|
|
|
|
 |
|||
|
|||
Relationship of glutamate and aspartate to the periaqueductal gray- raphe magnus projection: analysis using immunocytochemistry and microdialysis
AJ Beitz
Department of Veterinary Biology, University of Minnesota, St. Paul 55108.
This study tested the hypothesis that the excitatory amino acid transmitters glutamate and/or aspartate are associated with the periaqueductal gray (PAG)-raphe magnus (NRM) projection. Retrograde neuroanatomical tracing procedures utilizing the tracers WGA-HRP or D- [3H]-aspartate were combined with immunocytochemical localization of glutamate or aspartate to determine if glutamate and/or aspartate immunostained neurons projected to the NRM. Both glutamate- and aspartate-immunoreactive cells in the PAG were found to project to the NRM. Double labeling immunocytochemichemical procedures indicated that glutamate and aspartate are co-localized in many PAG neurons, suggesting the following possibilities: (a) one of these two amino acids may serve as a precursor to the other; (b) both amino acids may be co-released from the same PAG neuron; or (c) both amino acids are present in high levels in the perikarya for metabolic purposes. At the EM level, both glutamate- and aspartate-immunoreactive terminals were identified in the NRM, strengthening the concept that both amino acids participate in synaptic transmission in this medullary nucleus. To determine if glutamate and aspartate are in fact released from PAG-NRM axons, the PAG was stimulated chemically with homocysteic acid (HCA) and amino acids were collected from the NRM using a microdialysis probe. Microinjection of HCA, but not vehicle, into the PAG resulted in the release of both glutamate and aspartate in the nucleus raphe magnus. These data suggest that both glutamate and aspartate are released from PAG fibers terminating in the NRM and provide strong support for the hypothesis that excitatory amino acids play a neurotransmitter role in the PAG-NRM pathway.
Volume 38,
Issue 12,
pp. 1755-1765,
12/01/1990
Copyright © 1990 by The Histochemical Society
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  I. D. Meng, J. P. Johansen, I. Harasawa, and H. L. Fields Kappa Opioids Inhibit Physiologically Identified Medullary Pain Modulating Neurons and Reduce Morphine Antinociception J Neurophysiol, March 1, 2005; 93(3): 1138 - 1144. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Miki, Q.-Q. Zhou, W. Guo, Y. Guan, R. Terayama, R. Dubner, and K. Ren Changes in Gene Expression and Neuronal Phenotype in Brain Stem Pain Modulatory Circuitry After Inflammation J Neurophysiol, February 1, 2002; 87(2): 750 - 760. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. Pose, S. Sampogna, M. H. Chase, and F. R. Morales Cuneiform Neurons Activated during Cholinergically Induced Active Sleep in the Cat J. Neurosci., May 1, 2000; 20(9): 3319 - 3327. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Cui, Y. Feng, D. J. McAdoo, and W. D. Willis Periaqueductal Gray Stimulation-Induced Inhibition of Nociceptive Dorsal Horn Neurons in Rats Is Associated with the Release of Norepinephrine, Serotonin, and Amino Acids J. Pharmacol. Exp. Ther., May 1, 1999; 289(2): 868 - 876. [Abstract] [Full Text]
|
|
| Guidelines | Subscriptions | About | exPRESS - Current - Archive | Business Information | Contact |