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Structure
editThe Autonomic Nervous System
editThe autonomic nervous system controls involuntary responses to regulate physiological functions.[1] The brain and spinal cord from central nervous system are connected with organs that have smooth muscle, such as heart, bladder, and other cardiac, exocrine, and endocrine related organs, by ganglionic neurons.[1] The most notable physiological effects from autonomic activity are pupil constriction and dilation, and salivation of saliva.[1] The autonomic nervous system is always activated, but is either in the sympathetic or parasympathetic state.[1] Depending on the situation, one state can overshadows the other, resulting in a release of different kinds of neurotransmitters.[1] There is a lesser known division of the autonomic nervous system known as the enteric nervous system.[2] Located only around the digestive tract, this system allows for local control without input from the sympathetic or the parasympathetic branches, though it can still receive and respond to signals from the rest of the body.[2] The enteric system is responsible for various functions related to gastrointestinal system.[2]
The Sympathetic Nervous System
editThe sympathetic system is activated during a “fight or flight” situation in which great mental stress or physical danger is encountered.[1] Neurotransmitters such as noradrenaline (NA), norepinephrine (NE), and adrenaline (Ad) are released,[1] which increases heart rate and blood flow in certain areas like muscle, while simultaneously decreasing activities of non-critical functions for survival, like digestion.[2] The systems are independent to each other, which allows activation of certain parts of the body, while others remain rested.[2]
The Parasympathetic Nervous System
editPrimarily using the neurotransmitter acetylcholine (ACh) as a mediator, the parasympathetic system allows the body to function in a “rest and digest” state.[2] Consequently, when the parasympathetic system dominates the body, there are increases in salivation and activities in digestion, while heart rate and other sympathetic response decrease.[2] Unlike the sympathetic system, humans have some voluntary controls in the parasympathetic system. The most prominent examples of this control are urination and defecation.[2]
Development
editThe development of both the peripheral and central nervous system (PNS, CNS) for any vertebrate begins in the embryo. Both the CNS and PNS derive from the two bodily structures known as the neural tube, which aids in supporting the embryonic body, and the neural crest, respectively. Additionally, both the neural tube and neural crest are formed from the neural plate, which is a thin strip of tissue along the center of the back on the embryo. It is the center of this strip of tissue that folds into the neural tube and develops into the CNS, while the outskirts of the neural plate strip form the neural crest cells, which correspondingly develop into the peripheral nervous system. The process begins with the notochord, which aids in supporting the embryonic body, initiating neural plate formation following the stabilization of the intact neuroectoderm. This neuroplate is subsequently folded over along its central axis resulting in two foci, or neural folds as well as the neural groove along the center. Ultimately, these two neural folds come together and pinch off the neural plate forming the neural tube, which is subsequently developed into the central nervous system. Formed along this neural tube are the two strips of tissue mentioned previously known as the neural crest. Finally, both the neural tube and neural crest continue to mature and develop into the corresponding nervous systems. This entire process of development from neural plate, to neural tube and neural crest is known as neurulation. The neural crest continues to develop, differentiating into a large variety of cells found in the body that continue to grow and mature, especially into those specific to the peripheral nervous system. Some of the specialized cells including melanocytes, craniofacial cartilage and bone, peripheral and enteric neurons and glia, and smooth muscle all come from neural crest development. More specific to the PNS, from this neural crest we get the development of the neurons of the dorsal root ganglia, the autonomic ganglia, and the paraganglia which includes the adrenergic neurons of the adrenal glands.
Pathology
editPeripheral Neuropathy is one of the most common forms of disease within the Peripheral Nervous System.[3] Damage or malfunction in peripheral nerves generates not only acute and chronic pain, but also changes in sensory pathways.[3] In response to such nerve damage, restorative processes, including Inflammation and other proinflammatory processes, create hyperexcitability within the sensory neurons, called peripheral sensitization.[3] These peripheral nerve fibers are then able to associate with nociceptive fibers and are then able to elicit pain.[3] This sensitization pathway is not functioning during either normal tissue operation or lack of inflammation unless the sensory neurons are been permanently damaged.[3] The pain that stems from Peripheral Neuropathy stems from NMDA receptors and the release of the neurotransmitter glutamate from sensory neurons in the brain. [3] Release of glutamate and coupled neurotransmitters that connect neurokinin receptors causes release of magnesium and calcium ions while simultaneously activating NMDA receptors.[3] This causes postsynaptic cells to send a painful signal to the brain.[3] Upon interaction with calcium, the NMDA receptors become more sensitive and the neuronal threshold is lowered.[3] Mononeuropathy is a subset under the broad context of Peripheral Neuropathy and occurs only when a single nerve outside of the Central Nervous System is affected.[3] The most common forms of mononeuropathy are when physical stress is placed on a particular nerve, known more specifically as compression neuropathy.[3] One of the most common forms of mononeuropathy is carpal tunnel syndrome.[3] Common symptoms of carpal tunnel syndrome include pain and numbness in the thumb, index and middle finger.[3] One of the major causes of carpal tunnel syndrome is demyelination of axons through mechanical stress.[3] A lack of myelin can prevent nervous transmission and eventually, development of an endoneural edema.[3] This culminates in the degeneration of axons and release of pro inflammatory molecules, causing pain and redness.[3] Other subsets of peripheral neuropathy include polyneuropathy which causes pain in similar areas on both sides of the body, diabetic neuropathy or nerve damage associated with diabetes mellitus, and autonomic neuropathy which consists of peripheral nerve damage that directly affects the autonomic nervous system.[3]
References
edit- ^ a b c d e f g Laight, David (September 2013). "Overview of peripheral nervous system pharmacology". Nurse Prescribing. ISSN 1479-9189.
- ^ a b c d e f g h Matic, Agnella Izzo (2014). "Introduction to the Nervous System, Part 2: The Autonomic Nervous System and the Central Nervous System". AMWA Journal: American Medical Writers Association Journal (AMWA J). ISSN 1075-6361.
- ^ a b c d e f g h i j k l m n o p q Vanotti, Alessandra; Osio, Maurizio; Mailland, Enrico; Nascimbene, Caterina; Capiluppi, Elisa; Mariani, Claudio (2007). "Overview on Pathophysiology and Newer Approaches to Treatment of Peripheral Neuropathies". CNS Drugs. ISSN 1172-7047.