sensory and emotional

30
Q

ID of nociceptive neurons

A

-tease nerve out of skin and do recordings
-at the same time do stimulation on skin
-increase force of pressure
-with the blunt probe, no response
-with the pinprick from a needle, the nerve started firing APs
-with serrated forceps, even more APs are fired

31
Q

small-to-medium DRG neurons initiate pain

A

-large neuron (40 microns) has a thick axon that is wrapped with myelin —> very fast conduction velocities and is involved with light touch and body position
-medium neuron has a smaller axon with thinner myelin and slower conduction velocity and is involved in initial sharp pain
-small neuron make up the majority of DRG neurons and they are un-myelinated axons with slow conduction velocities and involved with delay burning pain

32
Q

nociceptors can allow us to detect pain in different modalities

A
  1. mechanical pain- pinprick
  2. thermal pain- <15 degrees celsius or >45 degrees celsius
  3. chemical pain- hydrogen, ATP, capsaicin
  4. electrical pain
    -certain nociceptors are dedicated to each type of modality
33
Q

what molecules are implicated in pain activation?

A

-voltage gated Na, K, Ca channels- allow these neurons to propagate APs
-ligand-gated cation channels- very diverse and activated by specific pain stimuli like acid, ATP, and temperature
-G protein-coupled receptors are activated by specifical molecules and modulate ion channel activities —> opioid receptors inhibit the channel and prostaglandin receptors potentiate channel

34
Q

transient receptor potential vanilloid 1 (TRPV1)

A

-molecular sensor for heat greater than 45 degrees celsius
-culture DRG neuron —> take it out and disassociate them and culture them then give them capsaicin
-found that capsaicin activates a subset of the DRG neurons with Ca influx
-use the Ca dye to look at activation —> kow that Ca channel in DRGs of nociceptors

35
Q

expression of TRPV1 cloning

A

-express into heterologous cells and these cells usually do not have any capsaicin channels so they put cDNA into the cells for expression cloning
-generate DRG cDNA library- collect mRNA from DRG and convert them to cDNA
-express different pool of cDNAs in heterologous cells
-monitor capsaicin activation by calcium imaging

36
Q

DRG-11

A

-in DRG-11 there are certain neurons that light up after capsaicin addition
-narrow it down to one gene VR1 or TRPV1
-express gene and the majority of cell expression respond to capsaicin

37
Q

TRPV1 protein sequence and structure

A

-structure qualifies to every feature of ion channels
-has pore domain that opens for ions to flow in —> recording of the channel found there was inward current when capsaicin is added and if you use heat there is also inward current
-expressed in small diameter nociceptors
-found that it has threshold of 42 degrees celsius to open in response to temperature increase, which correlates well with human psychophysics

38
Q

generation of TRPV1 knockout mice

A

-found that for moderate heat (45 degrees celsius), many WT neruons responded however in knockout mice no response
-for higher temps, certain neurons respond in both WT and knockout —> may be another ion channel controlling for higher temperatures

39
Q

behavior tests for DRG neurons

A

-von frey test- single filament hair used to poke hindpaw of mice
-different strands of filaments —> as the filament strains increase, so does pressure
-found in the WT and knockout, no difference in mechanical force so TRPV1 is not involved in mechanical pain
-thermal pain: at 48 degrees celsius, knockout take a little bit longer to withdraw tail and on hot plate, if they feel pain they jump as the temperature increases —> not completely gone in knockout
-TRPV1 single channel responds above 42 or 45 but many other channels compensate

40
Q

temperature spectrum + TRPV1 channels

A

-over temperature spectrum, different TRPV1 channels cover different temperatures
-TRPV2 can activate over 55 and may explain why knockout mice still respond to temps over 55
-TRPM8 can be activated at lower than 20 degrees

41
Q

peripheral sensitization

A

-injury- pain becomes exaggerate
-touch an injury site and it feels painful —> nociceptors become sensitized under chronic pain sites so normally less or non-painful stimuli can become stronger
-increased expression of ion channels so detect more pain
-increased sensitivity of ion channels
-reduced inhibitory channels
-mainly mediated by G-coupled receptors

42
Q

endogenous agents that activate or sensitize nociceptive neurons

A

-when there is a lesion/injury, the nerve site can release factors including ATP proton acid, lipids, serotonn —> these can activate their GPCRs expressed on nerve endings to sensitize nerves
-sensitization from bradykinin, prostalglandins, substance P, CGRP, and NGF
-edema and vasodilation are from substance P and CGRP

43
Q

what do GPCR signaling pathways do?

