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Retrograde suppression of GABAergic currents in a subset of SCN neurons
Author(s) -
Gompf Heinrich S.,
Irwin Robert P.,
Allen Charles N.
Publication year - 2006
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2006.04850.x
Subject(s) - depolarization , gabaergic , postsynaptic potential , neuroscience , postsynaptic current , retrograde signaling , chemistry , inhibitory postsynaptic potential , biology , biophysics , excitatory postsynaptic potential , microbiology and biotechnology , receptor , signal transduction , biochemistry
Many postsynaptic neurons release a retrograde transmitter that modulates presynaptic neurotransmitter release. In the suprachiasmatic nucleus (SCN), retrograde signaling is suggested by the presence of dendritic dense‐core vesicles. Whole‐cell voltage‐clamp recordings were made from rat SCN neurons to determine whether a retrograde messenger could modulate the activity of afferent γ‐aminobutyric acid (GABA)ergic inputs. The frequency and amplitude of spontaneous GABAergic currents was significantly reduced in a subpopulation of SCN neurons (eight out of 13) following a postsynaptic depolarization. Similarly, a postsynaptic depolarization significantly reduced the amplitude of evoked GABAergic currents during both day and night recordings. A postsynaptic depolarizing pulse eliminated paired‐pulse inhibition of GABAergic currents consistent with a presynaptic mechanism. Muscimol‐activated currents were not altered by postsynaptic depolarization, demonstrating that the activity of GABA A receptors was not altered. Depolarization‐induced inhibition of the GABAergic currents was not observed when a Ca 2+ chelator was included in the microelectrode. Postsynaptic depolarization significantly increased the Ca 2+ concentration in both the soma and dendrites. The dendritic Ca 2+ levels increased faster, to a higher concentration and decayed faster than in the soma. The depolarization‐induced inhibition of the evoked GABAergic current was blocked by the G‐protein uncoupling agent N‐ethylmaleimide, suggesting that the retrograde messenger acts on a pertussis toxin‐sensitive G‐protein‐coupled receptor. Because the majority of SCN neurons receive GABAergic input from neighboring cells, these results describe a retrograde signaling mechanism by which SCN neurons can modulate GABAergic synaptic input.