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Họ và tên học viên Nữ đang tìm kiếm từ khóa Where are the cell bodies of sympathetic preganglionic neurons located in the spinal cord được Cập Nhật vào lúc : 2022-12-19 05:00:12 . Với phương châm chia sẻ Kinh Nghiệm Hướng dẫn trong nội dung bài viết một cách Chi Tiết 2022. Nếu sau khi Read Post vẫn ko hiểu thì hoàn toàn có thể lại Comment ở cuối bài để Ad lý giải và hướng dẫn lại nha.Within the ciliary ganglion are postganglionic neuronal cell bodies that receive synapses from the preganglionic nerve fibers. The postganglionic nerve fibers, for the most part, travel within the short ciliary nerves and enter the sclera on the temporal side of the globe. These nerves innervate the ciliary muscles and iris sphincter muscles; roughly 95% go to the ciliary muscles and 5% innervate the sphincter muscles. Thus, this parasympathetic innervation is responsible for pupil constriction in response to light as well as for accommodation needed for near vision.
Nội dung chính Show- Neural Regulation of Gastrointestinal Blood Flow29.3.2.2 Parasympathetic NeuronsOVERVIEW OF THE DIGESTIVE SYSTEMParasympathetic nervesPhysiology: The Regulation of Normal Body FunctionCommon Theme 7: Autonomic Nervous SystemNeurobiology of Autonomic GangliaGanglionic Transmission and Rate of Nerve FiringMolecular Signaling in the Gut–Brain Axis in StressSpinal Efferent PathwayTrigeminal NeuralgiaIntroduction and HistoryMale Sexual Behavior during Aging1. Neural ComponentWhere are the cell bodies of preganglionic neurons?Where are cell bodies of preganglionic parasympathetic neurons located?Where is the cell body toàn thân of a sympathetic preganglionic neuron located quizlet?
It should also be noted that experimental evidence demonstrates that intraocular parasympathetic projections also can arise from the pterygopalatine ganglion. These fibers arrive in the orbit by either (1) joining the retro-orbital plexus and then traveling anteriorly to the globe with the ciliary artery, long ciliary nerve, short ciliary nerve, and/or within the optic nerve sheath, or (2) they travel retrogradely with the ethmoidal or infratrochlear nerves and join the long ciliary nerves to enter the globe.
An additional source of parasympathetic innervation to the globe itself is supported by the fact that removal of the ciliary ganglion only reduces the cholinergic nerve fibers within the cornea, iris, and choroid by 60%.
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Neural Regulation of Gastrointestinal Blood Flow
Peter Holzer, in Physiology of the Gastrointestinal Tract (Fifth Edition), 2012
29.3.2.2 Parasympathetic Neurons
The parasympathetic innervation of the GI tract is provided by the vagus and pelvic nerves. While the preganglionic nerve fibers in the pelvic nerves originate in the sacral spinal cord, those running in the vagus nerves emanate from the vagal nuclei (dorsal vagal motor nucleus and nucleus ambiguus) of the brain stem and project to the enteric ganglia of the GI tract, where they impinge on enteric neurons within the myenteric plexus.41–43 Thus, within the gut there are no distinct postganglionic parasympathetic neurons, and the effects that parasympathetic pathways have on GI blood flow are relayed by the enteric nervous system (Figure 29.1). It has been suggested, however, that pelvic parasympathetic neurons may directly innervate mesenteric arteries and veins supplying the human colon.26
The principle transmitter of the preganglionic parasympathetic neurons is acetylcholine, which is also the major mediator of the postganglionic parasympathetic pathways in the enteric nervous system. However, the chemical coding of enteric neurons is highly elaborate,43–46 and the enteric vasodilator neurons that receive input from preganglionic parasympathetic nerve fibers have been little characterized. Vasoactive intestinal polypeptide (VIP) may be one vasodilator messenger of these pathways, given that vagal efferent fibers make contact with myenteric neurons containing VIP.41 Nitric oxide (NO) synthase and gastrin-releasing peptide have also been found in enteric neurons receiving vagal efferent input,41 but it is not known whether these neurons supply GI blood vessels.
