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Flashcards in Ascending Sensory Systems Deck (22):

This class of sensory receptor has its nerve ending surrounded by a capsule of connective tissue. Give specific corpuscle examples.

Encapsulated (duh). Types include meissner and pacinian.


What is the function, location, and fibers of the meissner corpuscle?

The function is discriminative touch (2 point discrimination).
Location: concentrated in finger tips.
Fibers: A-beta fast conducting.


What is the function, location, and fiber type associated w pacinian corpuscles?

Function: detection of vibrations.
Location: fingers and palm.
Fibers: A- beta fast conducting.


What do free nerve endings detect?

Pain, crude touch, and temperature.


What is the axon reflex?

a response elicited by peripheral nerve stimulation; attributed to impulses traveling proximally from the stimulation site along motor axons, encountering a branch point, and then passing distally down the other branch to activate local arterioles (to cause vasodilation) or muscle (to cause contractions).


What are steps of the triple response?

1. Red line- occurs from scratching of the skin.
2. Flare- the skin reddens due to capillary dilation.
3. Wheal- increased capillary permeability.

Further explanation-
1. the triphasic response to the firm stroking of the skin. Phase 1 is the sharply demarcated erythema that follows a momentary blanching of the skin and is the result of release of histamine from the mast cells. Phase 2 is the intense red flare extending beyond the margins of the line of pressure but in the same configuration, and is the result of arteriolar dilation; also called axon flare because it is mediated by axon reflex. Phase 3 is the appearance of a line wheal in the configuration of the original stroking.


What are rexed laminate?

These are located in the posterior horn and consist of ten segments of gray matter. Those that are important for us are specifically laminae I, II, and V.


Which lamina is/are responsible for fast pain transmission and what fiber is used?

That's lamina I which is a A-delta fiber.


Which lamina is/are used in slow pain transmission and which fiber is used?

There are two lamina involved- II and V and the fiber is C.


Which lamina is/are responsible for pain regulation?

That's lamina II.


Discriminative touch includes....

Touch, pressure and vibration


Describe the discriminative touch pathway

This pathway is located in the posterior column system. It is collateral to lamina II, decussates in the medulla, relays in the thalamus and terminates in the post central gyrus.


Describe the fast pain pathway

This pathway is associated w lamina I. The pathway decussates in the cord, relays in the thalamus and terminates in the post central gyrus.

Further explanation- The key points are that the primary afferents ascend all the way to the medulla, on the ispilateral side of the cord, in the posterior columns. The secondary afferents cross in the medulla and ascend as the medial lemniscus. In the thalamus they synapse in the VPL (the ventroposterior lateral nucleus) and finally ascend to cortex.


Fast pain description for you benefit:

Fast pain, often called sharp or pricking pain, is usually conducted to the CNS over type A delta fibers. These ultimately excite lateral spinothalamic tract fibers which go directly to the VPL of the thalamus on the contralateral side. From here third-order fibers project to the cerebral cortex where they are somatotopically organized and sharply localized. Somatotopic organization means that each minute area of the sensory cortex receives input from a distinct peripheral area. A person can sharply localize a pain if he is able to tell exactly where it is originating


Explanation of slow pain

Slow pain, often called burning pain, is conducted to the CNS over smaller-diameter type C fibers. After entering the cord these fibers stimulate lateral spinothalamic tract neurons which send collaterals into the brainstem reticular formation. Fibers from the reticular formation diffusely project to the thalamus, hypothalamus, and possibly other areas as well, perhaps giving rise to the emotional component of pain. Pain signals following this route are poorly localized.


Describe slow pain pathway

The signal comes from lamina V in the spinal cord which travels to the reticular formation in the brainstem. From there the signal relays in the thalamus ( in the intra laminar nuclei) and are lastly sent to many cortex regions


Describe the pain regulation pathway

Once the pain stimulus is detected in the periaquiductal gray region of the midbrain, the signal is sent to and synapses on the nucleus raphe Magnus. From here, the signal is sent through the raphe spinal tract and synapses on an inhibitory interneuron located posterior column. Stimulus to the inhibitory interneuron in lamina II causes pain suppression.


Further pain regulation explanation- gate theory of pain

The theory suggests that collaterals of the large sensory fibers carrying cutaneous sensory input activate inhibitory interneurons, which inhibit (modulate) pain transmission information carried by the pain fibers. Non-noxious input suppresses pain, or sensory input “closes the gate” to noxious input (Figure 8.1). The gate theory predicts that at the spinal cord level, non-noxious stimulation will produce presynaptic inhibition on dorsal root nociceptor fibers that synapse on nociceptors spinal neurons (T), and this presynaptic inhibition will block incoming noxious information from reaching the CNS (i.e., will close the gate to incoming noxious information).


What is the periaquiductal gray region of the brain

Periaqueductal gray (PAG; also called the "central gray") is the gray matter located around the cerebral aqueduct within the tegmentum of the midbrain. It plays a role in the descending modulation of pain and in defensive behaviour.


What is the input to the PAG?

Prefrontal cortex


What are the neurotransmitters involved in pain regulation?

During PAG stimulatin, serotonin (5-HT) is also released from ascending and descending axons in subcortical nuclei, in spinal trigeminal nuclei and in the spinal cord. This release of 5-HT modulates pain transmission by inhibiting incoming sensory activity. Depletion of 5-HT by electrical lesion of the raphe nuclei or by a neurotoxic lesion results in blocking the ability of both opiate (intracranial and systemic) and electrical stimulation to produce analgesia.

Basically serotonin is involved. In addition there is an endogenous opioid system that dulls pain. It uses morphine receptors.


Give an example of an uncapsulated sensory receptor

Merkle nerve ending