Figure 2.

Glutamate transporter currents and AMPA receptor currents can be evoked in outside-out patches from Bergmann glia. (A) l-glutamate (10 mM) activates a transient current that is blocked by NBQX and GYKI-52466 and a smaller biphasic current in patches using a KSCN internal solution. V_m = −90 mV. (B) Complete substitution of extracellular Li⁺ for Na⁺ blocks the transporter current evoked by 10 mM l-glutamate. V_m = −90 mV. (C and D) The current-voltage relationship of the transporter current is inwardly rectifying and does not reverse. Responses in C were recorded at membrane potentials of −10, −30, −50, −70, and −90 mV. In D, each point is an average of responses from six patches normalized to the peak response at −110 mV. (E) In the presence of NBQX (10 μM) and GYKI (25 μM), THA (300 μM) produces a steady-state inward current and occludes the response to a pulse of 10 mM l-glutamate. The outward current elicited by l-glutamate in the presence of THA probably reflects the replacement of THA with l-glutamate, which is likely to occur at these concentrations. V_m = −110 mV. (F) l-aspartate (2 mM) activates a transporter current but not an AMPA receptor current. The control responses and those recorded in NBQX (10 μM) and GYKI (25 μM) are superimposed. This result also indicates that at these concentrations neither NBQX nor GYKI alter transporter function. KSCN-based internal solutions were used in all recordings. The uppermost traces in each figure are the “open-tip” response obtained by solution exchanges after disrupting the membrane patch. In each case the concentrations listed were used, except in F, where ACSF was diluted with 50% dH₂O to increase the size of the junction current. Traces are averages of 5–15 responses.