Open AccessRebound Bursts in GABAergic Neurons of the Thalamic Reticular Nucleus in Postnatal Mice
Author(s) -
X Wang,
Guang-Di Yu,
Xin Hou,
Jing Zhou,
Bo Yang,
L Zhang
Publication year - 2010
Publication title -
physiological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 70
eISSN - 1802-9973
pISSN - 0862-8408
DOI - 10.33549/physiolres.931617
Subject(s) - depolarization , gabaergic , bicuculline , chemistry , gabaa receptor , neuroscience , reticular connective tissue , patch clamp , electrophysiology , membrane potential , thalamic reticular nucleus , nucleus , medicine , biophysics , biology , receptor , anatomy , inhibitory postsynaptic potential , biochemistry
Whole cell patch-clamp recordings from GABAergic cells ofthalamic reticular nucleus (RTN) in thalamocortical slices madefrom postnatal day 6 (P6) to 10 (P10) were used to investigatethe pattern of rebound bursts (RBs) triggered by an injection ofhyperpolarizing current into RTN cells. The number of RBs in theRTN and the overlying Na+/K+ spikes changed in an agedependent manner. The generation of RBs depended largely onthe amplitude of the after-hyperpolarizations (AHPs). RB patternsin response to hyperpolarizing current injection into relay cellswere markedly different from RB patterns in RTN cells with anafter-depolarization. GABAA receptor antagonist bicucullinemethiodide (BMI) changed burst firing patterns, increasing theduration of RB and decreasing the amplitude of AHP in RTN cells.Furthermore, local puffs of NMDA in the presence of BMI inducedRBs. K+ channel blocker 4-aminopyridine partially mimicked theeffect of BMI on AHPs. The shapes of RBs were altered by aselective CaMKII inhibitor KN-62, but not by an inactive analogKN-04.