A glutamate antagonist blocks perforant path stimulation-induced reduction of dynorphin peptide and prodynorphin mRNA levels in rat hippocampus

Brain Res. 1991 Oct 25;562(2):243-50. doi: 10.1016/0006-8993(91)90627-8.

Abstract

Stimulation of the perforant path elicits a behavioral response, wet dog shakes (WDS), and reduction in hippocampal dynorphin A(1-8) immunoreactivity (DYN-IR) and prodynorphin mRNA (DYN mRNA) in rats. This study examined whether glutamate, the proposed endogenous transmitter released by perforant fibers, mediated the above responses. A glutamate antagonist, gamma-D-glutamylglycine (DGG, 25 micrograms/0.5 microliters), or artificial cerebrospinal fluid (ACSF, 0.5 microliters) was injected into the ventral hippocampus 10-20 min prior to acute or daily stimulation of the left perforant path in rats. In acute stimulation experiments, 4 consecutive stimulation trials elicited a total of 73 +/- 4 WDS at an average threshold intensity of 0.46 +/- 0.03 mA in ACSF-treated rats. The hippocampal DYN-IR in these animals decreased by more than 40% in both dorsal and ventral hippocampus relative to sham-stimulated rats. DGG injections significantly elevated the threshold for WDS (0.78 +/- 0.05 mA, P less than 0.01), reduced the number of WDS (45 +/- 6, P less than 0.01), and partially antagonized stimulation-induced reduction of DYN-IR in the ventral, but not dorsal, hippocampus. In daily stimulation experiments, rats received a single trial of stimulation once per day for 6 days. Daily DGG pretreatment almost completely abolished WDS at control threshold intensities, and significantly inhibited stimulation-induced decrease of DYN-IR in both dorsal and ventral hippocampus. In situ hybridization using a 35S-labeled oligodeoxyribonucleotide probe demonstrated a clear depletion of DYN mRNA signal in the dentate granule cell layer of ACSF-treated animals. This depletion was completely prevented in DGG-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Dipeptides / pharmacology*
  • Dynorphins / drug effects
  • Dynorphins / metabolism*
  • Enkephalins / genetics*
  • Excitatory Amino Acid Antagonists*
  • Glutamic Acid
  • Hippocampus / drug effects*
  • Hippocampus / metabolism
  • Histocytochemistry
  • Male
  • Neural Pathways / drug effects*
  • Neural Pathways / physiology
  • Peptide Fragments / drug effects
  • Peptide Fragments / metabolism*
  • Protein Precursors / genetics*
  • RNA, Messenger / drug effects
  • RNA, Messenger / metabolism*
  • Rats
  • Rats, Inbred F344
  • Tremor / drug therapy

Substances

  • Dipeptides
  • Enkephalins
  • Excitatory Amino Acid Antagonists
  • Peptide Fragments
  • Protein Precursors
  • RNA, Messenger
  • gamma-glutamylglycine
  • Glutamic Acid
  • Dynorphins
  • dynorphin (1-8)
  • preproenkephalin