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Neuropeptides and electroconvulsive treatment.

A A Mathé1

  • 1Karolinska Institute, Institution of Clinical Neuroscience, Stockholm, Sweden.

The Journal of ECT
|April 6, 1999
PubMed
Summary

Electroconvulsive treatment (ECT) increases neuropeptides like NPY and somatostatin (STS) in cerebrospinal fluid and brain regions. These neuropeptide changes, linked to clinical recovery, suggest a key mechanism of action for ECT in treating psychiatric disorders.

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Area of Science:

  • Neuroscience
  • Psychiatry
  • Molecular Biology

Background:

  • Neuropeptides such as corticotropin-releasing factor (CRF), neuropeptide Y (NPY), and somatostatin (STS) are implicated in depression and anxiety.
  • Neurotransmitters like neurotensin (NT), calcitonin gene-related peptide (CGRP), and tachykinins are linked to the dopaminergic system.
  • Psychotomimetic and antipsychotic drugs, along with lithium, influence neuropeptide synthesis, concentration, and release.

Purpose of the Study:

  • To investigate whether alterations in neuropeptide levels are a mechanism underlying the therapeutic effects of electroconvulsive treatment (ECT).
  • To examine the impact of electroconvulsive stimuli (ECS) on neuropeptide concentrations in both human cerebrospinal fluid (CSF) and rat brain models.

Main Methods:

  • Human CSF samples were analyzed before and after ECT.

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  • Brains from healthy and depression model rats were studied following electroconvulsive stimuli (ECS) or sham treatment.
  • Neuropeptide-like immunoreactivity (LI) and messenger RNA (mRNA) levels were measured in various brain regions (hippocampus, frontal cortex, occipital cortex, striatum).
  • Effects of ECS were compared to generalized seizures induced by kainic acid or pentylenetetrazole.
  • The influence of seizure-reducing agents (benzodiazepines, MK-801) on neuropeptide changes was assessed.

    • Main Results:

    • A series of ECTs increased CSF concentrations of NPY-LI, STS-LI, and CRF-LI, correlating with clinical recovery.
    • Repeated ECS, but not single ECS, elevated NPY-LI, neurokinin A (NKA)-LI, and STS-LI in the hippocampus and cortex, but not other regions.
    • ECS increased NPY and STS mRNA levels, indicating an effect on peptide synthesis.
    • Neuropeptide changes persisted for at least one week post-treatment and were mimicked by other seizure-inducing agents.
    • Seizure-reducing drugs did not alter the magnitude of neuropeptide changes despite reducing seizure duration.

    Conclusions:

    • Neuropeptides are demonstrably involved in the mechanism of action of electroconvulsive treatment (ECT).
    • ECT-induced changes in neuropeptides may contribute to its therapeutic efficacy in conditions like schizophrenia and depression.
    • A hypothesis is proposed that specific combinations of neuropeptide and monoamine alterations underlie ECT's effects on distinct disease symptoms, potentially irrespective of diagnosis.