Immunolocalization of mGluR1alpha in specific populations of local circuit neurons in the cerebral cortex.

By coupling glutamate to the IP(3) signaling pathway, group I metabotropic receptors can increase intracellular Ca(2+) concentration, and might thus contribute to excitotoxicity. To identify neurons that might be vulnerable to such injury, we performed immunofluorescence histochemistry for metabotropic glutamate receptor 1alpha (mGluR1alpha) in the cerebral cortex of adult rat. mGluR1alpha was in somata and dendrites of a subset of non-pyramidal neurons scattered throughout the cerebral cortex. To further characterize mGluR1alpha-positive neurons, we investigated its colocalization with several neurochemical markers. Nearly all mGluR1alpha-positive cells were interneurons immunopositive for gamma-aminobutyric acid. The majority (70-80%) of mGluR1alpha-immunopositive neurons were double-labeled for somatostatin. Approximately half of calretinin-positive neurons and 30% of calbindin-positive neurons expressed mGluR1alpha. In contrast, parvalbumin-expressing neurons were rarely positive for mGluR1alpha. Neurons staining strongly for mGluR1alpha were also positive for GluR1. These results indicated that mGluR1alpha is expressed by specific classes of GABAergic neurons in the neocortex, and suggests a mechanism by which these neurons may be especially vulnerable to excitotoxic injury.