A ROLE FOR NON-NMDA EXCITATORY AMINO-ACID RECEPTORS IN REGULATING THEBASAL ACTIVITY OF RAT GLOBUS-PALLIDUS NEURONS AND THEIR ACTIVATION BYTHE SUBTHALAMIC NUCLEUS

Citation
Rp. Soltis et al., A ROLE FOR NON-NMDA EXCITATORY AMINO-ACID RECEPTORS IN REGULATING THEBASAL ACTIVITY OF RAT GLOBUS-PALLIDUS NEURONS AND THEIR ACTIVATION BYTHE SUBTHALAMIC NUCLEUS, Brain research, 666(1), 1994, pp. 21-30
Citations number
72
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
666
Issue
1
Year of publication
1994
Pages
21 - 30
Database
ISI
SICI code
0006-8993(1994)666:1<21:ARFNEA>2.0.ZU;2-U
Abstract
We have investigated the hypothesis that excitatory amino acid (EAA) r eceptors in the globus pallidus (GP) play a significant role in mainta ining the firing rates of GP neurons under basal conditions and follow ing activation of the subthalamic nucleus (STN). Drugs were infused di rectly into the GP and/or STN while the extracellular single unit acti vity of Type II GP neurons was recorded in ketamine-anesthetized rats. Local infusions of the EAA agonists NMDA (30-300 pmol/200 nl) or AMPA (0.1-1 pmol/200 nl) elicited increases in the firing rate of GP neuro ns in a dose-dependent fashion. Infusion of the GABA(A) receptor antag onist bicuculline methiodide (1-10 pmol/100 nl) into the STN also elic ited dose-related increases in the firing rate of GP neurons. Intrapal lidal infusion of the non-NMDA (AMPA/kainate) receptor antagonist NBQX (0.1-1.0 nmol) reduced the basal firing rate of GP neurons by 40%. In contrast, the NMDA antagonist MK-801 (0.01-0.1 nmol) produced no sign ificant effect on basal firing rate. Intrapallidal infusion of the non -selective EAA receptor antagonist kynurenic acid or NBQX reversed or blocked the increase in firing rate of GP neurons following bicucullin e-induced activation of the STN. Similar treatment with MK-801, howeve r, had no significant effect on this response. These results indicate that tonic stimulation of non-NMDA receptors plays an important role i n maintaining the basal activity of GP neurons and in mediating the ef fects of increased excitatory input from subthalamic afferent neurons.