P/Q-type CA2+-channels are required for acid-sensing ion channels 1A (ASIC1A)-mediated inhibition of neuromuscular transmission in mice

LINO N.G.,VATTINO L.G.,URBANO F.J.,UCHITEL O.D.

Huerta Grande, Cordoba, Argentina.

Congreso; IIRCN- Second Joint Meeting of the Argentine Society for Neuroscience (SAN: XXV Reunión Anual de la Sociedad Argentina de Investigación en Neurociencias) and the Argentine Workshop in Neuroscience (TAN: XII Taller Argentino de Neurociencias).; 2010

SAN-TAN

CNS changes in pHO have considerable influence on the physiology of neurons, and in pathological conditions affect the outcome of neuronal injury. Acid-sensing ion channels (ASICs) have been proposed to regulate synaptic transmission in response to acidosis. Recently, we have described the presence of ASIC1a at the presynaptic terminals of neuromuscular junctions (NMJs), where they may exert an inhibition on neuromuscular transmission. Considering our evidence and the fact that several neurological diseases are characterized by an abnormally sustained synaptic transmission, the aim of this work was to investigate the modulatory role of ASIC1a in such pathological conditions. We initially studied miniature endplate potentials frequencies from mice lacking P/Q-type Ca2+-channels (α1A-/-) in the absence or presence of psalmotoxin. No significant difference was observed after the application of psalmotoxin (Student´s t-test, p= 0,278). Neither evoked endplate potentials during paired-pulse nerve-stimulation at 20 and 50 Hz change significantly after the application of psalmotoxin (Student´s t-test, p=0,314 and p=0,834, respectively). In conclusion, the lack of expression of the P/Q-type Ca2+-channels might preclude ASIC1a channels from inhibiting neuromuscular synaptic transmission in mice.