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Featured researches published by Robert L. Conner.


Physiology & Behavior | 1970

Parachlorophenylalanine and habituation to repetitive auditory startle stimuli in rats

Robert L. Conner; Jon M. Stolk; Jack D. Barchas; Seymour Levine

Abstract The relationship between brain serotonin levels and habituation of a skeletal-motor startle response was studied using parachlorophenylalanine (PCPA), a drug which inhibits the formation of serotonin. Depletion of brain serotonin by PCPA slows down, but does not prevent, habituation. PCPA given to rats that were habituated before starting drug treatment causes a transitory increase in startle response magnitude. Whether PCPA is administered before or after habituation, the treated rats exhibit heightened reactivity to startle stimuli following exposure to novel stimuli. These results suggest that brain serotonin plays a role in inhibitory processes.


Physiology & Behavior | 1968

Effects of rapid eye movement (REM) sleep deprivation on shock-induced fighting ☆ ☆☆

Bruce Morden; Robert L. Conner; George Mitchell; William C. Dement; Seymour Levine

Abstract The effects of REM sleep deprivation on shock-induced fighting behavior in rats were studied in three experiments. The experimental animals were selectively deprived of REM sleep by maintaining them on a small pedestal surrounded by water. One control group was maintained under similar conditions except that REM sleep was permitted to occur, while a second control group was conventionally housed. Fighting behavior was elicited by administering a train of brief electric shock pulses at five intensities to pairs of rats. In Experiment 1, fighting behavior was studied before, during, and after REM sleep deprivation. Experiment 2 replicated the first study except that fighting was not studied during the treatment period. REM sleep deprived animals showed dramatic increases in fighting frequency which persisted even after prolonged sleep recovery. In Experiment 3, the experimental group had a history of four previous cycles of REM sleep deprivation and recovery before fighting behavior was studied. The animals previously deprived of REM sleep fought significantly more than their controls. In Experiments 4 and 5 the adrenocortical stress response was examined in REM sleep deprived and control animals. Results indicated statistically significant but small changes in plasma corticosterone levels as a result of REM sleep deprivation.


Physiology & Behavior | 1970

The effect of parachlorophenylalanine (PCPA) on shock-induced fighting behavior in rats

Robert L. Conner; Jon M. Stolk; Jack D. Barchas; William C. Dement; Seymour Levine

Abstract Shock-induced fighting behavior was studied in rats treated with parachlorophenylalanine (PCPA). In the doses used, PCPA injections depleted brain serotonin to 10 per cent of the control animal levels. In the first study, injections were started prior to initial behavioral testing. In the second experiment, injections were started during a sequence of repeated behavioral testings in the shock-induced fighting situation. In neither case was there any evidence that PCPA injections had any effect on shock-induced fighting behavior in rats.


Psychopharmacology | 1971

Rubidium-induced increase in shock-elicited aggression in rats

Jon M. Stolk; Robert L. Conner; Jack D. Barchas

Daily treatment of rats with 0.3 or 0.6 meq/kg rubidium chloride (RbCl) causes an increase in shock-elicited aggressive behavior relative to potassium chloride-treated controls. Aggressive responses increase immediately with the higher dose of RbCl and are maintained for 12 days. The lower RbCl dosage increases fighting behavior significantly after 11 consecutive injection days. Measurements of flinch, jump, and vocalization threshold reveal no consistent pattern with treatment; thus, it is unlikely that threshold changes underlie the observed increases in aggression.


Physiology & Behavior | 1969

Avoidance conditioning and adrenocortical function in the rat

George A. Wertheim; Robert L. Conner; Seymour Levine

Abstract Six male rats were trained on an unsignaled (Sidman-type) avoidance schedule, on which each response postponed the next shock, and no warning signal was present. Measurement of plasma corticosteroid levels, during both the resting state and after exposure to ether stress, was made prior to training and at regular intervals during the course of several months of avoidance conditioning. It was found that animals exhibiting higher pre-training stress responses attained greater avoidance performance proficiency. Moreover, after individual differences in avoidance performance developed, greater proficiency was found to be accompanied by higher resting steroid levels. These data suggest that there may be a strong interrelation between the behavioral and endocrinological responses to stress of the kind present in aversive learning contingencies.


