A step-through locomotor passive avoidance task is described requiring the suppression of a spontaneous escape reaction from a cool toward a warm compartment in order to avoid an electric shock delivered in the warm side. We observed no lerning of this task at 9 days of age, a very low but significant level of acquisition at 11 days, a slow but progressive improvement of avoidance from the 13th until the 17th day when the adult capacity was achieved, and a marked increase in the rate between 17-20 days.

Passive avoidance learning was significantly impaired by atropine (5 mg/kg, IP) or scopolamine (0.5 mg/kg), but not by methyl-atropine (5 mg/kg) or methyl-scopolamine (0.5 mg/kg), from postnatal day 15 on. In contrast, an improvement was observed, not significant at 11 days and significant at 13 days, probably due to nonspecific effects. Retention of the response increased from 6 h at 13 days, to 24 h at 17 days. In treated rats, retention was abolished at 13 and 15 days, and impaired at 17 and 20 days. Acquisition of the response was also significantly impaired by bilateral injections of atropine (1, 5, and 20 micrograms) into the posteroventral hippocampo-entorhinal (VHE) area, from day 15 on. Concomitantly, extinction was accelerated. At 14 days, atropine had no influence. At 13 days, a facilitatory action was observed, with better acquisition and greater resistance to extinction, possibly linked to affective changes. The results confirm that central muscarinic cholinergic mechanisms are involved in passive avoidance learning from postnatal day 15 on, and demonstrate that some pathways of this system are located in the VHE area, become efficient at 15 days, and improve markedly between 17 and 18 days.

Passive avoidance learning was studied in young rats 7-20 days old, in control conditions and after bilateral injections of physostigmine into the lateral amygdaloid nucleus. Acquisition in controls was possible from postnatal Day 8 on, progressed markedly after Day 11, and nearly reached maturity by Day 20. Physostigmine differentially altered acquisition depending on the dose: facilitation with low doses, no effect with moderate doses, and impairment with high doses. Enhanced learning through small doses of physostigmine was observed at all ages from Day 8 on, and was greater with 0.2 microgram than with 0.1 microgram. Maturation of the cholinergic innervation of the amygdaloid region was also studied between Days 9-20 using acetylcholine-esterase histochemistry. The results suggest that passive avoidance learning is dependent on amygdaloid cholinergic mechanisms early in life. In addition, very immature cholinergic systems, which are known to be uninfluenced by anticholinergic agents, react to anticholinesterases.

No abstract

Young rats 11, 13, 16, and 20 days old were injected bilaterally with the nicotinic antagonist mecamylamine hydrochloride (5, 50, and 100 micrograms on each side) into the posteroventral hippocampo-entorhinal (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.