A

-modulate ion channel activities
-activated by a ligand that will modify the ion channels to make them sensitized

44
Q

bradykinin

A

-give neuron without adding bradykinin, neuron is activated at threshold of 42 degrees celsius
-add bradykinin, there is larger current and threshold shift from 42 to 35
-this means that added bradykinin could open the TRPV1 channels with normal body temp

45
Q

central sensitization

A

strengthen synaptic transmission between primary afferent neurons and second order neurons in the dorsal horn

46
Q

somatosensation

A

-small-to-medium DRGs mediate pain/itch
-feel pain —> withdraw, avoid the tissue damage
-feel itch —> scratch to remove the irritant and suppress itch

47
Q

itch

A

-initiated by small-to-medium DRG neurons
-unpleasant sensation to make you want to scratch

48
Q

different types of itch

A

histamine vs non-histamine

49
Q

relationship between pain and itch

A

antagonize each other —> suppress pain can cause itchiness

50
Q

animal model for itch

A

-inject chemical into skin of mouse
-if the animal feels the itch it will lift its hindpaw at high frequency

51
Q

animal model to distinguish pain and itch response

A

-inject chemical into cheek to distinguis pain and itch
-pain it wipes, grooms with both paws, and scratch with hindpaw
-inject histamine they scratch a lot but without wiping
-inject pain no scratching but a lot of wiping

52
Q

intensity theory

A

-single neuron can mediate pain and itch but depends on the stimuli —> stimuli strong you feel pain and stimuli weak you feel itch
-human skin has small spot that can give rise to pain and itch —> hypothesized that it was the same neuron

53
Q

evidence against intensity theory

A

-increased frequency of electrical stimuli showed an increase in feeling itchiness but no change from itch to pain
-in another test to look at pain, they lowered the frequency for pain and felt less pain but no transition to itch

54
Q

labelled line theory

A

dedicated populations for pain and itch

55
Q

evidence for labelled line theory

A

-after histamine injections, people reported itch and found that there was a specific subset of G-fibers respond to histamines
-this type of C-fiber is an itch specific fiber

56
Q

evidence against labelled line theory

A

in the same study, they found that the same fiber responded to histamine and capsaicin —> changed units of theory from specific to selected

57
Q

Mrg-expressing receptors expressed in subset of DRG neurons

A

-respond to itchy substances
-made MrgA3-GFP-Cre line (only expressed in 5% of DRG neurons)
-saw a neuron in live animals and applied different stimuli —> responded to CQ and histamine (itchy-like substance)
-also responded to capsaicin

58
Q

what do the MrgA3+ axons innervate?

A

the very apical surface of the skin

59
Q

ablation of MrgA3+ neurons in DRG

A

-express toxin to kill these neurons for experiment
-add CQ —> they scratch less and a lot of the itch sensation is reduced
-for pain it is completely normal
-specific

60
Q

what happens with specific activation of MrgA3+ neurons?

A

evokes only itch but not pain response

61
Q

what happens when you activate the 5% neurons with TRPV1?

A

-knock out TRPV1 and only use it in 5% neuron specific ones
inject capsaicin:
-WT mice have a lot of wiping and no scratching
-knockout for TRPV1 they do not feel pain
-mice with TRPV1 and 5% Mrg, they just scratch but do not feel pain

62
Q

for WT mice, you inject capsaicin and yo should activate both populations —> why only pain and not itch?

A

-inhibitory interneuron in spinal cord
-activate both populations and turn on inhibitory interneuron which blocks the itch sensation to only feel pain
-itch specific neurons in DRG but with inhibitory mechanisms from pain to itch to modify itch sensation

63
Q

what happens when you topically apply capsaicin?

A

you feel itch initially then as it penetrates the inhibition kicks in to become pain

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