scholarly journals Primary Afferent Activation of Thermosensitive TRPV1 Triggers Asynchronous Glutamate Release at Central Neurons

Neuron ◽  
2010 ◽  
Vol 65 (5) ◽  
pp. 657-669 ◽  
Author(s):  
James H. Peters ◽  
Stuart J. McDougall ◽  
Jessica A. Fawley ◽  
Stephen M. Smith ◽  
Michael C. Andresen
Keyword(s):  
Glutamate Release ◽  
Primary Afferent ◽  
Central Neurons ◽  
Afferent Activation

The effect of GABA on lumbar terminations of rubrospinal neurons in the cat spinal cord

1984 ◽  
Vol 223 (1230) ◽  
pp. 25-33 ◽  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Gaba Receptors ◽  
Red Nucleus ◽  
Chloride Content ◽  
Inhibitory Process ◽  
Primary Afferent ◽  
Peripheral Cell ◽  
Central Neurons

Although GABA and piperidine-4-sulphonic acid depolarize I a afferent terminations in the cat spinal cord by activation of bicuculline-sensitive GABA receptors, no evidence was obtained for a bicuculline-sensitive alteration by either gabamimetic of the electrical threshold of rubrospinal terminations in the spinal intermediate nucleus. The terminal axonal arborizations in the spinal cord of neurons in the red nucleus thus do not have GABA receptors similar to those on the cell bodies. The results are discussed in relation to the depolarizing action of GABA on some central neurons, and on neurons with peripheral cell bodies, and to probable differences in the intracellular chloride content of neurons having peripheral or central cell bodies, and thus of different embryological origin. A presynaptic depolarizing inhibitory process mediated by GABA appears to be confined to the terminals of primary afferent fibres in the mammalian central nervous system.

Glutamate release in parabrachial nucleus and baroreflex alterations after vagal afferent activation

1997 ◽  
Vol 272 (5) ◽  
pp. R1631-R1640 ◽  
Author(s):  
T. M. Saleh ◽  
L. G. Bauce ◽  
Q. J. Pittman
Keyword(s):  
Sodium Nitroprusside ◽  
High Performance ◽  
Vagal Stimulation ◽  
Glutamate Release ◽  
Male Rats ◽  
Parabrachial Nucleus ◽  
Glutamate Antagonists ◽  
Afferent Activation ◽  
Vagal Afferent ◽  
The Right

The parabrachial nucleus (PBN) is a regulatory nucleus that relays visceral information from the brain stem to the cortex. Immunohistochemical studies have shown that the levels of various neuropeptides in the PBN were changed after visceral afferent activation. Because the major transmitter relaying visceral information through the PBN is glutamate, the present study asked if glutamate release into the PBN also was changed after vagal afferent activation in anesthetized male rats. The distally crushed vagus was stimulated (50 Hz, 1-2 mA, 1 s on, 2 s off) for 2 h. Dialysates of the PBN were collected every 30 min and assayed for glutamate using high-performance liquid chromatography. Extracellular glutamate concentrations were reduced during the vagal stimulation, increased fourfold compared with prestimulated levels after the stimulation was terminated, and returned to prestimulated levels over the next 2 h poststimulation. These changes were not due to alterations in blood pressure because sodium nitroprusside infusion for the same interval resulted in a similar hypotension, but increased glutamate release. Phenylephrine and sodium nitroprusside were infused intravenously to measure the cardiac baroreflex before, during, and after vagal stimulation. The pressor (but not the depressor) response was elevated during the period of enhanced glutamate release, and the baroreflex curve was shifted to the right (increased threshold) without a change in gain. These changes in the cardiac baroreflex were reduced, but still seen, when the PBNs were dialyzed bilaterally with the glutamate antagonists MK-801 and 6-cyano-7-nitroquinoxaline-2,3-dione. Thus visceral activation alters glutamate release in the PBN and has enduring effects on cardiac baroreflex function.

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