The temperature-dependent modulation of an inhibitory circuit in hippocampal slices as revealed by a population spike recording is mediated by extracellular adenosine

Citation
S. Fujii et al., The temperature-dependent modulation of an inhibitory circuit in hippocampal slices as revealed by a population spike recording is mediated by extracellular adenosine, JPN J PHYSL, 51(5), 2001, pp. 545-554
Citations number
34
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Physiology
Journal title
JAPANESE JOURNAL OF PHYSIOLOGY
ISSN journal
0021-521X → ACNP
Volume
51
Issue
5
Year of publication
2001
Pages
545 - 554
Database
ISI
SICI code
0021-521X(200110)51:5<545:TTMOAI>2.0.ZU;2-H
Abstract
We examined the effects of temperature on excitatory synaptic transmission and the recurrent inhibitory loop in CA1 neurons in guinea pig hippocampal slices. Increasing the temperature of the perfusing medium from 30 to 49 de greesC resulted in attenuation of both the amplitude of the synaptically ev oked CA1 population spikes and the paired-pulse inhibition (PPI) of the spi kes. A bath application of 2 mum picrotoxin, alpha gamma -aminobutyric acid receptor antagonist, did not affect the amplitude of the CA1 population sp ikes, but it significantly reduced PPI during the early heating phase (30-3 2 degreesC). In contrast, the application of 1 mm theophylline or 50 muM 8- phenyltheophylline, a selective adenosine A1 receptor antagonist, resulted in significant augmentation of the PPI during the early phase of hypertherm ia (30-34 degreesC) and a significant increase in the amplitude of the CA1 population spikes at higher temperatures (34-43 degreesC). These results su ggest that increased activation of adenosine A1 receptors in response to a temperature increase depresses not only excitatory synaptic responses, but also the strength of the inhibitory circuit in CA1 neurons. Furthermore, hy perexcitability of CA1 pyramidal neurons was seen in the middle of the heat ing range (34-38 degreesC), excitatory responses still being present, but t he strength of the inhibitory circuit significantly reduced.