The responsiveness of the rat intergeniculate leaflet neurons to glutamatergic agonists.
The intergeniculate leaflet (IGL) has been shown to be a functional constituent of the circadian timing system. The IGL receives a monosynaptic input from the retina and is known to mediate some of the effects of light on the circadian clock. In the majority of retinal ganglion cells, glutamate functions as an excitatory neurotransmitter. The effect of monosodium glutamate and N-methyl-D-aspartate (NMDA), on the extracellularly recorded discharge activity of IGL neurons was studied in vitro. The application of monosodium glutamate induced either an excitatory, a biphasic or an inhibitory response. Application of NMDA induced an excitatory response in the majority of tested neurons. To determine the role of NMDA receptors in the response to glutamate application, the selective antagonist of NMDA receptors- AP-5, was applied to the incubation medium. The presence of AP-5 reduced the response of the IGL cells to focal application of glutamate and completely blocked their responsiveness to NMDA. To clarify whether GABAergic interneurons are involved in mediation of the inhibitory effects of glutamate, we repeated our experiments in the presence of bicuculline in the incubation medium. Since bicuculline did not influence the observed inhibitory effects, the involvement of GABAA receptors was excluded. The present study provides the first electrophysiological evidence that neurons in the rat IGL, respond to glutamate probably through NMDA receptors. However, our results also suggest that other types of glutamate receptors may play an additional role in mediating the action of this excitatory amino acid on the IGL neurons.
Błasiak
A
A
Department of Neurophysiology & Chronobiology, Chair of Animal Physiology, Jagiellonian University, Krakow, Poland.
Pekala
D
D
Lewandowski
M H
MH
D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D004594:Electrophysiology; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology*; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D005829:Geniculate Bodies / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D066298:In Vitro Techniques; D008297:Male; D016202:N-Methylaspartate / Q000494:pharmacology*; D009474:Neurons / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D016194:Receptors, N-Methyl-D-Aspartate / Q000819:agonists / Q000037:antagonists & inhibitors; D012970:Sodium Glutamate / Q000494:pharmacology*; D013493:Suprachiasmatic Nucleus / Q000166:cytology / Q000502:physiology
D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D016194:Receptors, N-Methyl-D-Aspartate; D016202:N-Methylaspartate; D015763:2-Amino-5-phosphonovalerate; D012970:Sodium Glutamate; D001640:Bicuculline