Somatosensory+System+I

=**Somatosensory System I**=


 * 1. Explain what the somatosensory system is, and what it does.**

The somatosensory system consists of the parts of the CNS and PNS that process sensory information from the body wall. PNS components include primary sensory neurons, and CNS components include spinal cord, brainstem thalamus and cortex.


 * 2. Point out the 4 somatosensory modalities of body feeling, and the adequate stimuli for each.**


 * Touch||Mechanical stimulus||
 * Proprioception||Mechanica stimulus||
 * Temperature||Thermal stimulus||
 * Pain||Noxious mechanical, thermal or chemical stimulus||


 * 3. Describe the receptors that transduce somatosensory stimuli, and indicate where different receptors are located in the body.**

Receptors are distributed in an orderly fashon in body wall tissue, for example meisners corpulcels are arranged in rows near the papillary ridges of glabrous skin on the distal fingers. Touch receptors are present in different densities at various parts of the body. This can be demonstrated using the two point discrimination test whose results show that fingertips face and toes are more sensitive then legs and arms for example.


 * Modality**||**Receptor type**||**Location**||
 * Touch||Meissners Corpuscle||Skin||
 * ||Pacinian Corpuscle||Skin||
 * ||Merkel Receptor||Skin||
 * ||Ruffini Corpuscle||Skin||
 * ||Hair Follicle||Skin||
 * Crude Touch||Free Nerve Ending||Skin, Viscera||
 * Proprioception||Muscle Spindle||Muscle||
 * ||Joint Receptor||Joint Capsule||
 * ||Ruffini Corpuscle|| ||
 * ||Pacinian Corpuscle|| ||
 * ||Golgi Tendon Organ||Tendon||
 * Temperature||Free Nerve Ending||Skin||
 * Pain||Free Nerve Ending||Most Tissue||


 * 4. Explain events underlying transduction by receptors.**

Receptors are proteins at the end of the distal axon of primary sensory neurons that transduce the four types of stimuli into electrical receptor potentials in the afferent neuron. The receptor are associated with ion channels in the membrane that open when activated to allow positive ions to enter. If the stimulation is large enough to reach threshold a receptor potential is setup in the distal sensory axon.


 * 5. Explain steps involved in the initiation of action potentials.**

Receptors change or transduce mechanical, thermal, or chemical energy of a stimulus into an electrical potential in the distal axon tip. These receptors are proteins inserted into the membranes of the distal axons of primary sensory axons and associated with ion channels. When the receptors are not stimulated, the ion channel is closed; when a stimulus delivers adequate threshold energy, the receptor is activated and causes the ion channel to open and cause a receptor potential as the distal axon ending is locally depolarized.


 * 6. Point out two ways that stimulus intensity is encoded by primary sensory fibers.**

More intense stimuli evoke larger receptor depolarization, leading to a greater number or higher rate of action potentials in sensory fibers. The stronger stimuli will also bring a larger number of fibers to threshold. Thus, stimulus intensity is encoded by frequency in single fibers and number of activated fibers.


 * 7. Explain what a receptive field is, how it contributes to localization of feelings, and how receptive field size varies across receptors.**

A receptive field of a touch fiber is an area of skin in which mechanical stimuli must arrive to cause a given touch fiber to respond. Different fibers with different receptors will have different sized receptive fields. Other receptor-fiber complexes have receptor fields (e.g., proprioception fibers with fields defined in terms of stretch or temperature fibers with fields defined in terms of thermal change.).

Regions of the body with high sensitivity are characterized by innervation by a large number of sensory fibers and sensory fibers with small receptive fields (high resolution). Because receptive fields of adjacent sensory fibers overlap, a stimulus to the skin can activate many sensory fibers and identify the location of the stimulus.


 * 8. Point out differences between rapid and slowly adapting fibers, give examples of each fiber, and explain their contributions to detecting rapid and slowly changing stimuli.**

In an unstimulated state, sensory fibers have low or no baseline levels of action potential discharge. If a stimulus is turned on in the receptive field and maintained for a long duration, rapidly adapting fibers will fire action potentials at the stimulus onset but not during the subsequence maintenance of the stimulus; instead, the response adapts back to baseline quickly. These rapidly adapting fibers are suited to signal stimuli that are transient or change quickly (e.g., pacinian corpuscles to vibration stimuli or Meissner corpuscles to movement across skin).

In contrast, slowly adapting fibers will fire action potentials at the stimulus onset and during maintenance of the stimulus; the response adapts back to baseline slowly. Slow adapting fibers are suited to signal tonically present stimuli (e.g., muscle spindles encoding present state of stretch or free nerve endings encoding continued presence of O MY FUCKING GOD MY HAND IS ON FIRE!!!).


