Theories of Biological Etiology of Affective Disorders

Davis, John M.

doi:10.1016/s0074-7742(08)60060-4

Cited by 67 publications

(15 citation statements)

References 185 publications

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“…1974], Although other interpretations can be of fered [BrambUia et al. 1978], we arc inclined to believe that in both PAD [Davis. 1970;Schildkraul.…”

Section: Control Subjectsmentioning

confidence: 85%

Anterior Pituitary Responsiveness to Hypothalamic Hormones in Anorexia Nervosa

Brambilla¹,

Nobile²,

Müller

1981

Neuropsychobiology

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7 women and 3 men with anorexia nervosa were tested with thyrotropin-releasing hormone (TRH) and luteinizing hormone-follicle stimulating hormone-releasing hormone (LH-RH) and the growth hormone (GH), prolactin (PRL), gonadotropin (FSH-LH) and thyrotropin (TSH) responsiveness of their anterior pituitaries (AP) to the two hypothalamic neurohormones were determined. Administration of TRH (500 µg i.v.) induced rises in plasma GH in 4 patients, while in 4 patients it induced rises in plasma FSH and/or LH. LH-RH (150 µg i.v.) induced rises in plasma GH in 3 patients, increased plasma PRL in 3 patients and plasma TSH in 1 patient. Collectively, in only 1 patient, who was in a phase of initial nutritional rehabilitation, was there conventional AP responsiveness to hypothalamic neurohormones. This demonstrates that there is a profound derangement of AP responsiveness to hypothalamic neurohormones in patients with anorexia nervosa, probably reflecting a primary alteration in brain neurotransmitter function.

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“…1974], Although other interpretations can be of fered [BrambUia et al. 1978], we arc inclined to believe that in both PAD [Davis. 1970;Schildkraul.…”

Section: Control Subjectsmentioning

confidence: 85%

Anterior Pituitary Responsiveness to Hypothalamic Hormones in Anorexia Nervosa

Brambilla¹,

Nobile²,

Müller

1981

Neuropsychobiology

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“…It is tempting to suggest that a similar biochemical brain abnormality is present in both conditions, at least with regard to hypothalamic GH regula tion, in 1 case linked to the psychosis and in the other to addiction. In primary affective disorders an impairment in brain monoamine metabolism has been suggested (Davis, 1970;Schildkraut, 1974). The effect of heroin on neutrotransmitters has not been fully clarified.…”

Section: Discussionmentioning

confidence: 99%

Growth Hormone Response to Thyrotropin-Releasing Hormone and Gonadotropin-Releasing Hormone Stimulation in Heroin Addicts

et al. 1980

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Previous endocrine investigations have demonstrated the presence of multiple impairments of pituitary-target gland function in heroin addicts suggesting a possible hypothalamic involvement. Since the response of the pituitary to nonspecific stimuli is considered an expression of hypothalamic dysfunction, indicating a disconnection between the central nervous system and the anterior pituitary, we thought it worthwhile to study the GH response to stimulation with thyrotropin-releasing hormone (TRH) or gonadotropin-releasing hormone (GnRH) in heroin addicts. 23 male heroin addicts, aged 18-40 years, with histories of addiction to heroin alone from 8 months to 4 years, and daily i.v. heroin intakes between 200 and 2,500 mg of the drug (containing 18% of pure heroin) were studied. 8 patients received TRH 500 µg, GnRH 150 µg and 5 saline only, intravenously, and GH levels were assayed radioimmunologically in bloods taken 3Omin before, at the moment of stimulation and 15, 30, 60, 90 and 120 min thereafter. The results show normal basal GH levels. Stimulation with TRH and GnRH induced marked GH hypersecretion in 8 of the 18 patients examined. These results suggest that the hypothalamopituitary function may be impaired in heroin addiction.

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“…According to the monoamine theory of affective disorders, the tricyclic antidepressant drugs exert their antidepressant effect by potentiating the pharmacological actions of monoamines at postsynaptic receptor sites in the brain (Schildkraut, 1965;Davis, 1970). It is generally believed that the monoamine potentiating effect of the tricyclic antidepressants is due to their ability to block the uptake of monoamines into monoamine-containing nerve terminals (Iversen, 1974).…”

Section: Introductionmentioning

confidence: 99%

Effects of Iprindole on Responses of Single Cortical and Caudate Neurones to Monoamines and Acetylcholine

Bevan

Bradshaw

Szabadi

1975

British J Pharmacology

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The technique of microelectrophoresis was used to study the effects of iprindole on single neurones in the cerebral cortex and caudate nucleus of the rat. Iprindole, when applied for a brief period, did not affect the firing rate of the vast majority of neurones tested. Both potentiation and antagonism of neuronal responses to noradrenaline, dopamine, and 5‐hydroxytryptamine could be observed after a brief application of iprindole. Potentiation and antagonism often occurred after the same application of iprindole, antagonism always preceding potentiation. Responses to acetylcholine were affected by iprindole similarly: both potentiation and antagonism of the responses could be observed. Responses to glutamate were not affected by iprindole. It is concluded that the potentiation of responses to monoamines by iprindole cannot be explained on the basis of uptake blockade; this potentiation may be due to the blockade of masked receptors on the post‐synaptic cell. It is suggested that the common pharmacological action of the tricyclic antidepressants may be the ability to block both monoamine and acetylcholine receptors in the brain.

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Theories of Biological Etiology of Affective Disorders

Cited by 67 publications

References 185 publications

Anterior Pituitary Responsiveness to Hypothalamic Hormones in Anorexia Nervosa

Anterior Pituitary Responsiveness to Hypothalamic Hormones in Anorexia Nervosa

Growth Hormone Response to Thyrotropin-Releasing Hormone and Gonadotropin-Releasing Hormone Stimulation in Heroin Addicts

Effects of Iprindole on Responses of Single Cortical and Caudate Neurones to Monoamines and Acetylcholine

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