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OVERVIEW OF THE DIGESTIVE SYSTEM
Margaret E. Smith PhD DSc, Dion G. Morton MD DSc, in The Digestive System (Second Edition), 2010
Parasympathetic nerves
Preganglionic nerves from both the cranial and sacral divisions of the parasympathetic nervous system supply the gastrointestinal tract. The cranial parasympathetic preganglionic nerve fibres travel in the vagus nerve, except for a few which innervate the mouth and pharyngeal regions. The vagal fibres innervate the oesophagus, stomach, pancreas, liver, small intestine and the ascending and transverse colon (Fig. 1.13). The preganglionic nerves of the sacral division of the parasympathetic nervous system, which innervate the tract, originate in the second, third and fourth segments of the sacral spinal cord and travel in the pelvic nerves to the distal part of the large intestine. The parasympathetic innervation of the tract is more extensive in the upper (orad) region and the distal (rectal and anal) regions than elsewhere. The preganglionic parasympathetic nerve fibres form excitatory synapses with postganglionic neurones in both the myenteric and submucosal plexi. These are mainly excitatory interneurones of the enteric nerve plexi. Stimulation of the parasympathetic nerves can have a diffuse, far-reaching effect to activate the entire enteric nervous system via these interneurones. In general, the effects of activity in the parasympathetic nerves is to stimulate secretion and motility in the gastrointestinal tract. The transmitter released by the preganglionic parasympathetic nerves is acetylcholine and it acts on nicotinic receptors on interneurones in the enteric nerve plexi.
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Physiology: The Regulation of Normal Body Function
Robert G. Carroll PhD, in Elsevier's Integrated Physiology, 2007
Common Theme 7: Autonomic Nervous System
The ANS is a major mechanism for neural control of physiologic functions. Discussions of ANS usually take one of three perspectives: (1) an anatomic perspective based on structure, (2) a physiologic perspective based on function, (3) a pharmacologic perspective based on the receptor subtypes involved. All three perspectives are valid and useful.
The anatomic perspective separates the ANS into a sympathetic and a parasympathetic branch, based in part on the origin and length of the nerves. The sympathetic nerves arise from the thoracolumbar spinal cord and have short preganglionic neurons. The preganglionic nerves synapse in the sympathetic chain, and long postganglionic nerves innervate the final target. Acetylcholine is the preganglionic nerve neurotransmitter, and norepinephrine is the postganglionic neurotransmitter, except for the sweat glands, which have a sympathetic cholinergic innervation. There is an endocrine component of the SNS. Circulating plasma norepinephrine levels come from both overflow from the sympathetic nerve terminals and from the adrenal medulla. Plasma epinephrine originates primarily from the adrenal medulla.
The parasympathetic nerves arise from the cranial and sacral portions of the spinal cord and have a long preganglionic nerve. They synapse in ganglia close to the target tissue and have short postganglionic nerves. The parasympathetic nerves use acetylcholine as the neurotransmitter for both the preganglionic and postganglionic nerves. There is not an endocrine arm to the PNS.
The physiologic perspective of the ANS is based on both homeostatic control and adaptive responses. The ANS, along with the endocrine system, regulates most body toàn thân functions through a standard negative feedback process. The adaptive component of the ANS characterizes the SNS as mediating “fight or flight” and the PNS as mediating “rest and digest.” This classification provides a logical structure for the diverse actions of the sympathetic and parasympathetic nerves on various target tissues.
The SNS is activated by multiple stimuli, including perceived threat, pain, hypotension, or hypoglycemia. The parasympathetic nerves are active during quiescent periods, such as after ingestion of a meal and during sleep. The specific ANS control of each organ is discussed in the appropriate chapter.
The pharmacologic division of the ANS is based on the receptor subtype activated. The SNS stimulates α- and/or β-adrenergic receptors on target tissues. The PNS stimulates nicotinic or muscarinic cholinergic receptors on the target tissues. Cells express different receptor subtypes, and the receptor subtype mediates the action of SNS or PNS on that cell.
