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Related Experiment Videos

Noradrenergic function in schizophrenia.

W M Glazer1, D S Charney, G R Heninger

  • 1Clinical Neuroscience Research Unit, Connecticut Mental Health Center, New Haven.

Archives of General Psychiatry
|October 1, 1987
PubMed
Summary

Yohimbine did not reveal significant noradrenergic dysfunction in schizophrenia or tardive dyskinesia (TD). While some schizophrenic patients showed increased MHPG and blood pressure, this did not support a central role for noradrenergic dysfunction in these conditions.

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Area of Science:

  • Neuroscience
  • Psychiatry
  • Pharmacology

Background:

  • Noradrenergic dysfunction has been hypothesized to play a role in schizophrenia and tardive dyskinesia (TD).
  • Yohimbine, an alpha 2-adrenergic receptor antagonist, enhances noradrenergic function.
  • Investigating the effects of yohimbine can help elucidate the role of the noradrenergic system in these conditions.

Purpose of the Study:

  • To investigate the effects of yohimbine on behavior, plasma MHPG levels, blood pressure, and heart rate in healthy subjects and schizophrenic patients.
  • To determine if schizophrenic patients, particularly those with TD, exhibit altered responses to yohimbine compared to healthy controls.
  • To assess the hypothesis that noradrenergic dysfunction is centrally involved in the pathogenesis of schizophrenia and TD.

Main Methods:

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  • A double-blind, placebo-controlled study administering yohimbine to 16 healthy subjects and 18 drug-free schizophrenic patients (10 with TD, 8 without TD).
  • Outcome measures included behavioral changes, plasma 3-methoxy-4-hydroxy-phenylglycol (MHPG) levels, blood pressure, and heart rate.
  • Analysis compared responses between healthy controls, schizophrenic patients, and patients with TD.

Main Results:

  • A subgroup of six schizophrenic patients experienced dysphoric arousal after yohimbine administration, not observed in healthy subjects.
  • The overall schizophrenic group showed a trend towards greater yohimbine-induced increases in plasma MHPG and systolic blood pressure.
  • Patients with TD did not differ in their response to yohimbine compared to those without TD or healthy controls.

Conclusions:

  • The results do not strongly support a central role for noradrenergic dysfunction in the pathogenesis of schizophrenia or TD.
  • Further research into noradrenergic dysfunction in specific subgroups of schizophrenic patients is warranted.
  • Yohimbine's effects in schizophrenia may involve specific patient subgroups rather than a generalized noradrenergic deficit.