A comparative study of selective stimulation of raphe nuclei in the cat in inhibiting dorsal horn neuron responses to noxious stimulation

1981 ◽  
Vol 229 (2) ◽  
pp. 520-524 ◽  
Author(s):  
James L. Griffith ◽  
Glenn B. Gatipon
2005 ◽  
Vol 1057 (1-2) ◽  
pp. 134-140 ◽  
Author(s):  
Arun K. Senapati ◽  
Paula J. Huntington ◽  
Stacey C. LaGraize ◽  
Hilary D. Wilson ◽  
Perry N. Fuchs ◽  
...  

2020 ◽  
Vol 21 (14) ◽  
pp. 5120
Author(s):  
Victor Bergé-Laval ◽  
Christian Gestreau

Pharmacological neuromodulation of swallowing may represent a promising therapeutic option to treat dysphagia. Previous studies suggested a serotonergic control of swallowing, but mechanisms remain poorly understood. Here, we investigated the effects of the serotonergic agonist quipazine on swallowing, using the arterially perfused working heart-brainstem (in situ) preparation in rats. Systemic injection of quipazine produced single swallows with motor patterns and swallow-breathing coordination similar to spontaneous swallows, and increased swallow rate with moderate changes in cardiorespiratory functions. Methysergide, a 5-HT2 receptor antagonist, blocked the excitatory effect of quipazine on swallowing, but had no effect on spontaneous swallow rate. Microinjections of quipazine in the nucleus of the solitary tract were without effect. In contrast, similar injections in caudal medullary raphe nuclei increased swallow rate without changes in cardiorespiratory parameters. Thus, quipazine may exert an excitatory effect on raphe neurons via stimulation of 5-HT2A receptors, leading to increased excitability of the swallowing network. In conclusion, we suggest that pharmacological stimulation of swallowing by quipazine in situ represents a valuable model for experimental studies. This work paves the way for future investigations on brainstem serotonergic modulation, and further identification of neural populations and mechanisms involved in swallowing and/or swallow-breathing interaction.


1997 ◽  
Vol 77 (3) ◽  
pp. 1087-1098 ◽  
Author(s):  
Peggy Mason

Mason, Peggy. Physiological identification of pontomedullary serotonergic neurons in the rat. J. Neurophysiol. 77: 1087–1098, 1997. Spinal serotonin is derived entirely from bulbar sources and plays an important role in spinal modulatory processes, including pain modulation. Establishing the electrophysiological properties of serotonergic bulbospinal neurons in the pontomedullary raphe and reticular formation is critical to understanding the physiological role of serotonin in the spinal cord. Neurons were characterized by their responses to noxious stimulation and their background discharge pattern in the lightly anesthetized rat. Characterized cells were intracellularly labeled with Neurobiotin, which was visualized with a Texas Red fluorophore. Sections containing the labeled cells were processed for serotonin immunocytochemistry with the use of a Bodipy fluorophore. Forty-seven intracellularly labeled cells were tested for serotonin immunoreactivity. The labeled neurons were located in raphe magnus, the nucleus reticularis magnocellularis, and the adjacent reticular and raphe nuclei at levels from the inferior olivary complex to the superior olivary complex. serotonergic cells were located in the raphe nuclei, in nucleus reticularis magnocellularis pars alpha, and in nucleus reticularis paragigantocellularis lateralis, but not in nucleus reticularis magnocellularis pars beta or nucleus reticularis gigantocellularis. Thirteen intracellularly labeled cells contained serotonin immunoreactivity. The background discharge rate of serotonergic cells averaged 1.8 Hz (range: 0.5–3.1 Hz). Discharge was steady and without sustained pauses or bursts in firing. Most serotonin-immunoreactive cells were unaffected or slightly excited by pinch and were unaffected by noxious heat. Three serotonergic cells were weakly excited by both noxious pinch and heat, whereas two serotonergic cells were briefly inhibited by these stimuli. Cells that lacked serotonin immunoreactivity were heterogeneous and included on, off, and neutral cells. Nonserotonergic cells differed from serotonergic cells in having an irregular discharge pattern and/or a high mean discharge rate. A linear discriminant function, employing background discharge characteristics as independent variables, was calculated that successfully classified 13 of 13 serotonergic and 32 of 33 nonserotonergic neurons. The probability of misclassification with the use of this discriminant function was estimated to be <10%. Employing the discriminant function on a test group of cells whose immunochemical content was unknown revealed a population of serotonergic-like cells that resembled the labeled serotonergic cells in background discharge pattern, response to noxious stimulation, and nuclear location. The discharge of pontomedullary serotonergic neurons is slow and steady, suggesting that these neurons may have a role in the tonic, rather than phasic, modulation of spinal processes.


2020 ◽  
Vol 6 (8) ◽  
pp. eaax4568 ◽  
Author(s):  
Sascha R. A. Alles ◽  
Filipe Nascimento ◽  
Rafael Luján ◽  
Ana P. Luiz ◽  
Queensta Millet ◽  
...  

Expression of the voltage-gated sodium channel NaV1.7 in sensory neurons is required for pain sensation. We examined the role of NaV1.7 in the dorsal horn of the spinal cord using an epitope-tagged NaV1.7 knock-in mouse. Immuno–electron microscopy showed the presence of NaV1.7 in dendrites of superficial dorsal horn neurons, despite the absence of mRNA. Rhizotomy of L5 afferent nerves lowered the levels of NaV1.7 in the dorsal horn. Peripheral nervous system–specific NaV1.7 null mutant mice showed central deficits, with lamina II dorsal horn tonic firing neurons more than halved and single spiking neurons more than doubled. NaV1.7 blocker PF05089771 diminished excitability in dorsal horn neurons but had no effect on NaV1.7 null mutant mice. These data demonstrate an unsuspected functional role of primary afferent neuron-generated NaV1.7 in dorsal horn neurons and an expression pattern that would not be predicted by transcriptomic analysis.


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