SYNAPTIC TRANSMISSION AND PAIRED-PULSE BEHAVIOR OF CA1 PYRAMIDAL CELLS IN HIPPOCAMPAL SLICES FROM A HIBERNATOR AT LOW-TEMPERATURE - IMPORTANCE OF IONIC ENVIRONMENT

To investigate the effects of ionic changes possibly associated with h ibernation, hippocampal slices prepared from golden hamsters were stud ied in artificial cerebrospinal fluid (ACSF) of variable composition ( K+ 3-5 mM, Ca2+ 2-4 mM, Mg2+ 2-4 mM, pH 7.0-7.7) at temperatures of 15 -20 degrees C, just above the temperature below which synaptic transmi ssion is blacked. Population action potentials (population spikes, PSs ) of CA1 pyramidal cells were evoked by stimulation of the Schaffer co llaterals/commissural fibers with paired pulses (interpulse interval 5 0 ms, interval between pairs 30 s). The responses evoked at given temp eratures were investigated as a function of extracellular ion concentr ations. In ACSF containing 3 mM K+, 2 mM Ca2+ and 2 mM Mg2+, PSs could be evoked at temperatures of > similar to 16 degrees C whereas at low er temperatures synaptic transmission was blocked. The threshold tempe rature was slightly higher for the first (PS1) than for the second PS (PS2) evoked by paired-pulse stimulation. The slices displayed paired- pulse facilitation (PPF) at all temperatures. Elevation of [K+](o) fro m 3 to 5 mM depressed the amplitudes of both PS1 and PS2, with a stron ger effect on PS2. PPF was reduced and, at near-threshold temperatures , turned into paired-pulse depression (PPD). Elevation of [Ca2+](o) fr om 2 to 4 mM increased the amplitude of PS1. The amplitude of PS2, in contrast, was reduced at near-threshold temperatures. PPF turned into PPD. Elevation of [Mg2+](o) from 2 to 4 mM reduced the amplitudes of b oth PS1 and PS2, with a stronger effect on PS1. Accordingly, PPF was i ncreased. Acidification by 0.3 pH units strongly depressed the amplitu des of PS1 as well as PS2 and increased PPF. Alkalization by 0.4 pH un its had only weak effects in the opposite direction. Changes in the io nic composition comparable to those investigated in the present study presumably occur in the brain interstitium of hamsters during entrance into hibernation. According to our results, such changes depress syna ptic transmission at low temperatures in the hamster hippocampus in vi tro. This modulation may be important for the regulation of neuronal a ctivity during entrance into hibernation.