Excitation Of Afferent Nerve Fibers Research Articles

BRUXISM AS A CAUSE OF NEUROPHYSIOLOGICAL ALTERATIONS IN THE TRIGEMINAL COMPLEX

All components of the dentoalveolar structures demonstrate close interconnections, especially in the intricate relationship between the nervous and muscular aspects of the temporomandibular joint (TMJ). The muscular system relies hierarchically on the regulatory mechanisms of the nervous system. Consequently, any disruption in the interaction between these components can lead to pathology affecting the overall function of the TMJ. One of the most prevalent myogenic disorders is bruxism, impacting 6-20% of the global population. However, pronounced signs of this condition are observed in only 3-5% of individuals. Bruxism is a multifactorial disorder, and its exact etiology remains unclear. Currently, a primary factor in bruxism is considered to be a disturbance in the body's adaptive capacity to cope with stress. Psychological stress induces hyperactivity in the masticatory muscles, leading to intense clenching of the dentition. This, in turn, results in an overload of the supporting tooth tissues, pathological abrasion of the dentition, dysfunction of the temporomandibular joint (TMJ), and the emergence of general clinical symptoms such as headaches, orofacial issues, and neurological symptoms. The pathophysiological foundation of bruxism lies in the excessive strain on the masticatory muscles, causing ischemia and inflammation in the muscle fibers. The inflammatory process in these fibers triggers a persistent excitation of afferent nerve fibers of type C, giving rise to a dull, aching pain. As bruxism is a chronic condition, there is a physiological restructuring of nerve fibers. This involves the initial peripheral and subsequent central sensitization of C-type nerve fibers, resulting in an inappropriate response of the body to physiological stimuli. For instance, the nervous system begins to interpret minor stimuli as painful (hyperalgesia). Currently, no treatment methods completely eliminate bruxism. Modern treatment approaches involve the use of intraoral dental appliances, pharmacotherapy (with muscle relaxants such as botulinum toxin type A and drugs from the benzodiazepine group), and psychotherapy courses aims to teach patients sleep hygiene, self-control, and the elimination of detrimental habits, including clenching the dentition as a response to psychological stress.

Effects of d-α-aminoadipate on excitation of afferent fibers in the lateral line of Xenopus laevis

The effects of d-α-aminoadipate (DαAA) on excitation of afferent nerve fibers in the Xenopus laevis lateral line were studied in vitro. DαAA reversibly suppressed spontaneous activity and excitation induced by water motion at concentrations as low as 0.25–0.5 mM. Higher concentrations (up to 10 mM) caused a greater suppression that was rapidly and fully reversible. l-α-Aminoadipate at 0.25–1.0 mM had no suppressive effects. Responses elicited by NMDA (1.0–2.0 mM) were the most sensitive to DαAA (0.25–0.5 mM), those elicited by l-aspartate and l-glutamate (1.0–2.0 mM) were less sensitive and similar, and those elicited by kainate (5–15 μM) were the least sensitive. The results provide evidence that the transmitter released by hair cells in the Xenopus lateral line interacts postsynaptically with NMDA-preferring receptors and that the transmitter is an excitatory amino acid, possibly l-glutamate of l-aspartate.

Excitation of afferent cardiac sympathetic nerves is modulated by nitroglycerin.

AbstractWe examined the effect of nitroglycerin on stimulation of sympathetic nerve fibers arising from receptor sites in the left ventricular wall during acute coronary artery occlusion. Sympathetic afferent nerve activity was recorded in single and multifiber nerve preparations dissected from slips of T3 white rami communicantes. Acute left anterior descending or left circumflex coronary artery occlusion produced an increase in segmental myocardial length and excitation of afferent cardiac sympathetic nerve fibers in the region of the myocardium supplied by the occluded artery. Intravenous administration of nitroglycerin in doses up to 100 μg/kg and sodium nitroprusside (50 μg/min) reduced systolic bulge during coronary occlusions and suppressed excitation of these myelinated and unmyelinated afferent fibers. Local intracoronary injection of nitroglycerin (100 μg) produced neither a change in systemic blood pressure nor a change in excitation of the afferent nerve fibers during coronary occlusion. Syste...

Excitation of afferent cardiac sympathetic nerve fibers induced by vagal stimulation.

The effect of vagal stimulation on activity of afferent sympathetic nerve fibers from the dog's left ventricle has been examined. During partial constriction of the coronary artery, a brief electrical stimulation of the cervical vagus nerves resulted in a decrease in blood flow of the constricted artery, systolic bulge of the left ventricle, elevation of the ST segment of electrocardiogram and excitation of the afferent nerve fibers, which continued for up to 15 min. These changes were not produced without coronary artery constriction. Intravenous injection of phentolamine eliminated the decrease in blood flow, and suppressed systolic bulge, elevation of the ST segment and excitation of afferent fibers. Propranolol could not eliminate the decrease in blood flow while suppressed the other changes. Atropine eliminated all of these changes. The results indicate participation of adrenergic alpha-receptors in sustained decrease of coronary blood flow and excitation of afferent cardiac sympathetic nerve fibers which can be produced by a brief vagal excitation.

Effect of propranolol on excitation of afferent sympathetic nerve fibers during myocardial ischemia.

The effect of propranolol on excitation of afferent cardiac sympathetic nerve fibers during myocardial ischemia has been examined. Using anesthetized dogs, the action potentials of the fibers were derived from either the 2nd or 3rd thoracic communicating ramus of the left side. Coronary artery occlusion resulted in excitation of the myelinated Aδfibers and unmyelinated C fibers, and in development of systolic bulge of the occluded area of the left ventricular wall. Eight to 16min after the systemic administrations of 0.5-5mg/Kg propranolol, development of systolic bulge was suppressed and the latency for excitation of the afferent nerve fibers became longer than that of the control occlusion experiments. The number of the action potentials per second during occlusion was significantly smaller than that of the control occlusion and percent change in number per second was close to that of heart rate. Resultantly, the num-ber of the action potentials per cardiac beat was not different from that of the control occlusion experiments. It is considered that propranolol suppressed excitation of the afferent cardiac sympathetic nerve fibers through reduction in heart rate.

Nitroglycerin-induced suppression of excitation of afferent cardiac sympathetic nerves during myocardial ischemia.

The effect of nitroglycerin on excitation of afferent cardiac sympathetic nerve fibers has been examined. Using anesthetized dogs, action potentials of the fibers were derived from either the 2nd or 3rd thoracic communicating ramus of the left side.Occlusion of the anterior descending branch of the left coronary artery resulted in development of systolic bulge of the anterior wall of the left ventricle and in excitation of myelinated Aδ and unmyelinated fibers. Systemic administrations of nitroglycerin in a dose of over 30μg/Kg reduced or eliminated systolic bulge and suppressed excitation of the afferent nerve fibers. The maximum duration of its inhibitory effect on afferent discharge was 240sec and it was produced with 60μg/Kg. The inhibitory effect of nitroglycerin was not observed during hypotension produced by the injections of regitine. The systemic administrations of regitine in a dose of over 100μg/Kg and a fall in systemic blood pressure produced by occlusion of the caval veins also eliminated systolic bulge and suppressed the afferent discharge.It is concluded that the inhibitory action on excitation of afferent cardiac sympathetic nerve fibers during myocardial ischemia is not specific for nitroglycerin and that the inhibitory action of nitroglycerin is dependent on the level of systemic blood pressure.