Carbonic anhydrase modulates short term plasticity at central synapses

C. GONZÁLEZ INCHAUSPE; LUCÍA COLL; OSVALDO D. UCHITEL

Córdoba

Congreso; XXIX CONGRESO ANUAL de la Sociedad Argentina de Investigación en Neurociencia (SAN); 2014

Sociedad Argentina de Investigación en Neurociencia (SAN)

Acetazolamide (AZ) is known to inhibit the action of carbonic anhydrase (CA), an enzyme responsible for regulating the extra- and intracellular pH. AZ is used to treat certain types of epilepsy and ataxia but its mechanism of action is still unknown. At the mouse neuromuscular junction our lab have reported that changes in buffer capacity, by inhibiting CA, produces changes in the mode of vesicle recycling and also affects short term synaptic plasticity. Our aim is to extend those studies to synaptic transmission at central synapses. Whole-cell voltage-clamp recordings were performed in brain stem slices at visually identified MNTB neurons and at the CA1 hippocampus pyramidal cells. Synaptic currents were evoked by stimulating their inputs. Transmitter release and pair pulse ratio (PPR) were not affected by AZ at normal Ca/Mg bicarbonate buffered external solution. However, studied in low release probability conditions showed that AZ reduces PPR at the Calyx of Held. In similar conditions AZ has no effect on excitatory input to CA1 pyramidal cells but in contrast increases the PPR at the inhibitory synapses. These results suggest that changes in pH during synaptic transmission may affect differentially excitatory and inhibitory synapses via a presynaptic vesicle recycling mechanism.