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Premenstrual tension was studied in 16 females, using both biochemical and psychological parameters during the pre- and postmenstrual phases. Uptake of serotonin (5-HT) and the levels of 5-HT in platelet-rich plasma and platelet-poor plasma were determined. Degrees of distress experienced pre- and postmenstrually were quantified via the Moos menstrual distress questionnaire. The mean V_max was significantly lower during the premenstrual (tension) phase (8.2 ± 0.9 pmol/min) as compared to the postmenstrual (normal) phase (14.4 ± 3.2 pmol/min). There was no significant difference in the K_m values. A highly significant (p < 0.001) reduction in the levels of 5-HT in platelet-rich plasma (–23.2%) and platelet-poor plasma (-19.1%) was found during the premenstrual phase. There were correlations between the kinetic parameters of 5-HT uptake and some of the Moos symptoms.

A series of experiments was performed to characterize the nature of local tissue reactions to cocaine. The time‐course of tissue injury was assessed over a 21‐day period by gross and microscopic examination of the skin of rats administered 0.1–2.0% cocaine hydrochloride by i.e. or s.c. injection. Pronounced blanching, progressively severe hemorrhage, delayed extravasation of Evans blue dye, and eventual scar formation were seen grossly at injection sites. Marked engorgement of blood vessels, small hemorrhagic foci, and hyalinization of scattered muscle bundles of the pannieulus carnosus were apparent microscopically at 15 min post‐injection. Subsequent changes during (he next 3 h included progressively severe hemorrhage and loss of muscle bundles, degeneration of hair follicles and necrosis of the vascular endothelium and epidermis. Healing of cocaine‐induced lesions, as monitored for 21 days, was relatively rapid and complete. A hyperplastic epidermis covered formerly ulcerated areas by 6 days. Destroyed cellular structures in the derm is were replaced by collagen. Since cocaine's local tissue toxicity has been ascribed to vasoconstriction, the toxic potential of cocaine was contrasted with that of a potent vasoconstrictor, epinephrine (EPI). Although 0.1% EPI produced greater vasoconstriction than did cocaine, s.c. injection of EPI did not result in skin damage. The slight acidity of cocaine hydrochloride solutions appeared to be of little consequence, since s.c. injection of pH 5 and 6 saline had little effect on tissues. Our results suggest that cocaine is directly cytotoxic, though ischemia resulting from vascular injury and vasoconstriction may contribute to the local tissue injury caused by the drug.

Following repeated injection in the rat, cocaine decreased the concentration of serotonin in the septum-caudate and increased the metabolism of hypothalamic norepinephrine and also striatal dopamine to a lesser extent. Furthermore, cocaine significantly decreased the activity of the rate-limiting enzyme, tryptophan hydroxylase. In a comparative study d-amphetamine and methylphenidate were found to exert an effect opposite to cocaine in the activation of tryptophan hydroxylase. These findings indicate that cocaine may lower central serotonin function by decreasing its availability for neural transmission. This could account for the stimulation of locomotor activity observed after cocaine administration.

Rats were trained in a two-lever operant procedure to discriminate either 1.0 mg/kg (+)amphetamine or 1.5 mg/kg DOM from saline. Rats trained to discriminate DOM from saline showed generalization with the DOM training condition when tested with mescaline or 2,5-dimethoxy-4-ethylamphetamine (DOET), but not when tested with (+)amphetamine or methylphenidate. Both isomers of DOM generalized with racemic training compound, the (-)isomer being more potent. The DOM stimulus was completely blocked by the serotonin (5-HT) antagonists cinanserin and methysergide, but not by the peripheral 5-HT antagonist xylamidine nor the dopamine antagonist haloperidol. Rats trained to discriminate (+)amphetamine from saline generalized with the amphetamine training condition when tested with methylphenidate but not when tested with mescaline, DOET, racemic DOM, or either isomer of DOM. The amphetamine stimulus was blocked by pretreatment with haloperidol but not by cinanserin, methysergide, or xylamidine. The results show that, despite their structural similarity, amphetamine and DOM induce pharmacologically distinct stimuli.

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Levels of platelet monamine oxidase activity, state anxiety and trait anxiety were quantified twice in 20 drug-free subjects with generalized anxiety and an equal number of healthy drug-free controls at 4-week intervals. Fifteen subjects in each groups also had plasma epinephrine and norepinephrine measured. The index group received relaxation training during the interval between the two evaluation sessions. Post-relaxation training values for monoamine oxidase, epinephrine, norepinephrine and the anxiety levels were found to be significantly lower than the pre-treatment values for the index group. No significant changes were seen in the control group values. For the index group, catecholamine levels and monoamine oxidase activity were seen to correlate significant before and after relaxation training.

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