Abstract
In the anterior cingulate cortex (ACC), GluR5-containing kainate receptor mediated the small portion of excitatory postsynaptic current. However, little is known about its role in modulation of neurotransmitter release in this brain region. In the present study, we address this question by using selective GluR5 agonist and antagonist, as well as GluR5-/- mice. Our results showed that activation of GluR5 induced action potential-dependent GABA release, which is also required for the activation of voltage-dependent calcium channel and Ca2+ influx. The effect of GluR5 activation is selective to the GABAergic, but not glutamatergic synaptic transmission. Endogenous activation of GluR5 also enhanced GABA release to ACC pyramidal neurons and the corresponding postsynaptic tonic GABA current. Our results suggest the somatodendritic, but not presynaptic GluR5, in modulation of GABA release. The endogenous GluR5 activation and the subsequent tonic GABA current may play an inhibitory role in ACC-related brain functions.
Original language | English (US) |
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Pages (from-to) | 146-157 |
Number of pages | 12 |
Journal | Developmental Neurobiology |
Volume | 67 |
Issue number | 2 |
DOIs | |
State | Published - Feb 2007 |
Keywords
- Anterior cingulate cortex
- GABAergic transmission
- GluR5
- Kainate receptor
- Mice
- Tonic GABA current
ASJC Scopus subject areas
- Developmental Neuroscience
- Cellular and Molecular Neuroscience