Thyrotropin-releasing hormone selectively depresses glutamate excitation of cerebral cortical neurons.
The microiontophoretic application of thyrotropin-releasing hormone causes a selective reduction in neuronal excitation evoked by L-glutamate but not by acetylcholine in rat cerebral cortex. Thyrotropin-releasing hormone has no influence on the activity of acetylcholinesterase or on choline uptake and release from cerebral synaptosomes. This evidence for a selective interaction between a centrally acting peptide and an excitatory amino acid neurotransmitter may indicate a specific locus of thyrotropin-releasing hormone action at glutamate-activated receptor sites.
D000109:Acetylcholine / Q000378:metabolism; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001224:Aspartic Acid / Q000037:antagonists & inhibitors; D002540:Cerebral Cortex / Q000187:drug effects* / Q000502:physiology; D018691:Excitatory Amino Acid Antagonists; D008297:Male; D051381:Rats; D017981:Receptors, Neurotransmitter / Q000187:drug effects; D009435:Synaptic Transmission / Q000187:drug effects; D013973:Thyrotropin-Releasing Hormone / Q000494:pharmacology*
D018691:Excitatory Amino Acid Antagonists; D017981:Receptors, Neurotransmitter; D001224:Aspartic Acid; D013973:Thyrotropin-Releasing Hormone; D000109:Acetylcholine