CGRP prevents electroconvulsive shock-induced amnesia in rats

A. Kovács, G. Telegdy

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

The effects of calcitonin gene-related peptide (CGRP) on electroconvulsive shock (ECS)-induced amnesia and the possible involvement of neurotransmitters in this action were studied in rats. ECS-induced amnesia was elicited in a passive avoidance paradigm. The possible roles of different transmitters involved in mediating CGRP action were followed by pretreating the animals with different receptor blockers in doses which themselves could not influence the paradigm. CGRP facilitated learning in the passive avoidance paradigm and prevented ECS-induced amnesia in a dose-dependent manner. Pretreatment with atropine, naloxone, phenoxybenzamine, or propranolol blocked the antiamnesic action of CGRP. Other receptor blockers, such as bicuculline, methysergide, and haloperidol, were ineffective. The results support our previous finding that CGRP facilitates passive avoidance learning and prevents ECS-induced amnesia. In the antiamnesic action of CGRP, cholinergic, opiate, and α- and β-adrenergic mediators are involved.

Original languageEnglish
Pages (from-to)121-125
Number of pages5
JournalPharmacology, Biochemistry and Behavior
Volume47
Issue number1
DOIs
Publication statusPublished - 1994

Fingerprint

Electroshock
Amnesia
Calcitonin Gene-Related Peptide
Rats
Opiate Alkaloids
Avoidance Learning
Methysergide
Phenoxybenzamine
Bicuculline
Haloperidol
Naloxone
Atropine
Propranolol
Adrenergic Agents
Cholinergic Agents
Neurotransmitter Agents
Transmitters
Animals
Learning

Keywords

  • CGRP
  • ECS-induced amnesia
  • ICV administration
  • Passive avoidance behaviour
  • Transmitter mediation

ASJC Scopus subject areas

  • Biochemistry
  • Behavioral Neuroscience
  • Pharmacology

Cite this

CGRP prevents electroconvulsive shock-induced amnesia in rats. / Kovács, A.; Telegdy, G.

In: Pharmacology, Biochemistry and Behavior, Vol. 47, No. 1, 1994, p. 121-125.

Research output: Contribution to journalArticle

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