Annals of the New York Academy of Sciences | 1969

HORMONAL DETERMINANTS OF AGGRESSIVE BEHAVIOR

Robert L. Conner; Seymour Levine; George A. Wertheim; Juliann F. Cummer

It has been suggested (Young, 1961; Harris, 1964) that one of the major differences between genetic males and females lies in the differential organization of the central nervous system (CNS). Circulating androgens emanating from the testes of the newborn male animal may lead to a differentiation, or increased sensitivity, of the neural structures underlying the expression of male sex behavior. In the absence of androgens during this critical period, e.g., in genetic females, the neural structures mediating female patterns of sex behavior continue to develop. In adulthood, then, the hormones are involved in the arousal of sex behavior, and the sexually differentiated brain is more susceptible to the action of specific gonadal hormones. This concept of a dual role of gonadal hormones is supported by the results of many studies dealing with the hormonal control of sex behavior in animals. Although members of each sex may exhibit some components of the mating pattern of the other sex (Beach, 1938), adult animals will usually respond more readily to treatment with hormones of their own genetic sex than to treatment with hormones of the other sex. For example, females do not usually show complete patterns of male sex behavior in response to injected testosterone, and males do not usually show female patterns of sex behavior even after supramaximal doses of estrogen and progesterone. This sex difference in response to hormone administration cannot readily be accounted for on the basis.of the functioning of the pituitary gland, since Harris and Jacobsohn (1952) have shown that the pituitary is a sexually indifferent organ. Thus, it is most likely that such differences lie in the organization of the CNS. Further evidence for this view has been provided by studies in which gonadal hormones were directly manipulated early in infancy (e.g., Pfeiffer, 1936). Neonatally castrated male rats differ from adult castrates and normal intact males in several ways: in the neonatal castrate, a transplanted ovary will form corpora lutea, thus indicating a femalelike cyclic pattern of pituitary gonadotrophin release; neonatally castrated males also show classic patterns of female sex behavior. Analogous findings have been observed in female rats: neonatal treatment with large doses of testosterone propionate (TP) results in persistent vaginal cornification, thus indicating a malelike acyclic pattern of gonadotrophin release. Further, these androgenized females usually cannot be made sexually receptive by treatment with large doses of estrogen and progesterone. This body of data suggests that the differential sensitivity to gonadal hormones shown by males and females is one important aspect of the sex difference that is present at the level of the CNS. These data also indicate that the sensitivity to gonadal hormones in adulthood may be experimentally controlled by either castrating male rats neonatally or by injecting female rats with TP neonat ally. The experiments which are described herein were designed to study the role


Physiology & Behavior | 1971

Preshock-produced intensification of passive avoidance responding and of elevation in corticosteroid level

John Madden; James Rollins; D. Chris Anderson; Robert L. Conner; Seymour Levine

Abstract The adrenocortical steroid response and passive avoidance behavior were studied in rats that had been exposed to inescapable intense shock (preshock). Previously preshocked animals exhibited a greater adrenocortical steroid response to mild shock than nonpreshocked controls; in addition, passive avoidance behavior was facilitated in the preshocked animals.


Psychonomic science | 1967

Shock-induced fighting in septal-lesioned rats

Allan Wetzel; Robert L. Conner; Seymour Levine

Emotionality ratings of rats with bilateral lesions in the septal area were elevated two days and 30 days after lesion placement. At approximately 85 days after lesioning, pairs of septal animals exhibited significantly more fighting in response to electric shock stimulation than control animals even though at this time their emotionality ratings did not differ from those of control animals.


Cellular and Molecular Life Sciences | 1969

Effects of chronic melatonin and saline injections on pituitary adrenal secretion

Jack D. Barchas; Robert L. Conner; Seymour Levine; Joan Vernikos-Danellis

Es wurde festgestellt, dass Melatonin, ein angebliches Hormon aus der Pinealis, keine spezifische Wirkung auf die Sekretion von ACTH aus dem Hypophysenvorderlappen hat.


Nature | 1971

Stress, fighting and neuroendocrine function.

Robert L. Conner; Joan Vernikos-Danellis; Seymour Levine

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