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Benzodiazepine involvement in LTP of the GABA-ergic IPSC in rat hippocampal CA1 neurons.
Brain Res. 2005 Nov 16; 1062(1-2):134-43.BR

Abstract

Benzodiazepine binding sites are present on gamma-aminobutyric acid (GABA) receptors in hippocampal neurons. Diazepam is known to potentiate the amplitude and prolong the decay of GABA(A) receptor-mediated inhibitory postsynaptic currents (IPSCs). In this study, benzodiazepine involvement in long-term potentiation (LTP) of the IPSC was examined. Whole-cell recordings of IPSCs were made from rat hippocampal CA1 neurons in a slice preparation. LTP was induced by a tetanic stimulation in the stratum radiatum (2 trains of 100 Hz for 1 s, 20 s inter-train interval) while pharmacologically blocking ionotropic glutamate receptors. During LTP, the amplitude of the IPSCs was potentiated in the majority of neurons with the IPSC decay and shape unaffected. Diazepam (5 microM) potentiated the IPSC amplitude and prolonged the decay when applied before, but not during, LTP. In neurons in which LTP could not be induced by a tetanic stimulation, diazepam did not increase the amplitude of the pre-tetanic IPSC. Flumazenil, at a concentration (10 microM) that blocked the enhancement of the IPSC by applied diazepam, had no effect on the IPSC amplitude when applied before LTP induction but significantly decreased the IPSC when applied during LTP maintenance. The antagonist, when applied during the tetanic stimulation, did not block LTP, suggesting that benzodiazepine receptors do not participate in LTP induction. These results indicate that the maintenance of LTP of the IPSC involves (a) the release of endogenous benzodiazepine agonist(s) and/or (b) the participation of benzodiazepine binding sites on subsynaptic GABA(A) receptors.

Authors+Show Affiliations

Neuroscience Research Laboratory, Department of Pharmacology and Therapeutics, Faculty of Medicine, The University of British Columbia, Vancouver, Canada.No affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

16266690

Citation

Xu, J-Y, and B R. Sastry. "Benzodiazepine Involvement in LTP of the GABA-ergic IPSC in Rat Hippocampal CA1 Neurons." Brain Research, vol. 1062, no. 1-2, 2005, pp. 134-43.
Xu JY, Sastry BR. Benzodiazepine involvement in LTP of the GABA-ergic IPSC in rat hippocampal CA1 neurons. Brain Res. 2005;1062(1-2):134-43.
Xu, J. Y., & Sastry, B. R. (2005). Benzodiazepine involvement in LTP of the GABA-ergic IPSC in rat hippocampal CA1 neurons. Brain Research, 1062(1-2), 134-43.
Xu JY, Sastry BR. Benzodiazepine Involvement in LTP of the GABA-ergic IPSC in Rat Hippocampal CA1 Neurons. Brain Res. 2005 Nov 16;1062(1-2):134-43. PubMed PMID: 16266690.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Benzodiazepine involvement in LTP of the GABA-ergic IPSC in rat hippocampal CA1 neurons. AU - Xu,J-Y, AU - Sastry,B R, Y1 - 2005/11/02/ PY - 2005/06/23/received PY - 2005/09/01/revised PY - 2005/09/25/accepted PY - 2005/11/4/pubmed PY - 2006/2/10/medline PY - 2005/11/4/entrez SP - 134 EP - 43 JF - Brain research JO - Brain Res VL - 1062 IS - 1-2 N2 - Benzodiazepine binding sites are present on gamma-aminobutyric acid (GABA) receptors in hippocampal neurons. Diazepam is known to potentiate the amplitude and prolong the decay of GABA(A) receptor-mediated inhibitory postsynaptic currents (IPSCs). In this study, benzodiazepine involvement in long-term potentiation (LTP) of the IPSC was examined. Whole-cell recordings of IPSCs were made from rat hippocampal CA1 neurons in a slice preparation. LTP was induced by a tetanic stimulation in the stratum radiatum (2 trains of 100 Hz for 1 s, 20 s inter-train interval) while pharmacologically blocking ionotropic glutamate receptors. During LTP, the amplitude of the IPSCs was potentiated in the majority of neurons with the IPSC decay and shape unaffected. Diazepam (5 microM) potentiated the IPSC amplitude and prolonged the decay when applied before, but not during, LTP. In neurons in which LTP could not be induced by a tetanic stimulation, diazepam did not increase the amplitude of the pre-tetanic IPSC. Flumazenil, at a concentration (10 microM) that blocked the enhancement of the IPSC by applied diazepam, had no effect on the IPSC amplitude when applied before LTP induction but significantly decreased the IPSC when applied during LTP maintenance. The antagonist, when applied during the tetanic stimulation, did not block LTP, suggesting that benzodiazepine receptors do not participate in LTP induction. These results indicate that the maintenance of LTP of the IPSC involves (a) the release of endogenous benzodiazepine agonist(s) and/or (b) the participation of benzodiazepine binding sites on subsynaptic GABA(A) receptors. SN - 0006-8993 UR - https://www.unboundmedicine.com/medline/citation/16266690/Benzodiazepine_involvement_in_LTP_of_the_GABA_ergic_IPSC_in_rat_hippocampal_CA1_neurons_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(05)01317-X DB - PRIME DP - Unbound Medicine ER -