(A1) The group I mGluR agonist 3,5-DHPG (100 µM, 11 s)
produced [Ca2+]i increases (upper
trace) but not membrane currents (bottom). (A2)
Pre-application of LY341495 (10 µM, 11 s) followed by
co-application of 3,5-DHPG (10 µM, 11 s) completely blocked the
3,5-DHPG-induced [Ca2+]i elevation.
Three min later, 3,5-DHPG (10 µM, 11 s) again provoked a
[Ca2+]i elevation in the same
cell. (B1) Region of interest with five NG2/EYFP cells (bar,
20 µm) which was selected for focal application of Fluo-4 AM
(B2). Arrows mark NG2 cells from which
[Ca2+]i elevations were
recorded (also seen in C1). Note Fluo-4 labeled,
EYFP-negative cells located in the lower left corner.
(C1–C3)
[Ca2+]i elevations upon
3,5-DHPG in the presence (middle) and absence (left, control; right,
wash) of subtype-specific mGluR antagonists. Antagonists were
pre-applied for 23 s, followed by 11 s co-application with 3,5-DHPG (10
µM, gray boxes). Applications were separated by 3 min.
(C1) The mGluR1 specific antagonist 3-MATIDA (50
µM) mostly exerted partial block of
Ca2+-responses. (C2) In most cells,
3,5-DHPG-mediated [Ca2+]i
elevations were abolished by the mGluR5 specific antagonist, MPEP (20
µM). (C3) In a few cells, co-application of both
antagonists failed to inhibit 3,5-DHPG-induced
[Ca2+]i elevations. Experiments
shown in (C1–C3) were performed in the
presence of the blocking cocktail described in the text. Each row
represents one individual brain slice.