PASSIVE-AVOIDANCE TRAINING INDUCES ENHANCED LEVELS OF IMMUNOREACTIVITY FOR MUSCARINIC ACETYLCHOLINE-RECEPTOR AND COEXPRESSED PKC-GAMMA AND MAP-2 IN RAT CORTICAL-NEURONS

Changes in neocortical immunoreactivity (ir) for muscarinic acetylchol ine receptors (mAChRs), protein kinase C gamma (PKC gamma), microtubul e-associated protein 2 (MAP-2), and the calcium-binding protein parval bumin (PARV) induced by the performance of a one-trial passive shock a voidance (PSA) task were studied in young adult male Wistar rats. In e xperiment I, four groups of animals were formed: three control groups (M, naive; H, habituated hut nonshocked; and S, habituated and shocked ), and a fully trained group (T, habituated and shocked, followed by a retention trial 24 hr after the footshock). Compared to naive animals , the H, S, and T animals all revealed enhanced cortical ir for mAChRs , PKC gamma, and MAP-2 in discrete subsets of cortical neurons in laye rs 2, 3, and 5, while no changes were found for PARV. The neurons disp laying enhanced levels of ir are of the pyramidal and nonpyramidal cel l type and are arranged in a columnar manner. Immunofluorescent double -labeling experiments for mAChR, PKC gamma, and MAP-2 revealed that in dividual cortical neurons localized within the columns display enhance d ir for all three functionally related proteins. Compared to naive an imals, all experimental groups revealed significant increases in the t otal size of cortical areas showing enhanced ir (H, S, and T over N). A further significant increase is found in animals receiving a footsho ck over nonshocked animals (S over H, respectively). The retention tri al, however, did not induce a further increase (T over S). In some of the animals the patterns appeared to be lateralized, in either the lef t or right hemisphere. In order to test the role of cholinergic innerv ation in the induction of enhanced mAChR-ir, unilateral lesions of the nucleus basalis magnocellularis (nbm) were performed in experiment II . Apparently, an intact cholinergic innervation from the nbm is not re quired for the occurrence of the aforementioned columnar patterns. How ever, when the enhanced columnar patterns in the sensory areas of the cortex are cholinergically deprived, clear deficits in PSA performance are observed. These results indicate that although ACh is not a prere quisite for the induction of enhanced ir for mAChRs in cortical cells, such neurons demand cholinergic neurotransmission for optimal retenti on of the shock experience. The alterations in ir for coexpressed mACh R, PKC gamma, and MAP-2 in a discrete subset of cholinoceptive cortica l neurons arranged in characteristic patterns most likely represent pa rt of the neuronal substrate involved in functional cortical plasticit y related to PSA training.