CHANGES IN CORTICAL NICOTINIC ACETYLCHOLINE-RECEPTOR NUMBERS FOLLOWING UNILATERAL DESTRUCTION OF PYRAMIDAL NEURONS BY INTRASTRIATAL VOLKENSIN INJECTION

Experimental lesions using the retrogradely transported toxic lectin, volkensin, were used in conjunction with quantitative autoradiography to investigate the cellular localization of nicotinic and adenosine A( 1) receptors. Lesions were produced by unilateral intrastriatal inject ion of volkensin, ricin (another toxic lectin but not transported in t he central nervous system), quinolinate, and unilateral intrathalamic injection of ibotenate. Volkensin injection significantly reduced the number and mean cell size of large, infragranular pyramidal neurones i n cortical areas Fr1/Fr2 (close to the midline) and more laterally in Par1/Par2. Selective destruction of these cells was accompanied by sig nificant increases in the binding of [H-3] nicotine in cortical areas contralateral to the lesion. A small but significant reduction in the binding of [H-3] 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) to adenosi ne A(1) receptors was observed only in deep layers of Fr1/Fr2 on the s ide ipsilateral to the lesion. No other toxin consistently changed the binding of either ligand in control animal groups with the exception of [H-3] nicotine where small reductions were observed in the middle l ayers of one thalamic injection group. These data indicate differentia l plasticity of nicotinic receptors compared with other receptors stud ied previously using this paradigm. In the light of these findings, ni cotinic receptors are discussed as targets for pharmacological manipul ation of the activity of pyramidal neurones. (C) 1995 Academic Press L imited.