Adrenergic Fiber, The Heart Fixer

Cholinergic fibers carried in the vagus are responsible for lowering heart rate. Increased cholinergic tone is the primary mechanism for abrupt bradycardia, as is often observed during exposure to hypoxia, at the initiation of burst swimming, and with visual and olfactory stimuli. Vagotomy or atropine injections abolish bradycardia. It is likely that acetylcholine, released from the large number of cholinergic nerve terminals in the sinoatrial region, hyperpolarizes pacemaker cells and slows the pacemaker rate. However, the specific action of neurotransmitter release on pacemaker cells in fish probably needs reexamining, since find that in amphibian and mammalian cardiac cells, acetylcholine applied as a pharmacological agent causes pacemaker hyperpolarization whereas acetylcholine released as a result of vagal stimulation does not.

The cholinergic mechanisms that control heart rate are affected by temperature acclimation. For example, the level of cholinergic inhibition of heart rate is greater in cold-acclimated compared with warm-acclimated Scyliorhinus canicula and rainbow trout.
Peripheral adrenergic and cholinergic fibers are present and provide innervation to a number of organelles in the skin including hair follicles, blood vessels, sweat glands and arrector pili muscles. Unmyelinated nociceptive C fibers pierce the basement membrane to innervate the epidermis from a subdermal plexus that runs just below the basement membrane. Clinical skin biopsies can be stained with the pan-axonal marker protein gene product and imaged by light microscopy to highlight the nerve fibers that surround the sweat gland tubules. The complexity of sweat gland innervation limits the utility of descriptive and semiquantitative methods for determining sudomotor density. Hair follicles extend from the deeper dermal tissue, through the basement membrane and epithelial layer and extend beyond the border of the skin. Arrector pili muscles anchor hair follicles by attaching the shaft of the hair follicle to the dermal tissue. Upon stimulation, the contracting muscles cause piloerection with the formation of cutis anseri, or goose bumps. The decline in both sudomotor and pilomotor nerve fiber density parallels overall neuropathy progression and is associated with longer duration of diabetes and higher glycosylated hemoglobin levels.

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