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Mechanisms regulating norepinephrine‐mediated α 2 ‐IPSCs in the rat locus coeruleus
Author(s) -
Barclay Samantha Lee,
Ford Christopher
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.903.1
Subject(s) - dnqx , locus coeruleus , dopamine , ventral tegmental area , chemistry , glutamate receptor , medicine , ionotropic effect , neuroscience , ampa receptor , stimulation , endocrinology , receptor , biology , central nervous system , dopaminergic
Dopamine (DA) in the ventral tegmental area (VTA) and norepinephrine (NE) in the locus coeruleus (LC) provide feedback inhibition that allows these cells to auto‐regulate their excitability. Previously, we characterized DA D 2 ‐receptor‐mediated inhibitory postsynaptic currents (D 2 ‐IPSCs) in the VTA. Here, we characterized NE α 2 ‐receptor‐mediated IPSCs (α 2 ‐IPSCs) in the LC. Both D 2 and α 2 receptors activate potassium channels. Despite analogous signaling, the duration of the D 2 ‐IPSC was about one‐fourth that of the α 2 ‐IPSC (D 2 ‐IPSC tau: 347 ms, n=8; α 2 ‐IPSC tau: 1346 ms, n=17). To characterize transmission, we evoked IPSCs with varying‐intensity stimulations. In the VTA, increased stimulus intensity increased the amplitude, but not the time course, of the D 2 ‐IPSCs (tau = 92 + 4%, n =12). In contrast, in the LC, increased stimulation intensity increased the amplitude and duration of the α 2 ‐IPSCs (tau = 142 + 13%, n = 13). Increased stimulus intensity may evoke spillover of NE. To examine glutamate input, we applied the AMPA receptor antagonist DNQX. DNQX had no effect on the amplitude or duration of the D 2 ‐IPSCs, but reduced the amplitude and duration of the α 2 ‐IPSC (control tau: 1282 ms, DNQX tau: 660 ms, n=9). Thus, stimulation of the LC may drive glutamate release that potentiates NE release. These data indicate that different mechanisms may regulate catecholamine transmission. Support: DA026417.