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In a series of experiments the effects of p-chloroamphetamine (PCA) on shock-elicited aggression in rats were investigated. 15 min after 5 mg/kg PCA, shock elicited aggression was inhibited. 2 h to 4 weeks after PCA, fighting was facilitated. Both the inhibitory and the excitatory effects of PCA were directly related to the dose of PCA (1.5, 2.5 or 5 mg/kg) and were blocked by pretreatment wtih p-chlorophenylalanine but not by α-methyl-p-tyrosine. PCA-increased pain thresholds 15 min after injection and then decreased pain thresholds over the next 24 h but not thereafter, even though shock-elicited aggression continued to to facilitated. The results are consistent with the idea that inhibition of shock-elicited aggression is associated with enhanced release of serotonin whereas enhancement of shock-elicited aggression is associated with serotonin depletion.

In a series of 6 experiments the effects of p-chloroamphetamine (PCA) on the acoustic startle response in rats were investigated. 15 min after 5 mg/kg PCA startle amplitude was inhibited, 2-15 hr after PCA startle was facilitated. Rate of habituation however was not altered. Both the inhibitory and excitatory effects of PCA were blocked by pretreatment with p-chlorophenylalanine but not by alpha-methyl-p-tyrosine. 24 hr, 1 week and 4 weeks after PCA, initial startle amplitude was unchanged but PCA increased rate of sensitization over successive tone blocks. Increased sensitization was most pronounced at 10 mg/kg and absent at 2.5 mg/kg. The early inhibitory effect of PCA but not the later facilitatory effect was eliminated by reducing the level of background noise. The results suggest that inhibition of startle sensitization is associated with enhanced release of serotonin (5-HT) whereas enhancement of startle sensitization is associated with 5-HT depletion.

LSD is the prototype for a cat behavior model for the study of hallucinogens. The model's specificity was tested with the nonhallucinogen methysergide, a d-lysergic acid amide derivative structurally similar to LSD. The frequencies of occurrence of the model behaviors limb flicking, grooming, and head plus body shaking show statistically significant dose dependency after i.p. methysergide (62.5–1000 μg/kg), and the maximum frequencies of the methysergide-elicited behaviors occur between 1–3 h post-dose. Methysergide produces statistically significant tolerance to limb flicking and grooming 24 h following an acute dose, and there is statistically significant methysergide-LSD and LSD-methysergide cross tolerance to limb flicking at 24 h. In addition, pretreatment with methysergide 15 min before LSD or lisuride antagonizes their elicitation of model behaviors. The dose-response, time course, and tolerance results with methysergide are analogous to those observed after LSD, showing that methysergide has all of the key properties of the model's prototype and, therefore, that the cat behavior model is not specific for hallucinogens.

C.N.S. lesioned or drug pretreated male albino rats were subjected to a 1 hr horizontal oscillation stress. An analysis of forebrain 5-HT and 5-HIAA levels indicated that p-CPA pretreatment or M.F.B. lesions facilitated 5-HT turnover in response to stress. Raphe lesions, on the other hand, prevented this latter facilitation of indolamine turnover. The results obtained were explained on the basis of an operative negative feedback system in stressed rats. The lack of a change in raphe lesioned rats, further reinforced the concept that most forebrain 5-HT containing neurons are the result of axons extending from this nucleus.