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Acute effects of lysergic acid diethylamide (LSD) and chlorimipramine on tryptophan uptake into rat brain synaptosomes were studied in rats treated chronically with dietary lithium and in control rats. The acute drug treatments did not change V max or K m for trytophan uptake in control rats. In lithium-treated rats, chlorimipramine increased and LSD decreased V max . These results indicate that, rather than stabilizing serotonin production through tryptophan uptake changes, chronic lithium treatment may increase the responsiveness of tryptophan uptake to changes in serotonin utilization.

Summary Amphetamine was given intraperitoneally in doses of 5 mg and 10 mg to cats which had been chronically implanted with electrodes in the lateral hypothalamus and midbrain reticular formation. The attack on an anesthetized rat which could be elicited by electrical stimulation of the lateral hypothalamus was facilitated by amphetamine. The facilitation of this attack by simultaneous electrical stimulation of the midbrain reticular formation was further enhanced by amphetamine, provided that the combined stimulation did not exceed a certain level above the level the attack behavior was inhibited. The facilitation occurred between the onset of stimulation and the first translational movement and between the first movement and moment of attack. It is postulated that the action of amphetamine is similar to direct electrical stimulation of the midbrain reticular formation but with some differences occurring as a result of concomitant indirect actions.

Electrical stimulation of the lateral hypothalamus in cats gave rise to directed attacks on an anesthetized rat. This electrically initiated attack was facilitated by concurrent stimulation of the midbrain reticular formation. By itself, the midbrain stimulation that facilitated attack produced only minimal alerting. At higher intensities, stimulation of the midbrain alone gave rise to tegmental reactions, and to attack and flight. These last two reactions occurred either with or without a marked display. The mesencephalic reticular formation can accelerate and intensify behavioral sequences. It both facilitates and inhibits the appropriate reflexes to bring about a well coordinated behavioral response.

Two large aggregates of serotonin-containing neurons are situated in the dorsal and median raphe nuclei of the caudal midbrain. Small electrolytic lesions placed in these nuclei and the suprachiasmaticnucleus (which receives axon terminals from the raphe nuclei) and the paraventricular nucleus of the hypothalamus were examined with the electron microscope 2–7 days post lesion. Many degenerating terminals were found in the suprachiasmatic nucleus but few were noted in the paraventricular nucleus. The degeneration was manifested by increased osmiophilia of nerve-ending ground substance, a dissolution of vesicular and mitochondrial membranes, and later, by a marked proliferation of glial lamellae. Both axosomatic and axodendritic terminals showed such changes; large granular vesicles were frequently observed in the involved endings. These results are in accord with the delineation of the serotonin-containing neuronal pathway based on the fluorescence histochemical method.