Alterations in the behavioral and biochemical effects of electroconvulsive shock with nicotine

Abstract

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 ...

Changes In Cholinergic Activity and Avoidance Behavior By Nicotine In Differentially Housed Mice

“…As summarized in Table I, the incidence of passive avoidance acquisition among aggregated mice was not significantly altered by prior treatment with nicotine sulfate (as previously indicated : Essman et al, 1968;Essman and Essman, 1971), however, the lower incidence of passive avoidance acquisition by isolated mice was significantly increased by nicotine treatment. Active avoidance response latency or escape response latency during the active avoidance training trials was not altered by either housing condition or drug treatment.…”

“…In previous reports (Essman et al, 1968;Essman and Essman, 1971) we have indicated that passive avoidance acquisition and retention was not notably altered by nicotine sulfate. The effects of the drug upon active avoidance conditioning is, in one respect, comparable with results obtained by Bovet et al (1966) and Bovet and Bovet-Nitti (1965); in these experiments a lower parented dose of nicotine sulfate facilitated avoidance acquisition among initially poor avoidance performing mice, while it impaired such acquisition among mice showing high avoidance performance.…”

“…This effect was attributed to the timedependent alteration, by nicotine, of changes in biogenic amines resulting from ECS (Essman, 1970a(Essman, , 1971a; these changes involve brain 5hydroxytryptamine (5-HT), as well as acetylcholine (Essman et al, 1968;Essman, 1971a). Relating to the above observations, have been data indicating that some of those changes in brain chemistry which parallel ECS-induced amnesia occur in the mouse as a consequence of isolation housing (Essman, 1971 b).…”

“…In prior experiments we have indicated a facilitative role for nicotine upon the memory consolidation process (Essman, et al, 1968) based upon the ability of this drug, when given 45 to 60 minutes prior to passive avoidance training, to reduce the amnesic effect of post-training electroconvulsive shock (ECS). This effect was attributed to the timedependent alteration, by nicotine, of changes in biogenic amines resulting from ECS (Essman, 1970a(Essman, , 1971a; these changes involve brain 5hydroxytryptamine (5-HT), as well as acetylcholine (Essman et al, 1968;Essman, 1971a).…”

Cigarette Smoking and Stimulus Selection

“…Although the physiological effects of smoking tobacco have been extensively studied in both man and animals (Rothe et aZ., 1944; Larson et al., 1961;Domino, 1967;Essman et al, 1968;Frankenhaeuser et al, 1968Frankenhaeuser et al, , 1969Frankenhaeuser et al, , 1970, few experimental studies have been made of changes in human performance that may ensue from smoking tobacco. Performance changes following smoking do occur ; Cotten et al (1971) found changes in simple reaction time following smoking, and repeated performance of a visual-search task is impaired (Johnston, 1966).…”