ANATOMY
Autonomic Nervous SystemThe sympathetic nerves originate in the intermediolateral horn of the spinal cord and exit the T1 through L2 spinal cord segments. The preganglionic nerve fibers synapse in either the paravertebral sympathetic chain ganglia or the prevertebral ganglia before the postganglionic nerve fibers run to the target tissue. The parasympathetic nerves exit the CNS through cranial nerves III, VII, IX, and X and through the S2 through S4 sacral spinal cord segments. The parasympathetic preganglionic nerve fibers usually travel almost all the way to the target before making the synapse with the postganglionic fibers.
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Neurobiology of Autonomic Ganglia
DAVID L. KREULEN, in Peripheral Neuropathy (Fourth Edition), 2005
Ganglionic Transmission and Rate of Nerve Firing
Autonomic control centers in the CNS regulate the activity in peripheral autonomic pathways, and therefore it is essential that impulses in preganglionic nerves are effectively conveyed through autonomic ganglia to the target organs. Some of the properties of ganglia discussed above might lead to the conclusion that the modulation of ganglionic transmission might prevent this. However, measurement of action potentials of preganglionic and postganglionic nerve fibers in vivo demonstrates that the rate of firing of preganglionic nerve fibers is approximately the same as the rate recorded from postganglionic nerve fibers. This suggests that, least under the conditions of the recordings, there is little modulation of preganglionic firing rate in autonomic ganglia. For example, preganglionic sympathetic fibers of the cat fire 0.1 to 5 Hz rest and 5 to 12 Hz during maximal reflex activation, and postganglionic sympathetic fibers fire 0.1 to 4 Hz rest and 4 to 8 Hz during maximal reflex stimulation. Parasympathetic fibers have been studied less and show a wider range of frequencies. Preganglionic parasympathetic nerves fire 0 to 20 Hz rest and 2 to 60 Hz after maximal activation. Postganglionic parasympathetic nerve fibers to the eye fire 0.1 to 20 Hz rest and greater than 30 Hz during maximal activation.41 The pattern of firing of postganglionic nerve fibers is also an important attribute, but regulation and alteration of the pattern of firing by ganglionic transmission have not been examined.
These observations suggest that strong synaptic connections dominate ganglionic transmission. They also suggest that a given preganglionic axon can form strong synaptic connections with more that one ganglionic neuron. Under the conditions of the in vivo experiments, it appears that the subthreshold or weak inputs to ganglionic neurons, which bring a neuron to firing threshold only when they summate, do not markedly increment the firing frequency of ganglionic neurons; in other words, they do not enhance the gain of ganglionic transmission. The exact physiologic role of these weak or modulatory pathways in ganglionic transmission awaits experimental examination, although first principles tell us that they must enhance it. Furthermore, in in vitro preparations ganglionic neurons can be brought to firing threshold by physiologic activation of mechanosensory afferents in the colon in the absence of preganglionic input (see below). Some insight into this is gained through the recording of activity in single ganglionic neurons in vivo.
