Brain tissue hydrolysate acts on presynaptic adenosine receptor in the rat hippocampus

H. Xiong, J. M. Wojtowicz, A. Baskys

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Adenosine is a potent inhibitory modulator in the brain. It suppresses glutamatergic synaptic transmission and possibly acts as a brain endogenous neuroprotective agent. In this study we have examined the effects of a clinically used porcine brain tissue hydrolysate, Cerebrolysin(TM), on synaptic transmission in the CA1 area of rat hippocampal slices. A major effect of the drug at doses approximating those administered clinically to demented patients was a depression of synaptic transmission at the Schaffer collateral-commissural pathway in CA1. Detailed analysis showed that the inhibition is presynaptic and can be reduced by low doses of a specific blocker of adenosine A, receptors, 8-cyclopentyltheophylline. Because Cerebrolysin(TM) does not contain a detectable amount of adenosine, the effect on adenosine A1 receptors must be indirect, perhaps by release of the endogenous agonist. This action of Cerebrolysin(TM) is consistent with a putative neuroprotective action underlying its clinical usage.

Original languageEnglish (US)
Pages (from-to)1194-1197
Number of pages4
JournalCanadian journal of physiology and pharmacology
Volume73
Issue number8
DOIs
StatePublished - Jan 1 1995

Fingerprint

Presynaptic Receptors
Purinergic P1 Receptors
Synaptic Transmission
Hippocampus
Adenosine
Brain
Adenosine A1 Receptors
Neuroprotective Agents
Swine
Pharmaceutical Preparations
cerebrolysin

Keywords

  • Adenosine
  • Brain slices
  • Cerebrolysin(TM)
  • Hippocampus
  • Synaptic transmission

ASJC Scopus subject areas

  • Physiology
  • Pharmacology
  • Physiology (medical)

Cite this

Brain tissue hydrolysate acts on presynaptic adenosine receptor in the rat hippocampus. / Xiong, H.; Wojtowicz, J. M.; Baskys, A.

In: Canadian journal of physiology and pharmacology, Vol. 73, No. 8, 01.01.1995, p. 1194-1197.

Research output: Contribution to journalArticle

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