CALCITONIN GENE-RELATED PEPTIDE IN THE AMYGDALOID COMPLEX OF THE RAT - IMMUNOHISTOCHEMICAL AND QUANTITATIVE DISTRIBUTION, AND DRUG EFFECTS ON CALCIUM DEPENDENT, POTASSIUM-EVOKED INVITRO RELEASE

The amygdaloid complex is an area with a high concentration of calcitonin gene-related peptide. In the present paper, immunohistochemical studies revealed a dense innervation of the central nucleus originating most probably from the bed nuclei of the stria terminalis. For determination of tissue concentrations of calcitonin gene-related peptidelike immunoreactivity, the amygdaloid complex was dissected into four parts. The distribution was found to be uneven with the highest concentration (1153.3 fmol/mg protein) in the portion including the nucleus amygdaloideus centralis. High performance liquid chromatographic analysis from an extract of amygdaloid tissue showed that 97% of the calcitonin gene-related peptidelike immunoreactivity measured by radioimmunoassay is authentic rat calcitonin gene-related peptide alpha or beta. Release of calcitonin gene-related peptidelike immunoreactivity was measured in superfused slices of amygdalae pooled from three rats. High potassium (60 mM) caused a significant release of calcitonin gene-related peptidelike immunoreactivity (from 0.88% of total tissue content to 1.91%) from the amygdaloid complex in vitro, which was blocked in calcium-free buffer. Pretreatment with haloperidol or clozapine caused a significant reduction of the 60 mM potassium-evoked release, compared with a saline treated control group (control 21.0 fmol; haloperidol 2.8 fmol; clozapine 8.8 fmol) and an increase of tissue levels after haloperidol treatment by 43%. These results demonstrate that calcitonin gene-related peptide is integrated in amygdaloid functions and possibly a target for actions of neuroleptic drugs.