Involvement of Ionotropic Glutamate Receptors and Nitric Oxide in DOPA-Induced Depressor Responses in the Nucleus Tractus Solitarii
L-Dihydroxyphenylalanine (DOPA) is proposed to be a neurotransmitter for the primary baroreceptor afferents terminating in the nucleus tractus solitarii (NTS),1 and it produces glutamate-like depressor responses when microinjected into the NTS of anesthetized rats. Little is known about the mechanism of such an excitatory action of DOPA. In striata, exogenous DOPA induces glutamate release and endogenous DOPA is a causal factor for the ischemic glutamate release and resultant delayed neuronal death.2 In the present study, we tried to clarify whether glutamate receptors and/or nitric oxide (NO), an important modulator for central cardiovascular regulation, are involved in the DOPA-induced cardiovascular responses in the NTS of anesthetized rats.
KeywordsNitric Oxide Glutamate Receptor Cardiovascular Response Nucleus Tractus Solitarii Ionotropic Glutamate Receptor
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- 2.N. Furukawa, N. Arai, Y. Goshima, T. Miyamae, E. Ohshima, F. Suzuki, K. Fujita, and Y. Misu, Endogenously released DOPA is a causal factor for glutamate release and resultant delayed neuronal cell death by transient ischemia in rat striata, J. Neurochem. 76, 815–824 (2001).PubMedCrossRefGoogle Scholar