L-glutamate conditionally modulates the K+ current of Müller glial cells.

L-Glutamate inhibits the K+ conductance that dominates the electrical behavior of a Müller glial cell. The effect of glutamate is enhanced by simultaneous exposure to dopamine. L-Glutamate acts at a metabotropic receptor that controls the K+ conductance through two pathways. A rapid pathway produces a partial inhibition in less than 2 s. Thereafter, a slow pathway progressively inhibits the conductance with a half-time of minutes. Pathways initiated by L-glutamate and dopamine appear to converge on and stimulate adenylyl cyclase. A subsequent step is the activation of a cAMP-dependent protein kinase, PKA. The local overflow of L-glutamate from active synapses may functionally remove K+ channels from nearby glial membranes. A uniform rise in extracellular L-glutamate concentration, as might occur during pathological conditions, should suppress a glial cell's K+ conductance and allow other voltage-dependent processes to be influenced by depolarization.