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Anatomy and Function of the Intrathoracic Neurons Regulating the Mammalian Heart
Published in Irving H. Zucker, Joseph P. Gilmore, Reflex Control of the Circulation, 2020
The locations of the somata of afferent neurons that innervate the heart have been studied relatively extensively due, in part, to the relevance of the subject to our understanding of the symptomatology of cardiac pain. The somata of cardiac afferent neurons lie in the nodose (Kalia and Mesulam, 1980) and dorsal root (Kuo et al., 1984; Vance and Bowker, 1983) ganglia. Since cardiac pain is referred most frequently to the left upper limb and thorax, it has been assumed that the majority of the somata of afferent neurons innervating the heart is located in left-sided dorsal root ganglia (White, 1957; Whitteridge, 1948). However, afferent neurons that innervate the heart are located primarily throughout the nodose ganglia bilaterally, with lesser numbers being in the C7–T4 dorsal root ganglia bilaterally (Hopkins and Armour, 1989). As the majority of the somata of afferent neurons innervating any cardiac region are in the nodose ganglia rather than in the dorsal root ganglia and since they are distributed relatively evenly bilaterally, it appears that the locations of the first-order afferent neurons innervating the heart cannot fully account for the perceived anatomical localization of angina that occurs during cardiac disease. Presumably integration at the level of central nervous system neurons accounts, in part, for this symptomatology (Foreman et al., 1986).
Baroreflex Failure
Published in David Robertson, Italo Biaggioni, Disorders of the Autonomic Nervous System, 2019
Below this the nerve again thickens to form the much larger nodose ganglion. The vagus then lies in close proximity to the accessory (XI) and the glossopharyngeal nerves, and the internal jugular vein. The vagus continues to descend between the internal (then common) carotid and the internal jugular vein (Brodal, 1957).
Neuroactive Substances in the Control of Cardiovascular and Visceral Responses: An Overview
Published in I. Robin A. Barraco, Nucleus of the Solitary Tract, 2019
Removal of the nodose ganglion itself, or degeneration of vagal afferents, leads to a number of physiologically relevant events. Specifically, concentrations and release of some putative transmitters diminishes significantly in NTS.64,65,98 Deafferentation may also cause altered receptor binding. In some cases, changes in affinity of receptors for putative transmitters have been consistent with denervation supersensitivity94 that have been further supported by physiological studies.99
Communication between the gut microbiota and peripheral nervous system in health and chronic disease
Published in Gut Microbes, 2022
Tyler M. Cook, Virginie Mansuy-Aubert
As illustrated in Fig.1 and 2, vagal and spinal afferent neurons innervate the digestive tract, monitoring mechanical, chemical, thermal, and nociceptive signals related to the diet and microbiota.40–45 It is important to note that some enteric neurons are also characterized as afferent and they are labeled as “intrinsic”, while spinal and vagal neurons which originate outside of the gut are “extrinsic”. Vagal afferent neurons transmit signals up from the viscera, their cell bodies are located in the nodose ganglia (NG), and they synapse into the solitary nucleus (NTS) in the brainstem (Figure 2). The NTS integrates vagal afferent signals and relays the information up to higher brain regions such as the hypothalamus, or reflexes back down to the dorsal motor nuclei of the brainstem where vagal efferent neurons project out to effector organs.46 Spinal neurons, with cell bodies in the dorsal root ganglia (DRG), project into the dorsal horn of the spinal cord. These signals are relayed up to the brain and integrated, or they induce reflex activation of motor neurons which may bypass the brain. The spinal nerves can be subdivided into 5 divisions: cervical, thoracic, lumbar, sacral, and coccygeal, based on their projections into and out of the vertebrae.
The Vagus Nerve and the Celiaco-mesenteric Ganglia Participate in the Feeding Responses Evoked by Non-sulfated Cholecystokinin-8 in Male Sprague Dawley Rats
Published in Endocrine Research, 2020
Amged I. Dafalla, Thaer R. Mhalhal, Kenneth Hiscocks, John Heath, Ayman I. Sayegh
The vagus nerve comprises the main parasympathetic innervation of the gastrointestinal tract, with cell bodies located in the nodose ganglia (the sensory/afferent portion) and the dorsal motor nucleus of the vagus (DMV, the motor/efferent portion).9,10 The splanchnic nerve comprises the main sympathetic innervation of the gut and also contains visceral afferent and efferent fibers. The cell bodies of the first-order neurons of this nerve reside in the pre – and paravertebral ganglia along the spinal cord, whereas the cell bodies of the second-order neurons reside in the celiaco-mesenteric ganglia, located between the celiac and the cranial mesenteric arteries.11,12 Although both nerves contain efferent and afferent fibers, the majority of these fibers are afferents e.g. over 85% of the fibers in the vagus nerve are afferents.9,10,13,14
Tapia syndrome: an unusual complication following posterior cervical spine surgery
Published in British Journal of Neurosurgery, 2019
Adikarige HD Silva, Matthew Bishop, Hari Krovvidi, Declan Costello, Jasmeet Dhir
The neurological deficit is usually unilateral and spares the accessory cranial nerve (XI). This differentiates Tapia syndrome from other jugular foramen syndromes such as Vernet (IX, X and XI), Collet-Sicard (IX, X, XI and XII) and Villaret (Collet-Sicard and Horner’s syndrome). Symptoms include hoarseness of voice, ipsilateral tongue weakness and dysphagia due to tongue incoordination and vocal cord dysfunction. Signs include ipsilateral tongue deviation on protrusion and ipsilateral vocal cord paresis or paralysis confirmed on endoscopic visualisation. Atrophy of the denervated side of the tongue may also occur with chronic injury. Glottic sensation is often intact because the external branch of the vagus nerve providing its sensation branches off just below the nodose ganglion and before the likely site of compression and injury. Diagnosis relies on recognition of the concurrent paralyses (clinical examination and endoscopic examination; other invasive techniques such as laryngeal and tongue electromyography are often not required) and exclusion of other aetiologies. Treatment is supportive, with emphasis on empiric corticosteroids and dysphagia and vocal cord therapy. Recovery is excellent in 30% of patients, incomplete in 39% of patients and none in over 26% of patients.3