Activation of groups I or III metabotropic glutamate receptors inhibits excitatory transmission in the rat subthalamic nucleus
- PMID: 11445183
- DOI: 10.1016/s0028-3908(01)00047-8
Activation of groups I or III metabotropic glutamate receptors inhibits excitatory transmission in the rat subthalamic nucleus
Abstract
The subthalamic nucleus (STN) is a key nucleus in the basal ganglia motor circuit that provides the major glutamatergic excitatory input to the basal ganglia output nuclei. The STN plays an important role in the normal motor function, as well as in pathological conditions such as Parkinson's disease. Development of a complete understanding of the role of the STN in motor control will require a detailed understanding of the mechanisms involved in the regulation of excitatory and inhibitory synaptic transmission in this nucleus. Here, we report that activation of groups I or III metabotropic glutamate (mGlu) receptors, but not group II, causes a depression of excitatory transmission in the STN. In contrast, mGlu receptor activation has no effect on the inhibitory transmission in this nucleus. Further characterization of the group I mGlu receptor-induced effect on EPSCs suggests that this response is mediated by mGlu1 and not mGlu5. Further, paired pulse studies suggest that both the mGlu1 receptor and the group III mGlu receptor-mediated effects are due to a presynaptic mechanism. If these receptors are involved in endogenous synaptic transmission in the STN, these results raise the exciting possibility that selective agents targeting mGlu receptors may provide a novel approach for the treatment of motor disorders involving the STN.
Similar articles
-
Activation of metabotropic glutamate receptor 5 has direct excitatory effects and potentiates NMDA receptor currents in neurons of the subthalamic nucleus.J Neurosci. 2000 Nov 1;20(21):7871-9. doi: 10.1523/JNEUROSCI.20-21-07871.2000. J Neurosci. 2000. PMID: 11050106 Free PMC article.
-
Dual modulation of excitatory synaptic transmission by agonists at group I metabotropic glutamate receptors in the rat spinal dorsal horn.Brain Res. 2000 Dec 29;887(2):359-77. doi: 10.1016/s0006-8993(00)03066-3. Brain Res. 2000. PMID: 11134626
-
Group II and group III metabotropic glutamate receptor agonists depress synaptic transmission in the rat spinal cord dorsal horn.Neuroscience. 2000;100(2):393-406. doi: 10.1016/s0306-4522(00)00269-4. Neuroscience. 2000. PMID: 11008177
-
Serotonin regulation of subthalamic neurons.Rev Neurosci. 2014;25(4):605-19. doi: 10.1515/revneuro-2014-0004. Rev Neurosci. 2014. PMID: 24717335 Review.
-
Glutamate receptor ligands.Handb Exp Pharmacol. 2007;(177):217-49. doi: 10.1007/978-3-540-33823-9_8. Handb Exp Pharmacol. 2007. PMID: 17087125 Review.
Cited by
-
Group I metabotropic glutamate receptors in the monkey striatum: subsynaptic association with glutamatergic and dopaminergic afferents.J Neurosci. 2003 Aug 20;23(20):7659-69. doi: 10.1523/JNEUROSCI.23-20-07659.2003. J Neurosci. 2003. PMID: 12930805 Free PMC article.
-
Pesticides Drive Stochastic Changes in the Chemoreception and Neurotransmission System of Marine Ectoparasites.Int J Mol Sci. 2016 May 31;17(6):700. doi: 10.3390/ijms17060700. Int J Mol Sci. 2016. PMID: 27258252 Free PMC article.
-
Glutamate receptors and Parkinson's disease: opportunities for intervention.Drugs Aging. 2003;20(5):377-97. doi: 10.2165/00002512-200320050-00006. Drugs Aging. 2003. PMID: 12696997 Review.
-
Localization and expression of group I metabotropic glutamate receptors in the mouse striatum, globus pallidus, and subthalamic nucleus: regulatory effects of MPTP treatment and constitutive Homer deletion.J Neurosci. 2007 Jun 6;27(23):6249-60. doi: 10.1523/JNEUROSCI.3819-06.2007. J Neurosci. 2007. PMID: 17553998 Free PMC article.
-
Group II metabotropic glutamate receptor modulation of excitatory transmission in rat subthalamic nucleus.J Physiol. 2003 Dec 1;553(Pt 2):489-96. doi: 10.1113/jphysiol.2003.052209. Epub 2003 Sep 18. J Physiol. 2003. PMID: 14500768 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
