Nervous 3 Flashcards

1
Q

nociceptive input is recvied in what lamina of the spinal cord?

A

1 and 2, and also 5

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2
Q

mechanoreceptive input is received into which lamina of the spinal cord?

A

III-V

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3
Q

proprioceptive input is received into which lamina?

A

III and deeper into the ventral horn

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4
Q

what is the specificity theory? How do we know this isn’t true?

A

that there is a dedicated pathway for each sematosensory modality, for example, hot and cold. we know this isn’t true because there are receptors that carry both hot and cold stimuli

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5
Q

what is the intensity theory? how do we know this theory is not true?

A

the number of action potentials encodes the intensity of the stimuli, so more APs means it is more intense, or, over a certain threshold it becomes nociceptive.

we know this isn’t true because there are different receptors for touch and noxious stimuli and they go to different areas of the brain

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6
Q

why does rubbing a wound make it hurt less?

A

it is called the gate control theory. When there is a painful stimulus it acitvates the C fibers (nocipetion fibers) and these deactivate the inhibitory neurons (stopping inhibition) BUT when you have touch stimulus (A fibers) coming in at the same time, this signal activates the inhibitory neuron and so it inhiits the painful stimuli coming in, sort of counteracting the stimulus with another one

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7
Q

what is the difference between nociception and pain?

A

nociception is the physioligcal detetion and processing of noxious stimuli

pain refers to the cumulative experience as a result of the received input as well as biological, social, and psychological aspects which influence the perception of pain

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8
Q

____ and ____ nuclei relay sematosensory information from the spinal cord to the ______. Processing of nociceptive information between sematosensory cortex and other areas leads to ____

A

VPL

VPM

sematosensory cortex

the overall pain experience

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9
Q

what are the 3 general types of areas involved in interpreting pain?

A

areas of sensation

areas of remembering, rewarding, and addiction pathways (like the amygdala)

areas of descending modulation of pain (emotions, stress, like the hypothalamus)

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10
Q

what are the 3 aspects of desccending modulation to the spinal cord?

A
  1. periaqueductal Gray (PAG)
  2. locus coeruelus (LC)
  3. Rostral ventromedial medulla (RVM)
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11
Q

the periaqueductal Gray (PAG) projects to the spinal cord via _____. It releases _____ which there are 3 types: ____. it contains a high density of ______. it is one way in which opioids exert their _____ effetcs

A

LC or RVM

endogenous opiods

enkephalins, dynorphrins, endorphins

cannabinoid receptors

analgesic

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12
Q

Locus Coeruleus (LC) projects ______, releasing ______. Unlike the brain where it is excitatory, in the spinal cord this hormone binds to ____ which are _____, resulting in ______ otherwise known as ____. It is responsible for the concept that you can exceed your threshold

A

directly down the spinal cord

norepinepherine

alpha 2

inhibitory

analgesia

hysterical strength

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13
Q

the RVM projects ______, producing _____. It is thought to have some sort of ____ effect. in some patients, _____ may be helpful in treating chronic pain.

A

directly down the spinal cord

serotonin

analgesic

selective serotonin receptive inhibitors (SSRIs) or serotonin-epineperine reuptake inhibitors (SNRIs)

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14
Q

in a facial actio coding system, what indicates pain?

A

brow lowering, cheek raising, eyelid tighening, nose wrinkling, flattened ears, whiskers shift to be tight, narrow eyes

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15
Q

How do we know acute pain is necessary to survival?

A

those with mutations in the SCN9A gene that encodes for Nav1.7 channels (sodium gated voltage channel) aren’t able to feel pain, so they have hidden injuries like broken bones, dental issues, eye damage, etc. these injuries to progress to fatal

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16
Q

what is chronic pain?

A

pain that continues after the injury has healed or the stimulus isn’t there anymore

17
Q

what are the types of chronic pain?

A

inflammatory: result of tissue damage and inflammation
neuropathic: result of nerve damage

cancer pain: combination of the two

18
Q

all chronic pain syndromes are characterized by what 3 things?

A

hyperalgesia: there is more pain than expected
allodynia: something that shoulnd’t be painful is

spontaneous pain: like pain in the absence of nociceptive input

19
Q

what is the most common chronic pain condition in animals?

A

osteoarthritis

20
Q

what are the steps in the transition from acute pain to chronic pain?

A

acute injury–> nociceptor activation–>central sensitization–>neuronal modification and long term potentiation–> persistent pain

21
Q

what is peripheral sensitization?

A

tissue injury leads to the activation of immune cells which release inflammatory soup (histamine, etc). these molecules bind to ion channels which allows calcium and sodium to flow into the synapse of the nociceptors. this leads to an action potential. many of these inflammatory chemicals make it easier for the positive charge to get inside, aka, make it easier for the action potential to fire. they are essentially changing the threshold of the receptor so that you need less of a positive charge to result in an action potential

22
Q

what are some comon treatments for acute and chronic pain?

A

NSAIDS, opiods (for acute), gabapentin

exercise, physiotherapy, weight reduction

23
Q

why is it so hard to find effective treatments for pain?

A

our pain models may not be accurate: studies are usually done on one sex, one strain, one age, etc

there are biological, social, and psychological factors

24
Q

what is stress induced analgesia?

A

animals that stress may have fewer pain symptoms. there is higher cortisol

25
Q

acute stress blunts pain due to release of _____, which activates ____

A

cortisol, epinpherine, norepinepherine

descending modulation of pain

26
Q

chronic stress disorders change the way the body functions, ______ susceptibility to pain. chronic pain ____cortisol levels which over time leads to _____. Chronic pain can also lead to ____, creating a cycle

A

increasing

increases

immune system dysregulation

chronic stress

27
Q

what is central sensitization? What does wind-up refer to?

A

the first pain receptor at the synapse is releasing things like glutamate, substance P, etc. These bind to receptors on the 2nd pain receptor to allow positive ions into the neuron, increasing action potentials. there are also glial cells which are also releasing things like cytokines leading to an amplified signal. even when the stimulus is removed, this continues.

wind up refers to the progressive increase in AP firing in the dorsal horn via C fibers due to the release of chemicals like substance P that allow positive ions to flow into the neuron. the action potential threshold is decreased, meaning it takes less sodium and calcium for an action potential to be fired

28
Q

what is long term potentiation?

A

when there is sustained glutamate release, which binds to the AMPA receptor. This then triggers the AP, which causes the magnesium to no longer block the channel of the NMDA receptor. This allows calcium to enter the cell, and calcium activates cascades that induce transcription of proteins. This leads in more AMPA receptors being produced and put into the cell membrane, making the receptor more sensitive to glutamate, more output for the same input.

https://www.youtube.com/watch?v=vso9jgfpI_c