Kainic acid seizures in the rat

Serotonergic facilitation of facial motoneuron excitation.

Motor effects of serotonin in the central nervous system

Indoleamine structures in the brains of normal, pair-fed control, and thiamine deficient rats are selectively localized by autoradiography following monoamine oxidase inhibition and simultaneous intraventricular infusion of 3H-5HT (10−5 m) and cold d–1 norepinephrine (10−4 m). The locations of indoleamine neurons and their plexuses are comparable in the normal and control animals and are enumerated and mapped in detail. In addition to numerous labeled neurons in the raphe and reticular formation of pons and medulla, there are indoleamine neurons in several hypothalamic nuclei, in the mammillary, habenular, and interpeduncular nuclei. Labeled axonal plexuses occur in almost all areas of the brain but certain regions in spinal cord, medulla, midbrain, diencephalon, basal ganglia, and hippocampus are particularly rich. Thiamine deficiency causes lack of label in almost all indoleamine neurons and their processes in the midbrain and medulla; only a few dystrophic cells with hypertrophied axons are seen. In the diencephalon more indoleamine neurons and their axonal plexuses are visualized in these uptake studies. The periventricular regions of spinal cord, medulla, midbrain and diencephalon, the mammillary nuclei, habenular nuclei, and cerebellum – areas richly innervated by indoleamine axons in the normal brain – are the most severely affected. The ventricular and leptomeningeal indoleamine structures are preserved, however, and individual axons may hypertrophy. It remains to be resolved whether these changes reflect disturbances in the ability of certain indoleamine neurons to take up and retain 3H-5HT or true neuronal degeneration.

Indoleamine neurons and their processes in the normal rat brain and in chronic diet‐induced thiamine deficiency demonstrated by uptake of 3H‐Serotonin

Central nervous system metabolism in children with the syndrome of Gilles de la Tourette (TS) and contrasting pediatric patients was assessed by measuring the cerebrospinal fluid (CSF) metabolites of dopamine (homovanillic acid, HVA) and serotonin (5-hydroxyindoleacetic acid, 5-HIAA) with and without the administration of probenecid. Reduced accumulation of CSF HVA and 5-HIAA was found in TS. This may represent a primary decrease in brain turnover of dopamine and serotonin or a long-term adaptation to overactivity in these systems, perhaps as a result of changes in receptor sensitivity. In the CSF of a child with profound TS, an elevated level of the major metabolite of norepine.

Central biogenic amine metabolism in children with the syndrome of chronic multiple tics of Gilles de la Tourette: norepinephrine, serotonin, and dopamine.

5-hydroxytryptophan-induced myoclonus: Increased sensitivity to serotonin after intracranial 5,7-dihydroxytryptamine in the adult rat

A myoclonic syndrome consisting of tremor, myoclonus, and seizures was produced following the systemic administration of 5-hydroxytryptophan to adult rats previously given intracisternal injections of 5, 7-dihydroxytryptamine and systemic desmethylimipramine, but not in their controls. This behavioral response was blocked by pretreatment with the putative serotonin receptor blocking agents methysergide, lysergic acid diethylamide, and bromolysergic acid diethylamide, as well as centrally effective doses of the aromatic amino acid decarboxylase inhibitor Ro4-4602. Blockers of receptors of other neurotransmitters had little effect. This neurologic response in the adult rat may be relevant to some forms of clinical myoclonus and may be useful in testing potential agonists and antagonists of serotonin receptors in the mammalian central nervous system.

R. M. Stewart

Papers

5-hydroxytryptophan-induced myoclonus: Increased sensitivity to serotonin after intracranial 5,7-dihydroxytryptamine in the adult rat

Myoclonus after 5‐hydroxytryptophan in rats with lesions of indoleamine neurons in the central nervous system