Spontaneous GABA(A)-dependent synchronous periodic activity in adult rat ventral hippocampal slices.
The present study shows that adult rat transverse slices from the ventral hippocampus perfused with standard medium persistently generate spontaneous synchronous field potentials. In CA1 st. pyramidale this regular ventral hippocampus spontaneous synchronous activity (VHSSA) was positive with mean amplitude 0.18 +/- 0.02 mV (n=80 slices) and occurred every 0.48 +/- 0.02 s. Simultaneous intracellular recordings from CA1 pyramidal neurons demonstrated that concomitant hyperpolarizations invariably occurred in association to this field activity and could thus constitute its electrical generators. These hyperpolarizations, had mean amplitude 2.7 +/- 0.6 mV, duration at half amplitude 44.8 +/- 6.6 ms, they reversed at -72.6 +/- 1.5 mV (n=10 cells), they effectively suspended the depolarization-induced tonic neuronal firing of all ten pyramidal neurons and they were reversibly abolished, together with field potentials, by the GABA(A) receptor antagonist bicuculline (5 microM, n=4). VHSSA was also dependent on fast glutamatergic transmission, since it was blocked by the antagonist of AMPA/kainate receptors 6-Cyano-7-nitroquinoxaline-2,3-dione disodium (10 microM, n=3). We propose that, under standard in vitro conditions, synchronous GABA(A)-mediated hyperpolarizing potentials are spontaneously generated in pyramidal neurons presumably resulting from the phasic quasi-rhythmic discharge of a local interneuronal network of ventral hippocampus.
Papatheodoropoulos
Costas
C
Department of Physiology, Medical School, University of Patras, 26 500 Patras, Greece. cepapath@med.upatras.gr
Kostopoulos
George
G
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001683:Biological Clocks / Q000187:drug effects / Q000502:physiology*; D003344:Cortical Synchronization / Q000187:drug effects; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D058787:GABA-A Receptor Antagonists; D018698:Glutamic Acid / Q000378:metabolism; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D007395:Interneurons / Q000166:cytology / Q000378:metabolism*; D008297:Male; D009415:Nerve Net / Q000166:cytology / Q000378:metabolism*; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009924:Organ Culture Techniques; D010507:Periodicity; D017966:Pyramidal Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D018091:Receptors, AMPA / Q000037:antagonists & inhibitors / Q000378:metabolism; D011963:Receptors, GABA-A / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D058787:GABA-A Receptor Antagonists; D018091:Receptors, AMPA; D011963:Receptors, GABA-A; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid