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Psychological stress produced by intraspecies emotional communication in a communication box was studied to see whether it could be applied to a new screening method for anti-ulcer agents. There were two groups of mice, the 'sender' mice that received electrical foot shocks and showed emotional responses such as piloerection, abnormal squealing and jumping, and the 'responder' mice that were affected by the sender's emotional responses without foot shock. The gastric lesions (erosions) produced by conditioned emotional stimuli were observed in both groups. The effects of the anti-ulcer drugs cetraxate, cimetidine and gefarnate were examined. In 'senders', the gastric lesions were significantly suppressed by the administration of cetraxate at a dose of 200 mg/kg (p.o.) or cimetidine at doses of 30 and 100 mg/kg (p.o.). The gastric lesions in 'responders' were significantly suppressed by two administrations of cetraxate at doses of 100 and 200 mg/kg (p.o.), cimetidine at doses of 10-100 mg/kg (p.o.) or gefarnate at a dose of 200 mg/kg (p.o.). The gastric lesions of 'responders' were more sensitive to anti-ulcer drugs. The present results indicate that the gastric erosions of 'responders' are useful for the evaluation of anti-ulcer agents.

Arginine-vasopressin (AVP) microinjected into the medial preoptic area (MPOA) induces flank marking behavior, a form of olfactory communication, in the golden hamster. When exposed to the odors of conspecifics flank marking behavior occurs naturally in association with grooming of the flank gland region. The present study examined whether microinjection of AVP, oxytocin (OXY) and other biologically active peptides into the medial preoptic area (MPOA), lateral cerebroventricle (LV) or the ventromedial or lateral hypothalamus (VMH-LH) would elicit flank gland grooming. Microinjection of AVP and OXY produced 2-3 times more flank gland grooming when microinjected into the MPOA than saline, neurotensin or angiotensin II. Injection of AVP into the LV and VMH-LH produced significantly less flank gland grooming than when injected into the MPOA.

Male rhesus monkeys were trained to perform an instrumental avoidance conditioned response. They were then paired in the "cooperative conditioning" paradigm, a situation designed to measure the quality of nonverbal communication by changes in facial expression. A "responder monkey" was able to perform discriminated instrumental avoidance responses by processing facial expressive cues provided through a closed circuit television picture of a "stimulus monkey" which was receiving presentations of the conditioned stimulus. Oral administration of 1.0 mg/kg of delta-9-tetrahydrocannabinol (delta-9-THC) to the stimulus animal, the responder, both animals, or neither animal was given in all possible combinations of pairings to determine if delta-9-THC affects the expressiveness of the stimulus monkey or the sensitivity of the responder to the expressions of others. The drug impaired the display of facial expression in "stimulus" subjects but enhanced the ability of "responders" to discriminate the expressions of their partners. Measures of heart rate during cooperative conditioning revealed that delta-9-THC lowered cardiac rates of responder monkeys.

Flank marking, a form of olfactory communication displayed by hamsters, is dependent upon vasopressin-sensitive neurons in the anterior hypothalamus. In the present study two vasopressin type-1 (V1) receptor antagonists, d(CH2)5Tyr(Me)AVP and dPTyr(Me)AVP were tested for their ability to block flank marking stimulated by the microinjection of arginine vasopressin (AVP) into the anterior hypothalamus. Dose-response curves were established for AVP and flank marking in the presence or absence of different concentrations of each antagonist. DPTyr(Me)AVP was microinjected into the anterior hypothalamus 1 h before the microinjection of AVP while d(CH2)5Tyr(Me)AVP and AVP were prepared together and delivered as a single microinjection. This procedure was necessary because dPTyr(Me)AVP, but not d(CH2)5Tyr(Me)AVP, had agonist activity when initially injected into the anterior hypothalamus in concentrations ranging from 0.90-900 microM. The ED50 values (microM) for dPTyr(Me)AVP and AVP were 17.9 and 0.90, respectively. The initial agonist activity of dPTyr(Me)AVP was always followed by blocker activity. Both V1-receptor antagonists caused a dose-dependent decrease in AVP-stimulated flank marking. Maximal inhibition of AVP-stimulated flank marking was produced with approximately 1.0 mM of either antagonist. Both antagonists blocked AVP-stimulated flank marking behavior for over 12 h following their microinjection.