N-methyl-D-aspartate receptor-mediated modulation of monoaminergic metabolites and amino acids in the chick forebrain: an in vivo microdialysis and electrophysiology study.
The associative avian forebrain region medio-rostral neostriatum/hyperstriatum ventrale (MNH) is involved in auditory filial imprinting and may be considered the avian analogue of the mammalian prefrontal cortex. In search of the neurochemical and physiological mechanisms which play a role in this learning process, we introduced microdialysis and a combined microdialysis/electrophysiological approach in domestic chicks a few days old. With this technique, we were able to follow changes of the extracellular levels of glutamate, taurine, 5-hydroxyindoleacetic acid (5-HIAA), a metabolite of serotonin, and homovanillic acid (HVA), a metabolite of dopamine, and neuronal activity simultaneously in freely moving animals. We obtained first evidence of a modulatory interaction between glutamatergic and monoaminergic neurotransmission mediated by N-methyl-D-aspartate (NMDA) receptors. During local intracerebral infusion of 300 microM NMDA via reverse microdialysis, an increase of taurine and a decrease of 5-HIAA and HVA were detected, accompanied by enhanced extracellular spike rates. Glutamate was increased only during consecutive infusion of increasing NMDA concentrations, when higher (1 mM) NMDA concentrations were infused. The effects of NMDA were antagonized by D, L-2-amino-5-phosphonovaleric acid (1 mM). Infusion of high potassium induced similar changes in taurine, 5-HIAA, and HVA, as found during infusion of NMDA, but decreased extracellular spike rates, which indicates that different cellular mechanisms may underlie the observed neurochemical changes. Neither urethane anesthesia nor different delays between probe implantation and experiment influenced the neurochemical and electrophysiological results; however, changes of taurine were observed only in chronically implanted, awake animals. In summary, microdialysis in combination with electrophysiology provides a powerful tool to detect changes of neuronal activity and transmitter release in the avian brain, with which the role of transmitter interactions can be followed during and after different learning events.
Leibniz Institute for Neurobiology, Project Group Juvenile Learning, POB 1860, 39008 Magdeburg, Germany.
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D000596:Amino Acids / Q000378:metabolism*; D000818:Animals; D015306:Biogenic Monoamines / Q000378:metabolism*; D002552:Cerebral Ventricles / Q000187:drug effects / Q000502:physiology; D002645:Chickens; D004594:Electrophysiology; D005260:Female; D018698:Glutamic Acid / Q000378:metabolism; D006719:Homovanillic Acid / Q000378:metabolism; D006897:Hydroxyindoleacetic Acid / Q000378:metabolism; D007263:Infusions, Parenteral; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D017551:Microdialysis; D016202:N-Methylaspartate / Q000008:administration & dosage / Q000494:pharmacology*; D009474:Neurons / Q000502:physiology*; D011188:Potassium / Q000494:pharmacology; D016548:Prosencephalon / Q000187:drug effects / Q000502:physiology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology*; D013654:Taurine / Q000378:metabolism
D000596:Amino Acids; D015306:Biogenic Monoamines; D016194:Receptors, N-Methyl-D-Aspartate; D013654:Taurine; D018698:Glutamic Acid; D006897:Hydroxyindoleacetic Acid; D016202:N-Methylaspartate; D011188:Potassium; D006719:Homovanillic Acid