Abstract

Experimental lesions followed by binding of [3H]8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), [125I]cyanopindolol and [3H] paroxetine to cryostat sections and coverslip autoradiography were used to localize 5-HT1A, 5-HT1B and 5-HT uptake sites in rat posterior cingulate cortex. Ablations included: 1) undercutting for removal of all afferent axons; 2) destruction of the raphe nuclei; 3) cortical ibotenic acid injections for removal of neurons and 4) anterior thalamic and caudate nuclei injections of the immunotoxin OX7-saporin which destroys single classes of cortical projection neurons by retrograde axonal transport. Peak paroxetine binding was in layer Ia with low binding in layer Va and moderate amounts in other layers. Undercut lesions reduced binding only in layer Ia by 35%. Major loses were observed after raphe ablations with decreases of 40 to 72% across all layers. Cortical ibotenic acid injections did not alter paroxetine binding. Peak cyanopindolol binding was in layers Ia to Ic. Undercutting decreased binding significantly in layers Ia, Ib, III and IV, whereas after raphe lesions binding was decreased by 34 to 58% in layers Ia to IV. 5,7-Dihydroxytryptamine injection increased binding by 10 to 40% in layers Ib, II, III and IV. Cortical ibotenic acid injections reduced grain density in all layers with a range of 28 to 47%. Peak 8-OH-DPAT binding was in layer Vb. No change was observed after undercut lesions, whereas after cortical ibotenic acid injection, binding reductions of 44 to 75% were observed throughout all nine sublaminae. Thalamic OX7-saporin injections destroyed almost all layer VI neurons, which resulted in a 45% decrease in layer VI 8-OH-DPAT binding.(ABSTRACT TRUNCATED AT 250 WORDS)