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Passive avoidance learning was studied in young rats 13-30 days of age following bilateral injections of saline or antimuscarinic and/or muscarinic agents into three amygdaloid nuclei - lateral (L), basolateral (BL), and cortical (CO). While acquisition was not influenced by saline injections into various other cerebral structures, it was significantly altered by similar injections into these amygdaloid nuclei, especially by those into the BL nucleus, suggesting that this nucleus is particularly involved in passive avoidance learning. Atropine induced significant deficits from as early as 13 days on. These deficits increased and were of similar strength after injections into any of the three studied nuclei until day 16; after that age, they diminished slightly following CO and L nuclei administration, while remaining substantial after BL nucleus injections at all ages, even at 30 days. No facilitatory effects could be elicited by arecoline injected alone, while arecoline could antagonize the disturbing effect of atropine, when given in combination, from day 13 on. These results suggest a muscarinic cholinergic mediation of passive avoidance learning through the synaptic elements located in the basal lateral part of the amygdala in the young rat. [ABSTRACT FROM AUTHOR]

Young rats 10-30 days of age received bilateral injections of antinicotinic and/or nicotinic agents into the lateral (L), the basolateral (BL), or the cortical (CO) amygdaloid nucleus, and were trained to learn a cool-draft stimulus passive-avoidance task, 17 min later. Mecamylamine produced age-and dose-dependent acquisition deficits; these deficits appeared on day 11, increased similarly after injections into any of the three nuclei until day 16, and decreased thereafter, more rapidly after administration into CO nucleus than after injections into L and BL nuclei. In the latter nucleus, the deficits had nearly disappeared on day 30. Nicotine injected alone induced slight facilitatory effects, significant at 20 days but not reliable at earlier stages. However, nicotine could hinder the antagonistic effects of mecamylamine, when given in combination, as early as the 11th day of age on. The results suggest the existence of nicotinic synaptic elements in the basal lateral part of the rat amygdala; however, these seem to play an important role in passive avoidance learning only during the early stages of ontogenesis. [ABSTRACT FROM AUTHOR]

Young rats 11, 13, 16, and 20 days old were injected bilaterally with the nicotinic antagonist mecamylamine hydrochloride (5, 50, and 100 μg on each side) into the posteroventral hippocampoentorhinal (VHE) area and trained on a 'cool-draft-stimulus' passive avoidance task. The data showed impaired acquisition and reduced resistance to extinction. The deficits observed were age- and dose-dependent, rats being highly sensitive to the drug when 11 and 13 days old and decreasingly responsive up to day 20. The results may indicate that nicotinic cholinergic sites in the VHE area mediate passive avoidance learning in the young rat as soon as acquisition emerges. Muscarinic cholinergic mechanisms only develop later in this region, becoming progressively more important for passive avoidance behavior. [ABSTRACT FROM AUTHOR]