Effect of Long-Term Neuroleptic Treatment on Prolactin and Norepinephrine Levels in Serum of Chronic Schizophrenics: Relations to Psychopathology and Extrapyramidal Symptoms

Finkbeiner, C; Fischer, Bernard A.; Zander, Karl; Ackenheil, Manfred

doi:10.1159/000117751

Cited by 36 publications

(8 citation statements)

References 26 publications

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“…Continuous antagonistic exposure of risperidone on the D 2 receptors, which would be the case with minipump administration compared with injections, may desensitize the prolactin response. Indeed, several studies indicate that tolerance to antipsychotic-induced hyperprolactinemia may develop during chronic administration in human studies [60,61,62]. Finally, another explanation may be the diurnal variation of prolactin secretion compared with sample collection.…”

Section: Discussionmentioning

confidence: 99%

Risperidone Treatment Increases CB<sub>1</sub> Receptor Binding in Rat Brain

et al. 2009

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Background/Aims: Body weight gain is a common side effect of treatment with antipsychotics, but the mechanisms underlying this weight gain are unknown. Several factors may be involved in antipsychotic-induced body weight gain including the cannabinoid receptor 1 (CB₁), the serotonin receptor 2C, the ghrelin receptor, neuropeptide Y, adiponectin and proopiomelanocortin. We investigated whether the expression of these factors was affected in rats chronically treated with the antipsychotic risperidone. Methods: Male Sprague-Dawley rats were treated with risperidone (1.0 mg/kg/day) or vehicle (20% hydroxypropyl β-cyclodextrin) for 28 days. Expression of the aforementioned factors were examined together with plasma prolactin and ghrelin levels. Results: No difference in body weight gained during treatment was observed between risperidone and vehicle treated rats, but plasma risperidone levels positively correlated with visceral fat mass. Risperidone treatment increased CB₁ receptor binding in the arcuate nucleus (40%), hippocampus (25–30%) and amygdala (35%) without concurrent alterations in the CB₁ receptor mRNA. Risperidone treatment increased adiponectin mRNA. Conclusion: The present study showed that risperidone treatment altered CB₁ receptor binding in the rat brain. Risperidone-induced adiposity and metabolic dysfunction in the clinic may be explained by increased CB₁ receptor density in brain regions involved in appetite and regulation of metabolic function.

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Section: Discussionmentioning

confidence: 99%

Risperidone Treatment Increases CB<sub>1</sub> Receptor Binding in Rat Brain

et al. 2009

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“…Both the low baseline PRL-levels found in a few cases and the further tendency to an increase of PRL induced by reserpine in spite of continuous high dose neuroleptic treatment indicates tolerance to the DA blocking effect of neuroleptics in the tuberoinfundibular system (Naber et al, 1980). This hypothesis is also supported by the fact that 3 out of the 4 patients whose PRLlevels did not increase after 14 days of adjuvant reserpine treatment had the highest pre-reserpine PRL levels, presumably because of the lack of tolerance in these cases (see Fig.…”

Section: Discussionmentioning

confidence: 97%

Effect of adjuvant reserpine treatment on catecholamine metabolism in schizophrenic patients under long-term neuroleptic treatment

Bagdy

Perenyi

Frecska

et al. 1988

J. Neural Transmission

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The clinical and biochemical effects of adjuvant reserpine treatment were investigated in 12 chronic schizophrenic patients on long-term neuroleptic medication. The global severity of the symptoms using the Brief Psychiatric Rating Scale did not change significantly in the whole group, however, a moderate decrease in positive symptoms (factors though disturbance, activation and hostile-suspiciousness) was observed for 5 patients. Cerebrospinal fluid (CSF) noradrenaline levels showed a consistent decrease, but other biochemical parameters (CSF dopamine metabolites, platelet MAO and serum dopamine-beta-hydroxylase activities) did not change significantly. The changes of clinical symptoms and biochemical parameters did not show any correlation.

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“…20], How ever, in the great majority (i.e., in 18 out of 25) of our schizophrenic patients who had been treated with neuro leptics for 6 weeks, basal PRL values exceeded the nor mal range; this may easily explain the significantly higher basal PRL values at 14.00 and 24.00 h which were found in our neuroleptic-treated patients, in comparison to their pretreatment values. A well-known effect of neu roleptics is the elevation of the serum PRL level; by blocking dopamine receptors of the tuberoinfundibular system, these drugs prevent the dopamine-mediated in hibition of PRL secretion [21][22][23]. However, within 3-24 years of neuroleptic therapy many patients may de velop a tolerance to the PRL-incrcasing effect of neuro leptics in the tuberoinfundibular system which is revers ible [21][22][23],…”

Section: Discussionmentioning

confidence: 99%

“…A well-known effect of neu roleptics is the elevation of the serum PRL level; by blocking dopamine receptors of the tuberoinfundibular system, these drugs prevent the dopamine-mediated in hibition of PRL secretion [21][22][23]. However, within 3-24 years of neuroleptic therapy many patients may de velop a tolerance to the PRL-incrcasing effect of neuro leptics in the tuberoinfundibular system which is revers ible [21][22][23],…”

Section: Discussionmentioning

confidence: 99%

Effects of Six Weeks’ Neuroleptic Treatment on the Pituitary-Thyroid Axis in Schizophrenic Patients

et al. 1986

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In order to investigate (a) the effects of 6 weeks’ neuroleptic treatment on the pituitary-thyroid axis in 25 male schizophrenic patients, and (b) the diurnal variation in the thyrotropin (TSH) and prolactin (PRL) responses to thyrotropin-releasing hormone (TRH) in these patients, the TRH stimulation test was performed in each of them at 14.00 and 24.00 h of the same day, both before and after 6 weeks’ treatment with neuroleptics (chlorpromazine or fluspirilene). Also, serum thyroxine (T₄), in vitro radioactive triiodothyronine uptake (RT3 U) and free-thyroxine index (FTI) values were estimated from the pre-TRH blood sample. We found no evidence of diurnal variation in the TSH response to TRH in the schizophrenic patients, before or after 6 weeks’ neuroleptic treatment. Only drug-free schizophrenic patients had significantly higher PRL responses to TRH at 14.00 h than those at 24.00 h. After 6 weeks’ neuroleptic treatment, schizophrenic patients tended to have lower FTI values; also, they had significantly higher basal TSH and PRL values, as well as significantly augmented TSH and PRL responses to TRH, in comparison to their pretreatment values. These findings render possible the diagnosis of subclinical hypothyroidism in neuroleptic-treated schizophrenic patients.

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Effect of Long-Term Neuroleptic Treatment on Prolactin and Norepinephrine Levels in Serum of Chronic Schizophrenics: Relations to Psychopathology and Extrapyramidal Symptoms

Cited by 36 publications

References 26 publications

Risperidone Treatment Increases CB<sub>1</sub> Receptor Binding in Rat Brain

Risperidone Treatment Increases CB<sub>1</sub> Receptor Binding in Rat Brain

Effect of adjuvant reserpine treatment on catecholamine metabolism in schizophrenic patients under long-term neuroleptic treatment

Effects of Six Weeks’ Neuroleptic Treatment on the Pituitary-Thyroid Axis in Schizophrenic Patients

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