Effects of stress on the metabolism of noradrenaline, dopamine and serotonin (5HT) in the central nervous system of the rat (II) modifications of serotonin metabolism
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Tryptophan hydroxylase
Biogenic amine
Fatal familial insomnia (FFI) is a unique hereditary prion disease with characteristic disturbances of sleep. We studied the serotonergic system in 8 FFI-affected subjects by immunohistochemistry for the serotonin-synthesizing enzyme, tryptophan hydroxylase (TH). Quantification of neurons in median raphe nuclei showed no total neuronal loss in FFI but a substantial increase of TH+ neurons (∼62%) in FFI subjects compared with controls. Our data indicate an alteration of the serotonergic system that might represent the functional substrate of some typical symptoms of FFI. Ann Neurol 2000;48:788–791
Tryptophan hydroxylase
Fatal familial insomnia
Raphe
Raphe nuclei
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The concept of a major inhibitory role of serotonin in aggressive behavior is widely accepted by researchers. There were ample evidences that a pharmacologically-induced increase in serotonergic activity attenuates agonistic behavior, and the manipulations inhibiting the brain serotonergic system can elicit aggressiveness in animals. Ealier, experimental studies have demonstrated reduced metabolism in brain serotonergic system and specific changes in pharmacological sensitivity of 5-HT(1A) receptors in male mice with repeated experience of aggression. It has been shown that mRNA levels of the serotonergic genes in the midbrain raphe nuclei are reduced in aggressive males. After no-fight period expression of some genes is restored or becomes higher compared with the controls on the background of increased aggression. The review provides data supporting and contradicting the serotonin-deficiency hypothesis of increased aggressiveness, revealing non-specific role of serotonin in the control of aggressive behavior, and also provides information about the inhibition of serotonergic activity under repeated experience of aggression.
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The link between suicidality and serotonergic dysfunction is a consistent finding in biological psychiatry. In three independent studies we found weak intensity dependence of auditory evoked potentials, which may be related to high serotonergic activity, in psychiatric patients with a history of suicide attempts. This result seems to contradict studies reporting low serotonergic activity in acute suicidal patients. As an explanation for this discrepancy we propose that serotonergic activity may be low only in acute suicidal states, and that high serotonergic activity, as reflected by a weak intensity dependence, may characterize high-risk patients, in whom a transient decrease of serotonergic activity is accompanied by acute suicidality.
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Serotonergic agonists such as m-chlorophenylpiperazine (m-CPP) and fenfluramine may induce migraine attacks. This has led to opposing theories concerning the role of 5-hydroxytryptamine (5HT) in triggering migraine attacks; is there hyperfunction or hypofunction of the central serotonergic system. Our review of the literature strongly suggests that m-CPP and fenfluramine provoke migraine attacks by stimulating, directly or indirectly, the 5HT 2C /5HT 2B receptors, although there is no total agreement with this interpretation. Central 5HT hypersensitivity in migraine patients, probably due to 5HT neuronal depletion, is proposed on the basis of review of electrophysiological tests and neuroendocrine challenge paradigms.
5-HT1 receptor
Cortical Spreading Depression
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Citalopram
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Serotonin's role as a neuronal transmitter was established already forty years ago, and the anatomy and many of the functions of the major serotonergic systems have been carefully mapped. The intimate association of serotonergic mechanisms with central control of food intake has also been extensively studied. While the present concepts of serotonergic functions rely on the ascending, raphe nuclei-originating serotonergic pathways, there is an accumulating evidence to support that hypothalamic neurons may also exhibit many features normally attributed to serotonergic neurons only. Neurons in the hypothalamic arcuate and periventricular nuclei express tryptophan hydroxylase, the serotonin synthesizing enzyme, while they do not transport or synthesize serotonin. On the other hand, dorsomedial nucleus contains a select population of neurons that do actively accumulate serotonin, while they do not express tryptophan hydroxylase. These and some other serotonin-associated features of the hypothalamic neuronal groups are discussed. Finally the present data is projected against the prevailing concept of hypothalamic regulation of food intake.
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Raphe nuclei
Dorsal raphe nucleus
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After systemic administration of several serotonergic antagonists, female rats that had been ovariectomized, adrenalectomized, and estrogen-primed showed lordotic responding. Lordosis could also be elicited after direct placement of serotonergic receptor blockers into hypothalamic sites known to contain serotonergic terminals. None of the treatments activated the soliciting component of the estrous behavior pattern of the female rat. It is postulated that the hypothalamus contains serotonergic terminals which suppress lordotic responding.
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