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Molecular Signaling in the Gut–Brain Axis in Stress
Amanda J. Page, Hui Li, in Stress: Genetics, Epigenetics and Genomics, 2022
Spinal Efferent Pathway
Spinal efferent nerves represent the major pathway of the sympathetic nervous system. The spinal efferents have cell bodies located in the spinal cord and their axons terminate on preganglionic or postganglionic neurons. The activation of the sympathetic adrenal medullary system is an important mechanism of the body toàn thân's “fight or flight” response in stress. This system responds to stress faster than the HPA axis due to the nerve transmitted signaling. The modulation of this system on the GI tract is shown in Fig. 12.2. In response to stress, the sympathetic efferent nerves send brain signals to preganglionic nerve fibers to activate the adrenal gland to release catecholamines (adrenaline and noradrenaline). One major function of catecholamines is to increase blood pressure and divert blood flow from the GI tract to the muscle and brain, which serves to promote an immediate “fight or flight” reaction to stress. This effect has been shown to contribute to the genesis of stress induced GI ulceration. Further, evidence suggests that catecholamines can also modulate GI immune responses.14 In addition to the activation of the adrenal gland, spinal efferents also have axons that terminate on postganglionic neurons innervating the enteric nervous system, muscle, or blood vessels to modulate GI motility, mucosal secretion, or blood flow. It is reported that CRF2 receptor mediated spinal efferent activation and descending signals to the GI tract contribute to the stress induced delay in gastric emptying.5 In addition, spinal efferents also modulate the GI immune system, evidenced by the close proximity of adrenergic nerve fibers to GI immune cells, the expression of adrenergic receptors in the GI immune cells, and the reduction of immune cell numbers by adrenaline treatment.15 Further the spinal efferent pathway may inhibit the GI immune response to stress, similar to the role of glucocorticoids released from the HPA axis.14
Figure 12.2. The modulatory effect of the sympathetic adrenal medullary system on the gastrointestinal (GI) tract. In response to stress the spinal efferent nerves send brain signals to preganglionic nerve fibers to activate the adrenal gland to release catecholamines, which can reduce GI blood flow and immune responses. The spinal efferents also innervate the GI tract via postganglionic neurons, modulating GI motility, mucosal secretion, blood flow, and immune responses.
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Trigeminal Neuralgia
David C. Straus, ... Laligam N. Sekhar, in Principles of Neurological Surgery (Fourth Edition), 2022
Introduction and History
Trigeminal neuralgia, first described in detail by Dr. James Fothergill in the 18th century, is an affliction of such severe facial pain that it has previously been dubbed the “suicide disease.” Early treatments primarily focused on peripheral neuroablative procedures. Carnochan documented the first successful surgical treatment of the disease in 1856, which used a transantral approach to follow the maxillary nerve back to the gasserian ganglion, which was subsequently excised. In the 1890s Victor Horsley developed a subtemporal approach to the gasserian ganglion where he sectioned the preganglionic nerve fibers. Also in the 1890s Hartley and Krause independently described the extradural approach for gasserian ganglionectomy. In the late 1890s Cushing developed a modification of this extradural ganglionectomy that utilized a more basal trajectory to avoid bleeding from the middle meningeal artery.1 Dandy was the first to perform a lateral suboccipital approach (“cerebellar route”2) to the trigeminal nerve for treatment of trigeminal neuralgia in the 1920s. Similar to other techniques, his involved sectioning of the preganglionic trigeminal nerve. As a result of his intracranial approach through the posterior fossa, he was the first to note the frequent incidence of vascular compression on the trigeminal nerve in its cisternal segment and postulate that sensory root compression may be an important factor in the pathogenesis of trigeminal neuralgia.3 Gardner4,5 furthered this theory in the 1960s and published successful results from vascular decompression of the nerve root. With the advent of the surgical microscope, Jannetta6–8 solidified the theory of vascular compression as the underlying etiology for trigeminal neuralgia and demonstrated the excellent response rate and surgical safety for microvascular decompression (MVD) of the trigeminal nerve in a large series of patients.
Percutaneous techniques also evolved in parallel to open surgical treatments for trigeminal neuralgia. As early as 1910, Harris documented the percutaneous injection of alcohol into the gasserian ganglion in the treatment of a patient with trigeminal neuralgia. In 1914 Härtel described the landmarks and trajectory for accessing the gasserian ganglion through an anterior trajectory. Sweet further established the methods of radiofrequency rhizotomy (RFR),9 and Mullan developed the balloon compression technique.10 The application of the radiation to achieve lesioning of the trigeminal nerve was the first clinical application of stereotactic radiosurgery (SRS) by Leksell in the 1950s.11 Taken together, these techniques—MVD, RFR, balloon compression, glycerol rhizotomy, and SRS—continue to represent the current interventional armamentarium for treating trigeminal neuralgia.
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Male Sexual Behavior during Aging
Helen Kuno, ... Thomas Mulligan, in Functional Neurobiology of Aging, 2001
1. Neural Component
Penile erection is a complex sự kiện, occurring as a result of the integration of central (cerebral and spinal) and local (smooth muscle and endothelium) factors (Anderson and Wagner, 1995). It arises in response to sensory stimuli, fantasy, or genital stimulation. Specialized areas in the hypothalamus and thalamus organize the autonomic response to these stimuli (Sachs, 1995).
