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. Author manuscript; available in PMC: 2014 Aug 1.
Published in final edited form as: J Comp Neurol. 2013 Aug 1;521(11):2416–2438. doi: 10.1002/cne.23305

Figure 11.

Figure 11

Kainate (KA) activation of immunocytochemically identified AC populations. A–C: Brain nitric oxide synthase (bNOS)-immunoreactive ACs were not activated by KA even at saturating levels (white arrowheads). D–F: Tyrosine hydroxylase (TH)-immunoreactive ACs also did not colocalize with KA-activated ACs at low or saturating KA concentrations (white arrowheads). G–I: Colocalization was evident between AGB and choline acetyltranferase (ChAT)-reactive ACs (white arrowheads). M–U: Parvalbumin (PV)-positive ACs were activated with KA concentrations exceeding 5 μM. M–O: No colocalization was observed for incubations with 5 μM KA (black arrowheads). P–R: At 20 μM, most PV ACs were colocalized (white arrowheads), but some remained AGB negative (black arrowheads). S–U: All PV-immunoreactive cells were colocalized with KA-activated cells at 80 μM (white arrowheads). V–X: Colocalization with KA-activated cells was observed for some calretinin-positive ACs (white arrowheads) but not others (black arrowheads). Similarly, some calretinin-reactive cells in the ganglion cell layer colocalized with KA-activated GCs (white arrow) and others did not (black arrow). Retinal layer annotations are the same as in Figure 2. Scale bar = 20 μm in X (applies to A–X).