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N-methyl-D-aspartate receptors in the spinal cord mediate pressor responses to stimulation of the rostral ventrolateral medulla in the rat.
Mills, E H; Minson, J B; Pilowsky, P M; Chalmers, J P.
Affiliation
  • Mills EH; Department of Medicine, Flinders Medical Centre, Bedford Park, South Australia.
Clin Exp Pharmacol Physiol ; 15(2): 147-55, 1988 Feb.
Article in En | MEDLINE | ID: mdl-2908430
ABSTRACT
1. Activation of bulbospinal neurons projecting from the C1 area of the rostral ventrolateral medulla evokes a pressor response. The nature of the neurotransmitters involved in mediating this response at spinal cord level has not been established. 2. Amino acid antagonists were introduced into the spinal subarachnoid space to investigate the role of spinal amino acid receptors in mediating this pressor response in the anaesthetized rat. 3. Intrathecal administration of the amino acid receptor antagonists 2-amino-phosphono valeric acid (2APV), gamma-glutamyl glycine, kynurenate or glutamic acid diethylester (GDEE) attenuated the pressor responses to stimulation of the C1 area. These compounds have been shown to antagonize N-methyl-D-aspartate (NMDA) sensitive receptors. 4. Intrathecal administration of 2APV significantly attenuated the increase in blood pressure produced by injection of NMDA into the spinal subarachnoid space. 5. These results suggest that the pressor response produced by stimulation in the area of the C1 neurons in the rostral ventrolateral medulla of the rat is mediated at least in part by NMDA receptors in the spinal cord.
Subject(s)
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Collection: 01-internacional Database: MEDLINE Main subject: Spinal Cord / Blood Pressure / Medulla Oblongata / Receptors, Neurotransmitter Limits: Animals Language: En Journal: Clin Exp Pharmacol Physiol Year: 1988 Document type: Article
Search on Google
Collection: 01-internacional Database: MEDLINE Main subject: Spinal Cord / Blood Pressure / Medulla Oblongata / Receptors, Neurotransmitter Limits: Animals Language: En Journal: Clin Exp Pharmacol Physiol Year: 1988 Document type: Article
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