Sympathetic preganglionic nerve fibers to the penis arise from neurons in the intermediolateral cell columns of T12–L2 spinal cord segments, while parasympathetic input to the penis arises in the S2–S4 sacral spinal cord segments. Sympathetic impulses travel via the hypogastric nerve, and parasympathetic impulses travel via the pelvic nerve. The pelvic plexus serves as the peripheral integration center for autonomic input to the penis. The pelvic plexus then branches into the cavernous nerves that traverse the posterolateral aspect of the prostate and continue on both sides of the urethra as the cavernosal nerves (Steers, 1990).
In the flaccid state, there is tonic contraction of the arterial and corporal smooth muscles mediated by α 2 adrenergic receptors which maintains high penile arterial resistance (Wagner et al., 1989). With erotic stimulation, there is a decrease in sympathetic tone and an increase in parasympathetic activity. Central to erection is a hemodynamic change which decreases penile arterial resistance with resultant increased penile blood flow (Lue and Tanagho, 1987).
Parasympathetic stimulation activates cholinergic receptors via acetylcholine, stimulating endothelial cells to produce a nonadrenergic, noncholinergic transmitter, nitric oxide (NO). NO relaxes trabecular smooth muscle (Saenz de Tejada et al., 1988), and is considered the major neurotransmitter controlling relaxation of penile smooth muscle (Kim et al., 1991; Rajfer et al., 1992). NO is formed by conversion of l-arginine into l-citrulline by the enzyme, nitric oxide synthase (NOS) (Burnett, 1995a). NOS is activated by the influx of calcium ions that occurs with parasympathetic stimulation. The increased oxygen levels derived from the arterialization of cavernosal blood flow further activates NOS and thereby maintains erection.
NO moves from cell to cell through gap junctions and by diffusion into smooth muscle cells providing the rapidity of the response within the penis (Korenman, 1998). NO activates guanylate cyclase thereby increasing production of cyclic guanidine monophosphate (cGMP). cGMP depletes intracellular calcium and further induces smooth muscle relaxation with resultant penile vasodilation (Burnett, 1995b; Ignarro et al., 1990; Lugg et al., 1995a; Moncada, 1992).
Other chemical entities have been implicated in the control of erection, including prostaglandins E1 (PGE1) and E2 (PGE2) and vasoactive peptide. PGE1, PGE2, and vasoactive peptide stimulate the production of cyclic adenosine monophosphate (cAMP) which decreases intracellular calcium and induces smooth muscle relaxation. Vasoactive peptide may also interact with either endothelial or corporal smooth muscle cells to stimulate local formation of NO, and thereby sustaining penile erection (Makhlouf and Grider, 1993; Said, 1992).
Genital stimulation elicits neural impulses which traverse the dorsal nerve of the penis to the pudendal nerve. From the pudendal nerve, the impulses travel to the sacral spinal cord (S2–S4). Efferent impulses travel along the parasympathetic pelvic nerves and produce an erection as described above.
Where are the cell bodies of preganglionic neurons?
The cell bodies of the preganglionic neurons are in the brainstem or spinal cord of the central nervous system (CNS). The cell bodies of the postganglionic neurons are in autonomic ganglia located peripherally. Axon terminal of preganglionic neurons synapse on dendrites and cell bodies of postganglionic neurons.Where are cell bodies of preganglionic parasympathetic neurons located?
Parasympathetic preganglionic neurons have their cell bodies in the central nervous system and make synapses in the ganglia close to or in the walls of the organs they supply.Where is the cell body toàn thân of a sympathetic preganglionic neuron located quizlet?
Explanation: Cell bodies of the sympathetic preganglionic neurons are located in the lateral horn of the spinal cord gray matter between T1-L2. Tải thêm tài liệu liên quan đến nội dung bài viết Where are the cell bodies of sympathetic preganglionic neurons located in the spinal cord