Chlorisondamine inhibits the nicotine-induced stimulation of c-fos in the pigeon brain for up to 2 weeks.

Chlorisondamine is a charged molecule that acts as long-acting nicotinic antagonist in many species, including pigeon. Evidence indicates that, despite the charged nature of chlorisondamine, it blocks some central effects of nicotine. The present study examined the time course of chlorisondamine's blockade of nicotine-induced c-fos expression in the pigeon brain. Chlorisondamine's central blockade was examined from 1 hr to 28 days prior to nicotine administration. Nicotine stimulated increases in c-fos mRNA in the hippocampus, hyperstriatum accessorium, hyperstriatum ventrale, nucleus accumbens, bulbus olfactorius, paleostriatum augmentatum, and stratum griseum et fibrosum superficiale. Nicotinic receptors labeled by [(125)I]-epibatidine were not always found in the same regions as nicotine-induced increases in c-fos expression. Acute chlorisondamine increased the level of c-fos mRNA in the cerebellum, hippocampus, hyperstriatum accessorium, locus parolfactorius, nucleus accumbens, tectum opticum, paleostriatum augmentatum, and stratum griseum et fibrosum superficiale but had no effect on its own 24 hr after administration. Chlorisondamine blocked nicotine-induced increases in c-fos RNA for 4 days in the nucleus accumbens, a week in the bulbus olfactorius, and 2 weeks in the stratum griseum et fibrosum superficiale. The time course of chlorisondamine's blockade of nicotine-induced c-fos expression is consistent with the time course of the ability of chlorisondamine to block behavioral and physiological responses to nicotine.     

NMDA receptor antagonism impairs reversal learning in developing rats.

Four experiments examined the effect of dizocilpine maleate (MK-801), a noncompetitive N-methyl-Daspartate (NMDA) receptor antagonist, on reversal learning during development. On postnatal days (PND) 21, 26, or 30, rats were trained on spatial discrimination and reversal in a T-maze. When MK-801 was administered (intraperitoneally) before both acquisition and reversal, 0.18 mg/kg generally impaired performance, whereas doses of 0.06 mg/kg and 0.10 mg/kg, but not 0.03 mg/kg, selectively impaired reversal learning (Experiments 1 and 3). The selective effect on reversal was not a result of sensitization to the second dose of MK-801 (Experiment 2) and was observed when the drug was administered only during reversal in an experiment addressing state-dependent learning (Experiment 4). Spatial reversal learning is more sensitive to NMDA-receptor antagonism than is acquisition. No age differences in sensitivity to MK-801 were found between PND 21 and 30. (PsycINFO Database Record (c) 2010 APA, all rights reserved)