No facilitation of amphetamine- or cocaine-induced hyperactivity in adult rats after various 192 IgG-saporin lesions in the basal forebrain.
Lesions of basal forebrain cholinergic neurons by intracerebroventricular (i.c.v.) injections of 192 IgG-saporin increased the locomotor response to 0.5 and 1.5 mg/kg of D-amphetamine in adult rats [A. Mattsson, S.O. Ogren, L. Olson, Facilitation of dopamine_mediated locomotor activity in adult rats following cholinergic denervation, Exp Neurol. 174 (2002) 96-108.]. In the present study, adult male rats were subjected to bilateral injections of 192 IgG-saporin either into the septum (Sp), the nucleus basalis magnocellularis (Nbm), both structures (SpNbm) or i.c.v. Locomotor activity was assessed in the home cage 23 days after surgery, and, subsequently, thrice after an intraperitoneal injection of D-amphetamine (1 mg/kg) and twice after an injection of cocaine (15 mg/kg). Analysis of AChE-stained material showed that Sp lesions induced preferentially hippocampal denervation, Nbm lesions induced preferentially cortical denervation, while both SpNbm and i.c.v. lesions deprived the hippocampus and the cortex of almost all AChE-positive reaction products. The spontaneous and drug-induced locomotor activity of all lesioned rats did not differ significantly from that of control rats, except in rats subjected to i.c.v. injections, in which the locomotor response was significantly increased after the second administration of cocaine. In addition, in Nbm and SpNbm rats, the locomotor reaction to cocaine was weaker right after the second injection. The present results do not confirm the report by Mattsson et al. on the potentiation of amphetamine-induced locomotion by i.c.v. injections of 192 IgG-saporin, but suggest that cocaine-induced locomotion can be increased by such lesions and, to some respect, attenuated by cholinergic damage in the Nbm.
Jeltsch
Hélène
H
Laboratoire de Neurosciences Comportementales et Cognitives, UMR 7521 Université Louis Pasteur/CNRS IFR 37 Neurosciences 12, rue Goethe 67000 Strasbourg, France.
Lazarus
Christine
C
Cosquer
Brigitte
B
Galani
Rodrigue
R
Cassel
Jean-Christophe
JC
D000110:Acetylcholinesterase / Q000378:metabolism; D000661:Amphetamine / Q000494:pharmacology*; D000818:Animals; D000911:Antibodies, Monoclonal; D020532:Basal Nucleus of Meynert / Q000187:drug effects / Q000473:pathology; D000697:Central Nervous System Stimulants / Q000494:pharmacology*; D018678:Cholinergic Agents; D003042:Cocaine / Q000494:pharmacology*; D003714:Denervation; D018765:Dopamine Uptake Inhibitors / Q000494:pharmacology*; D004347:Drug Interactions; D006624:Hippocampus / Q000187:drug effects / Q000473:pathology; D006948:Hyperkinesis / Q000139:chemically induced* / Q000503:physiopathology; D000922:Immunotoxins; D007276:Injections, Intraventricular; D008297:Male; D008845:Microinjections; D009699:N-Glycosyl Hydrolases; D016548:Prosencephalon / Q000187:drug effects* / Q000473:pathology; D051381:Rats; D020318:Rats, Long-Evans; D054789:Ribosome Inactivating Proteins, Type 1; D000076985:Saporins; D020665:Septum of Brain / Q000187:drug effects / Q000473:pathology
C085696:192 IgG-saporin; D000911:Antibodies, Monoclonal; D000697:Central Nervous System Stimulants; D018678:Cholinergic Agents; D018765:Dopamine Uptake Inhibitors; D000922:Immunotoxins; D054789:Ribosome Inactivating Proteins, Type 1; D000661:Amphetamine; D000110:Acetylcholinesterase; D009699:N-Glycosyl Hydrolases; D000076985:Saporins; D003042:Cocaine