Male mating behavior, biting attack, defensive threat, eating, grooming, yawning, investigating, and escape-like activity were produced by electrical stimulation of differentiated zones in hypothalamus and preoptic area of oppossums. Close anatomical correspondence with similar mechanisms in higher species suggested considerable phylogenetic continuity from early mammalian levels. Responses involving environmental goals were not performed without the objects, indicating that they were facilitated rather than directly elicited by the stimulation. The interelectrode variability in the completeness of complex response patterns suggested that each zone sends divergent facilitatory output to separate sensory-motor mechanisms for different response elements. The performance of the mating pattern without intromission was an effective reward in a maze.

Mice treated with nicotine sulfate (J.O mg/k g, i.p.) prior to training for a passive avoidance response showed antagonism toward the amnesic effect produced by a post-training electroconvulsive shock; this effect was particularly apparent when drug treatment was given 45 to 60 min prior to training. A reversal of the predicted effect of ECS upon brain serotonin level by nicotine suggested a possible CO"oiary of the drug-induced facilitation of memory consolidation.Prior studies have indicated' that the administration of electroconvulsive shock in close temporal proximity with training for the establishment of a response results in a significant degree of failure to perform that response when subsequent testing is carried out (Kopp et ai, 1966;Essman, 1968a). This phenomenon has been interpreted as an experimentally-induced retrograde amnesia which has been related in several respects to physiological as well as biochemical changes in the central nervous system, produced by electroshock. Recent concern in this laboratory has been with several of the biochemical changes attending cerebral electroshock and its sequelae (Essman, 1968b(Essman, , 1968c. Specifically, changes in the amnesic effect produced by post-training electroshock and several pharmacological agents, which have either acted to minimize the elevation in brain serotonin or alter its turnover rate as a consequence of electroshock, have also been indicated as means by which the ECS-induced amnesia is appreciably reduced (Essman, 1967). The purpose of the present study was to consider one such compound, nicotine sulfate, a central nervous system stimulant, that has been shown to alter the content of serotonin in the brain (Westfall et ai, 1967). Under these conditions, therefore, it was hypothesized that the changes in brain serotonin resulting from nicotine treatment could impose rate-limiting conditions upon the brain serotonin alteration produced by electroshock, and thereby affect the degree to which such electroshock treatment would lead to a retrograde amnesia. MethodMale CF-ls strain mice, weighing approximately 27 g, were assigned to five drug-treatment and two saline-treatment conditions, with 20 animals per group in the behavioral series and 10 animals per group in the biochemical series.Four groups of Ss were each given 1.00 mg/kg of nicotine sulfate intraperitoneally, and the animals in the remaining group were treated with an equivalent volume of 0.9% saline. A single training trial in an apparatus designed to establish a passive avoidance response (Essman & Alpern, 1964) was given to Ss at either 15, 30, 45, or 60 min following injection, with the latency of entry into an inner chamber from an outer vestibule recorded. Ss received a 3 mA foot shock upon entering the inner chamber. Ten sec following the training trial all animals were given a single electroconvulsive shock (10 rnA, 700 V, 200 msec), and were subsequently tested in the same apparatus at 24 h following training for the retention of the conditioned response, as indicated by ...