Activation of rostral ventromedial medulla neurons by noxious stimulation of cutaneous and deep craniofacial tissues.
نویسندگان
چکیده
The rostral ventromedial medulla (RVM) projects to the medullary and spinal dorsal horns and is a major source of descending modulation of nociceptive transmission. Traditionally, neurons in the RVM are classified functionally as on, off, and neutral cells on the basis of responses to noxious cutaneous stimulation of the tail or hind paw. On cells facilitate nociceptive transmission, off cells are inhibitory, whereas neutral cells are unresponsive to noxious stimuli and their role in pain modulation is unclear. Classification of RVM neurons with respect to stimulation of craniofacial tissues is not well defined. In isoflurane-anesthetized male rats, RVM neurons first were classified as on (25.5%), off (25.5%), or neutral (49%) cells by noxious pinch applied to the hind paw. Pinching the skin overlying the temporomandibular joint (TMJ) altered the proportions of on (39.2%), off (42.2%), and neutral (19.6%) cells. To assess the response of RVM cells to specialized craniofacial inputs, adenosine triphosphate (ATP; 0.01-1 mM) was injected into the TMJ and capsaicin (0.1%) was applied to the ocular surface. TMJ and ocular surface stimulation also resulted in a reduced proportion of neutral cells compared with hind paw pinch. Dose-effect analyses revealed that on and off cells encoded the intra-TMJ concentration of ATP. These results suggest that somatotopy plays a significant role in the functional classification of RVM cells and support the notion that neutral cells likely are subgroups of on and off cells. It is suggested that a portion of RVM neurons serve different functions in modulating craniofacial and spinal pain conditions.
منابع مشابه
Glutaminergic receptors in rostral ventrolateral medulla mediate the cardiovascular responses to activation of bed nucleus of the stria terminalis in female rats
The bed nucleus of the stria terminalis (BST) has been known to contain estrogen (E)-concentrating neurons. In addition, injections of E into BST have been reported to potentiate the sympathoinhibitory arterial pressure (AP) and heart rate (HR) responses elicited by glutamate (Glu) stimulation. In this study, the effect of glutamate antagonist receptors in the rostral ventrolateral medulla (RVL...
متن کاملGlutaminergic receptors in rostral ventrolateral medulla mediate the cardiovascular responses to activation of bed nucleus of the stria terminalis in female rats
The bed nucleus of the stria terminalis (BST) has been known to contain estrogen (E)-concentrating neurons. In addition, injections of E into BST have been reported to potentiate the sympathoinhibitory arterial pressure (AP) and heart rate (HR) responses elicited by glutamate (Glu) stimulation. In this study, the effect of glutamate antagonist receptors in the rostral ventrolateral medulla (RVL...
متن کاملGABAergic receptors in rostral ventrolateral medulla mediates the cardiovascular responses to activation of bed nucleus of the stria terminalis in the female rat
The bed nucleus of the stria terminalis (BST) is known to contain estrogen (E)- concentrating neurons. In addition, injections of E into BST have been reported to potentiate the sympathoinhibitory arterial pressure (AP) and heart rate (HR) responses elicited by glutamate (Glu) stimulation. In this study, the effect of GABA-A antagonist receptors, bicuculline methiodide (BMI), in the rostral ven...
متن کاملGABAergic receptors in rostral ventrolateral medulla mediates the cardiovascular responses to activation of bed nucleus of the stria terminalis in the female rat
The bed nucleus of the stria terminalis (BST) is known to contain estrogen (E)- concentrating neurons. In addition, injections of E into BST have been reported to potentiate the sympathoinhibitory arterial pressure (AP) and heart rate (HR) responses elicited by glutamate (Glu) stimulation. In this study, the effect of GABA-A antagonist receptors, bicuculline methiodide (BMI), in the rostral ven...
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عنوان ژورنال:
- Journal of neurophysiology
دوره 113 1 شماره
صفحات -
تاریخ انتشار 2015