Diminution of N-methyl-D-aspartate-induced perturbation of neurotransmission by dexmedetomidine in the CA1 field of rat hippocampus in vitro.
The effects of alpha(2)-adrenoceptor activation on N-methyl-D-aspartic acid (NMDA)-induced perturbation of neurotransmission and normal NMDA-receptor dependent function (long-term potentiation, (LTP)) were investigated in the hippocampal CA1 field in vitro. Bath perfusion of dexmedetomidine hydrochloride (50 nM), which was initiated before NMDA (100 microM) exposure, enhanced the extent of recovery of extracellular field excitatory postsynaptic potentials after NMDA infusion. On the other hand, the induction and early maintenance of LTP was normal in the presence of dexmedetomidine. Thus, dexmedetomidine can diminish acute NMDA-induced perturbation of neurotransmission while the same dose of this drug does not influence the normal activation of NMDA receptors.
Niittykoski
M
M
A.I. Virtanen Institute for Molecular Sciences, University of Kuopio, P.O. Box 1627, FIN-70211, Kuopio, Finland. minna.niittykoski@uku.fi
Haapalinna
A
A
Sirviö
J
J
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000818:Animals; D020927:Dexmedetomidine / Q000494:pharmacology*; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology*; D019706:Excitatory Postsynaptic Potentials; D006624:Hippocampus / Q000187:drug effects* / Q000502:physiology; D066298:In Vitro Techniques; D017774:Long-Term Potentiation / Q000502:physiology; D008297:Male; D016202:N-Methylaspartate / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D018341:Receptors, Adrenergic, alpha-2 / Q000187:drug effects; D016194:Receptors, N-Methyl-D-Aspartate / Q000819:agonists*; D009435:Synaptic Transmission / Q000187:drug effects*
D000316:Adrenergic alpha-Agonists; D018690:Excitatory Amino Acid Agonists; D018341:Receptors, Adrenergic, alpha-2; D016194:Receptors, N-Methyl-D-Aspartate; D016202:N-Methylaspartate; D020927:Dexmedetomidine