To investigate the hypothesis that psychopathic offenders would show less suppression of behavior as a function of punishment at varying levels of probability, three groups of subjects were selected. Fifty criminal offenders were divided into two groups of psychopathic and nonpsychopathic offenders based on clinical ratings. A third group of nonoffenders was also used. A probabilitylearning card game was developed that consisted of 10 different levels of punishment probability, with the punishment based on the response-cost technique of removing reinforcers (chips redeemable for money). A measure of suppression was obtained from the reduction of subjects' response rates. Results are reported that show psychopathic offenders to produce the least suppression and the lowest winnings, with these findings attributed to the psychopaths being least responsive when the probability of punishment is most uncertain. Additional data are presented to indicate that these results are best explained in terms of cognitive factors, with the element of magical or superstitious logic proposed as a major pathognomic characteristic of psychopathy.

Cholecystokinin (CCK) and substance P (SP) were measured in discrete areas of the rat brain at different stages of the estrous cycle. Significantly higher levels of CCK were found in the lateral septum during diestrus as compared to proestrus. In the parietal cortex, CCK concentrations were significantly higher in diestrus than in proestrus. In the amygdala, estrous levels of CCK were significantly higher than proestrous levels. SP concentrations were significantly higher in diestrus than in proestrus in the medial and lateral septum, and the medial and lateral preoptic area. In the amygdala and ventral tegmental area, SP concentrations were significantly higher in estrus than in proestrus. These data suggest that certain CCK and SP neuronal systems may play a role in regulating the hypothalamo-pituitary-gonadal axis and/or be involved in steroid-dependent behavior.

The effects of acute stress exposure upon cholecystokinin (CCK) and substance P (SP) concentrations in discrete hypothalamic regions of the adult male rat brain were studied. Animals were exposed to foot shock stress for periods of 2, 4, 10, 30 or 60 min duration; immediately afterwards they were decapitated; brains were frozen and subsequently microdissected. CCK and SP concentrations were assayed by a specific RIA, as were serum levels of ACTH, corticosterone, PRL, GH, LH and testosterone. Stress had no effect upon SP concentrations in the anterior or posterior parts of the arcuate nucleus (ARC), but led to elevated CCK levels in the posterior ARC following 60 min of exposure. In both the ventromedial and dorsomedial hypothalamic areas, stress induced depletions of both neuropeptides. In the anterior (but not the posterior) portions of the lateral hypothalamic area, CCK and SP concentrations were reduced by stress exposure. These studies demonstrate that discrete hypothalamic CCK and SP neuronal systems are responsive to stress. This suggests that endogenous hypothalamic CCK and SP participate, along with other neurotransmitters/neuromodulators, in the integrated hypothalamic stress response, and mediate stress-neuroendocrine interactions.

Adult male rats, either intact (N) or bearing complete hypothalamic deafferentations (CHD), were injected with delta 1-tetrahydrocannabinol (THC: 5 mg/kg BW, IP). Forty-five minutes later, they were decapitated and trunk blood was collected for serum ACTH and corticosterone (CS) determinations. In the N animals, serum levels of both ACTH and CS were markedly elevated in the drug-treated, as compared to the vehicle-treated group (approximately 8-fold and 10-fold, respectively). In CHD rats, on the contrary, THC administration did not significantly alter serum concentrations of either ACTH or CS. These results demonstrate (1) that acute treatment with THC stimulates the secretion of ACTH as well as of CS; and (2) that extrahypothalamic sites and/or neural pathways mediate this effect.

No abstract

The present findings show that nicotine given i.v. can within minutes induce increases of ACTH, vasopressin and prolactin secretion in the male rat, giving further evidence for the existence of nicotine-like cholinergic receptors involved in the regulation of these hormones. These changes were associated with rapid reductions of NA levels in the subependymal layer of the median eminence, in the nuc, dorsomedialis hypothalami and in the anterior and posterior periventricular hypothalamic area as revealed by quantitative microfluorimetrical measurements of CA fluorescence. Intraindividual correlations indicate the involvement of an inhibitory noradrenergic mechanism in the subependymal layer of the median eminence in the regulation of ACTH secretion, the involvement of noradrenergic mechanisms in the posterior periventricular area in the regulation of prolactin secretion and the involvement of dopaminergic mechanisms in the medial palisade zone of the median eminence in the regulation of prolactin secretion. A rapid rise of prolactin secretion seems to be associated mainly with a reduction of NA levels in the posterior periventricular area indicating the existence of a possible facilitatory noradrenergic mechanism in this region regulating prolactin secretion.

No abstract

In view of the involvement of limbic structures in adrenocortical regulation, their afferent projections to the mediobasal hypothalamus were investigated. Electrical stimulation via chronically implanted electrodes in the dorsal hippocampus, the medial septal nuclei, the basolateral amygdala or the mesencephalic reticular formation all elicited a significant increment in plasma corticosterone levels in adult male rats under pentobarbital anesthesia. Complete or anterior hypothalamic deafferentation blocked these adrenocortical responses completely, and posterior hypothalamic deafferentation attenuated them to a marked extent. In animals with bilateral medial forebrain bundle lesions, hippocampal stimulation had no effect upon plasma corticosterone levels. These studies demonstrate that extrahypothalamic effects upon adrenocortical secretion are neurally mediated, and that the integrity of neural pathways impinging upon the mediobasal hypothalamus from both the rostral and the caudal directions is essential to these effects.