Test 3 - 9/30 Lecture Flashcards
True/False: Spinothalamic and Anterolateral Tracts are used as interchangable terminology
True
True/False: Spinethalamic goes up to spine and to thalamus
True
Fast pain ascends to brain via what portion of the anterolateral tract
Lateral pathway
What neurotransmitter is used for fast pain?
Glutamate
What kind of fibers relay fast pain signals
A delta fibers
Fast pain is first sensed by what?
Nociceptors (free nerve endings)
Where does the cross over happen for fast pain? and at what level?
AWC at the level that the pain enters
Why does fast pain have a detailed localization?
It is sent to the parietal lobe from the thalamus and there it is in the same region as the DCML pathway so the pain can be interpreted in the portion of the parietal lobe that the pain is happening.
What lamina does fast pain interact with?
Lamina I (lamina marginalis)
Does Neospinothalamic tract correspond to fast or slow pain?
Fast
True/False: Neospinothalamic is described by Schmidt as a “newer pathway” that could have branched off of slow pain pathway.
True
What portion of the Anterolateral tract does slow pain get sent up?
Anterior pathway
What is the main neurotransmitter for slow pain
Substance P
What are the three neurotransmitters for slow pain as mentioned in lecture
Glutamate, Substance P, CGRP
What fibers transmit slow pain signals
C fibers
How does Glutamate work in fast pain vs slow pain?
In fast pain it releases, binds and generates AP fast.
In slow pain it does everything slower.
Why is there poor localization of slow pain?
It doesn’t make it to the parietal lobe where it can be localized, a lot of the info makes it to the top of brain stem and then stops.
What lamina are associated with slow pain?
Lamina II & III and then V
True/False: Paleospinothalamic Tract corresponds with slow pain
True
How many paths can the Pyramidal tract take?
3.
True/False. Slow pain can elicit more emotional responses
True
Where is the emotional center located?
Toward the middle of the brain where the brain stem meets the diencephalon.
True/False. Slow pain typically goes past the thalamus to the parietal lobe
False. It rarely goes past the thalamus.
What passes through the ventrobasal complex?
DCML and fast pain signals
What is the tissue at the top of the brain stem where slow pain signals terminate?
Reticular Formation
What are the four extrapyramidal tracts? What kind of pathway are these?
- vestibulospinal
- olivospinal
- reticulospinal
- rubrospinal
They are descending motor accessory pathways
What is the vestibulospinal tract used for?
Used for maintaining balance and focus eyes while body is in motion
What is the reticulospinal tract used for?
maintaining muscle tone (always have some baseline muscle tone)
what is the rubrospinal tract used for?
modulation of voluntary movements.
(similar to cerebellum tracts)
True/False. The descending pain system is inhibitory in nature
True
Why does the descending pain system get activated?
It is activated in response to pain.
True/False. The descending pain pathway will take the edge off of pain
True
How many neurons make up the DIC pathway?
3
What is the first order neuron in DIC?
Enkephalin
Where does the body for the first order neuron reside?
Originates in the periventricular nuclei or the periaqueductal grey
Enkephalin neurons release _____ neurotransmitters in the _____ which is located in the middle of the _____
Enkephalins.
Raphe magnus nucleus (RMN)
Pons
Are the neurotransmitters from the first order neuron (Enkephalin) excitatory or inhibitory?
Excitatory
Where is the periaqueductal gray located?
Near the cerebral aqueduct in the midbrain
Where is the periventricular nuclei located?
It sits in front of the 3rd ventricle
What is the 2nd order neuron in DIC?
Serotonergic neuron
The serotonergic neuron releases _____ in the _____.
Serotonin.
Dorsal horn
What is the 3rd order neuron in DIC?
Enkephalin neuron
Is the 3rd order neuron inhibitory or excitatory?
Inhibitory
How is the 3rd order neuron enkephalin inhibitory? How does it work on pain?
There is a pain receptor neuron (nociceptor) that enters via the dorsal horn, there are enkephalin receptors on the nociceptors and when the neurotransmitter is released it shuts down pain
What is the abbreviation for serotonin?
5-HT
Enkephalin is _____(endogenous/exogenous).
Endogenous
True/False. Enkephalin is a morphine analog. All of our opioid receptors are actually enkephalin receptors
True
If we implant electrodes into _____ or ______ and stimulate, that would generate an _____ pain signal that could _____ the amount of pain we perceive.
Periventricular nuclei
Periaqueductal grey
inhibitory
Reduce
Where does the first synapse occur in the DIC pathway?
Raphe magnus nucleus, located in the middle of the pons
What are things that can be perceived as pain in the periphery according to the lecture. (8)
- Physical damage
- Acid build up (lactic acid)
- Increase in ECF K
- Histamine
- Serotonin
- Ach
- PG’s
- Bradykinin
Why could a dialysis patient have more pain?
Their K could be messed up and the increase in K can depolarize cells and be interpreted as pain
Excess of protons usually means excess of _____
K
How can we decrease chronic pain via the serotonin neuron in the DIC?
Typically serotonin neurons have a natural reuptake system. If we inhibit this reuptake we will have more serotonin at the synapse and can augment the effects of the 3rd order inhibitory neuron.
Why are TCA’s not used as much now as an serotonin reuptake inhibitor?
The side effects. Caused drowsiness but people with chronic pain would probs benefit from that.
What is lateral inhibition? How does it work?
Pressure sensor and nociceptor run parallel to each other..they can talk to each other and the nearby pressure sensor can shut down pain.
If we hit our hand with a hammer and grab our hand and apply pressure we are doing what to the pain?
lateral inhibition
Where does lateral inhibition take place?
in the dorsal horn of grey matter
Acupuncture is an example of what?
lateral inhibition
What is the main glutamate receptor for pain synapse?
AMPA-r
How does the AMPA-r work?
Glutamate binds to receptor and opens a Na ion channel. Enough Na comes in and generates an AP to send info to brain
NMDA is a _____ receptor
Glutamate
How does the NMDA-r work?
Have to have depolarization and glutamate binding to receptor to activate. Once activated ion channel opens and allows primarily Ca through (some Na too)
Why do the NMDA-r need depolarization to be activated?
Bc Mg sits at the cell wall and blocks it. If we make the inside more + it will move away from the cell wall and it can open.
True/False. NMDA-r work faster than AMPA-r.
False. AMPA-r are faster
How is glutamate released from the nociceptor?
Voltage gated Ca+ channels open and move the glutamate to the outside of the nociceptor.
True/False. When we are born we dont have many NMDA-r, they are placed in nervous system as we grow
True
What are some examples of things that can block NMDA-r as mentioned in lecture? (5)
- Ethanol
- Lead poisoning
- Ketamine
- Nitrous
- Tramadol
Does ketamine work on both AMPA and NMDA?
No, only NMDA
What happens with the AMPA and NMDA receptors with chronic pain?
The more often the are activated, the more receptors get populated and are able to send more action potentials making us more sensitive to pain
What are the 3 ionitropic glutamate receptors mentioned in class?
- AMPA
- NMDA
- Kanate
How do the Ionitropic receptors work?
They increase cell wall permeability to ions
What is the one metabotropic glutamate receptor mentioned in class?
GCPR
