Role of N-methyl-D-aspartate and metabotropic glutamate receptors in corticothalamic excitatory postsynaptic potentials in vivo.
The ventrobasal thalamus is the principal somatosensory thalamic relay nucleus, and it receives two major sources of excitatory input: firstly an input from ascending sensory afferents, and secondly a descending projection from the primary somatosensory cortex. There is considerable anatomical evidence to suggest that both of these projections utilise the excitatory amino acid L-glutamate as their neurotransmitter. Previous work from this laboratory has shown that the sensory input to the rat ventrobasal thalamus in vivo is mediated by ionotropic excitatory amino acid receptors of both the N-methyl-D-aspartate and non-N-methyl-D-aspartate type. These findings are consistent with data from other studies in various thalamic relay nuclei. In contrast, there are considerably less data available concerning the synaptic pharmacology of the corticothalamic projection although there have been both speculation and studies concerning the functional significance of this pathway. There is some evidence to suggest an involvement of N-methyl-D-aspartate receptors and metabotropic glutamate receptors. The aim of this study was to determine which excitatory amino acid receptors might mediate cortically-elicited excitatory postsynaptic potential in the ventrobasal thalamus in vivo. Intracellular recordings were made, and neurotransmitter antagonists were applied on to rat ventrobasal thalamus neurons by microiontophoresis. Cortically-elicited excitatory postsynaptic potentials were reduced by the N-methyl-D-aspartate antagonist 3-[(+/-)-2-carboxy-piperazin-4-yl]-propyl-1-phosphonate, or the Group I metabotropic antagonist (S)-4-carboxyphenylglycine. These data indicate that both N-methyl-D-aspartate receptors and Group I (possibly metabotropic glutamate receptors type I) metabotropic receptors are involved in the mediation of corticothalamic transmission. Such a transmitter mechanism would allow a modulatory system that could selectively enhance other excitatory inputs. Some of these data have been reported in abstract form.
Eaton
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Department of Visual Science, University College London, UK.
Salt
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D000818:Animals; D002540:Cerebral Cortex / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009434:Neural Pathways / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D018094:Receptors, Metabotropic Glutamate / Q000037:antagonists & inhibitors / Q000502:physiology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors / Q000502:physiology*; D013569:Synapses / Q000187:drug effects / Q000502:physiology; D013787:Thalamic Nuclei / Q000166:cytology / Q000187:drug effects / Q000502:physiology*
D018094:Receptors, Metabotropic Glutamate; D016194:Receptors, N-Methyl-D-Aspartate