 * 9. Point out the difference between different classes of A fibers and between A and C fibers in terms of sensory modality, conduction velocity, diameter, myelination, and associated receptor types.**

Primary sensory fibers are classified on the basis of axon diameter, conduction velocity, myelination, rate of adaptation, receptor type, and threshold. Sensory fibers fall into 4 categories: A-alpha, A-beta, A-delta, and C fibers. A-alpha, A-beta, and A-delta are all myelinated while C-fibers are unmyelinated. The fiber that conduct signals fastest are associated with proprioception (e.g., A-alpha muscle spindles, golgi tendon organs), followed by touch (e.g., A-beta Meissner, Merkel, Pacinian, Ruffini, and hair follicle), followed by temperature, pain, and crude touch (e.g., A-delta and C free nerve endings). Fibers with high thresholds are activated only by painful, high-amplitude stimuli; all other fibers have low thresholds.


 * **Receptor Type** || **Sensory Fiber Class** || **Receptor-Sensory Fiber Adaptation** || **Threshold** ||
 * Muscle Spindle || A-alpha, A-beta || Slow || Low ||
 * Golgi Tendon Organ || A-alpha, A-beta || Slow || Low ||
 * Meissner Corpuscle || A-beta || Rapid || Low ||
 * Pacinian Corpuscle || A-beta || Rapid || Low ||
 * Merkel Receptor || A-beta || Slow || Low ||
 * Ruffini Corpuscle || A-beta || Slow || Low ||
 * Hair Follicle || A-beta || Rapid || Low ||
 * Free Nerve Ending || A-delta, C || Slow || High (pain); Low (Temperature) ||


 * 10. Explain what the labelled line principle is, and 3 factors which contribute to the labeled line modality specifically of a sensory fiber.**

Most primary sensory fibers are specialized to transmit information about one modality, a concept known as labeled line principle. Three factors contribute to the labeled line modality:

(1) //type of receptor// on its endings (mechanoreceptors, thermoreceptors, etc.) (2) //location// of endings in the body wall – fibers mediating touch and proprioception have receptors for mechanical energy while touch fibers are superficially located in the skin to detect light touch. (3) //threshold// for activation – fibers mediating touch and pain have receptors for mechanical energy but touch fibers have much lower thresholds for response to less intensive stimuli than pain fibers.

There is some overlap in the contribution that each sensory fiber makes to each modality (e.g. touch fibers sensitive to skin displacement are also activated by repositioning of the body and contribute to proprioception to some degree). Additionally, there is a small population of polymodal C fibers also transduce high amplitude mechanical, chemical, and thermal stimuli.


 * 11. Describe how inflammation can sensitize primary sensory neurons.**

Inflammation and tissue damage can results in the release of a variety of substances, including bradykinin, histamine, prostaglandins, serotonin, ATP and H+. The presence of these substance around free nerve endings can results in changes in receptor potential and action potential generating membranes of fibers. Specifically, these substances can:

(1) directly activate receptors (2) increased receptor sensitivity, leading to increased receptor potentials and activation of axons (3) decreased thresholds of voltage-gated channels that facilitate in generating action potentials in distal axons.

Due to these changes, tissue inflammation results in increased receptor potential amplitudes and increased firing of pain fibers from stimuli that normally would not cause action ptentials. This contributes to peripheral sensitization and tenderness/abnormally intense pain sensation from inflamed tissues (primary hyperalgesia). A molecular mechanism to explain peripheral sensitization proposes that inflammation results in increased levels of prostaglandin E2 (PGE2) in inflamed tissues. Binding of PGE2 to prostaglandin EP2 receptors in pain fibers result in increased intrafiber cAMP that activates protein kinase A (PKA). PKA phosphorylizes voltage-gated Na+ channels to increasing their sensitivity and their probability of initiating action potentials to smaller amplitude stimuli.


 * 12. Describe outcomes of sensory fiber regeneration after injury, and give examples of problems that may arise from regeneration.**

Sensory fibers are frequently injured between the cell body and distal end. Following serious injury, the part of the fiber distal to the injury site degenerates. The part of the fiber that remains connected to the cell body can regenerate at a rate of 1-4 mm/day. However, regenerated axons may fail to reassociate with their pre-injury type of end organ or regenerate to a different location. Reinnervation errors can result in abnormal sensations from reinnervated tissue and faulty localization of stimuli. Fibers can get misdirected and regenerate back towards the cell body – when this occurs for large numbers of regenerating fibers in a nerve, a neuroma can form at the injury site.