Nervous 3 Flashcards
nociceptive input is recvied in what lamina of the spinal cord?
1 and 2, and also 5
mechanoreceptive input is received into which lamina of the spinal cord?
III-V
proprioceptive input is received into which lamina?
III and deeper into the ventral horn
what is the specificity theory? How do we know this isn’t true?
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
what is the intensity theory? how do we know this theory is not true?
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
why does rubbing a wound make it hurt less?
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
what is the difference between nociception and pain?
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
____ and ____ nuclei relay sematosensory information from the spinal cord to the ______. Processing of nociceptive information between sematosensory cortex and other areas leads to ____
VPL
VPM
sematosensory cortex
the overall pain experience
what are the 3 general types of areas involved in interpreting pain?
areas of sensation
areas of remembering, rewarding, and addiction pathways (like the amygdala)
areas of descending modulation of pain (emotions, stress, like the hypothalamus)
what are the 3 aspects of desccending modulation to the spinal cord?
- periaqueductal Gray (PAG)
- locus coeruelus (LC)
- Rostral ventromedial medulla (RVM)
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
LC or RVM
endogenous opiods
enkephalins, dynorphrins, endorphins
cannabinoid receptors
analgesic
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
directly down the spinal cord
norepinepherine
alpha 2
inhibitory
analgesia
hysterical strength
the RVM projects ______, producing _____. It is thought to have some sort of ____ effect. in some patients, _____ may be helpful in treating chronic pain.
directly down the spinal cord
serotonin
analgesic
selective serotonin receptive inhibitors (SSRIs) or serotonin-epineperine reuptake inhibitors (SNRIs)
in a facial actio coding system, what indicates pain?
brow lowering, cheek raising, eyelid tighening, nose wrinkling, flattened ears, whiskers shift to be tight, narrow eyes
How do we know acute pain is necessary to survival?
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
what is chronic pain?
pain that continues after the injury has healed or the stimulus isn’t there anymore
what are the types of chronic pain?
inflammatory: result of tissue damage and inflammation
neuropathic: result of nerve damage
cancer pain: combination of the two
all chronic pain syndromes are characterized by what 3 things?
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
what is the most common chronic pain condition in animals?
osteoarthritis
what are the steps in the transition from acute pain to chronic pain?
acute injury–> nociceptor activation–>central sensitization–>neuronal modification and long term potentiation–> persistent pain
what is peripheral sensitization?
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
what are some comon treatments for acute and chronic pain?
NSAIDS, opiods (for acute), gabapentin
exercise, physiotherapy, weight reduction
why is it so hard to find effective treatments for pain?
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
what is stress induced analgesia?
animals that stress may have fewer pain symptoms. there is higher cortisol
acute stress blunts pain due to release of _____, which activates ____
cortisol, epinpherine, norepinepherine
descending modulation of pain
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
increasing
increases
immune system dysregulation
chronic stress
what is central sensitization? What does wind-up refer to?
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
what is long term potentiation?
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
