Influence of an extracellular acidosis on excitatory synaptic transmissionand long-term potentiation in the CA1 region of rat hippocampal slices

The effects of extracellular acidification on the synaptic function and neu ronal excitability were investigated on the hippocampal CA1 neurons. A decr ease of extracellular pH from 7.4 to 6.7 did not alter either the resting m embrane potential or the neuronal membrane input resistance. Extracellularl y recorded field excitatory postsynaptic potentials (fEPSPs) and population spikes (PSs) were significantly reduced by acidosis. Additionally, the amp litude of presynaptic fiber volley was also reduced. The sensitivity of pos tsynaptic neurons to N-methyl-D-aspartate, but not to alpha -amino-3-hydrox y-5-methylisoxazole-4-propionic acid, was depressed by acidosis. Lowering o f extracellular pH did not significantly affect the magnitude of paired-pul se facilitation (PPF) of synaptic transmission. Acidosis also reversibly li mited the sustained repetitive firing (RF) of Na+-dependent action potentia ls elicited by injection of depolarizing current pulses into the pyramidal cells. The limitation of RF by extracellular acidification was accompanied by the reduction of the maximal rate of rise (V) over dot (max) of the acti on potentials and the amplitude of aftevhyperpolarization. Neither the Na+/ H+ antiporter blocker 5-(N-ethyl-N-isopropyl)-amiloride nor the selective a denosine A(1) receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine, howev er, affected the acidosis-induced synaptic depression. It was also found th at acidosis did not affect either the induction or maintenance of long-term potentiation (LTP) at Schaffer collateral-CA1 synapses. These results sugg est that the extracellular acidosis-induced synaptic depression is likely t o result from an inhibition of presynaptic Na+ conductance, thereby decreas ing the amplitude of action potentials in individual afferent fibers or the number of afferent fiber activation to stimuli and then indirectly affecti ng the signaling processes contributing to trigger neurotransmitter release . J. Neurosci. Res. 62: 403-415, 2000. (C) 2000 Wiley-Liss, Inc.