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Rebound bursts in GABAergic neurons of the thalamic reticular nucleus in postnatal mice
X. Wang, G. Yu, X. Hou, J. Zhou, B. Yang, L. Zhang
Language English Country Czech Republic
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- MeSH
- 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine analogs & derivatives pharmacology MeSH
- 4-Aminopyridine pharmacology MeSH
- Action Potentials physiology drug effects MeSH
- GABA-A Receptor Antagonists MeSH
- Bicuculline analogs & derivatives pharmacology MeSH
- Potassium Channel Blockers pharmacology MeSH
- Financing, Organized MeSH
- GABA Antagonists pharmacology MeSH
- gamma-Aminobutyric Acid physiology MeSH
- Protein Kinase Inhibitors pharmacology MeSH
- Thalamic Nuclei cytology physiology MeSH
- Mice, Inbred ICR MeSH
- Mice MeSH
- Neural Inhibition physiology drug effects MeSH
- Neurons physiology MeSH
- Animals, Newborn MeSH
- Organ Culture Techniques MeSH
- Calcium-Calmodulin-Dependent Protein Kinase Type 2 antagonists & inhibitors metabolism MeSH
- Receptors, GABA-A physiology MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
Whole cell patch-clamp recordings from GABAergic cells of thalamic reticular nucleus (RTN) in thalamocortical slices made from postnatal day 6 (P6) to 10 (P10) were used to investigate the pattern of rebound bursts (RBs) triggered by an injection of hyperpolarizing current into RTN cells. The number of RBs in the RTN and the overlying Na+/K+ spikes changed in an agedependent manner. The generation of RBs depended largely on the amplitude of the after-hyperpolarizations (AHPs). RB patterns in response to hyperpolarizing current injection into relay cells were markedly different from RB patterns in RTN cells with an after-depolarization. GABAA receptor antagonist bicuculline methiodide (BMI) changed burst firing patterns, increasing the duration of RB and decreasing the amplitude of AHP in RTN cells. Furthermore, local puffs of NMDA in the presence of BMI induced RBs. K+ channel blocker 4-aminopyridine partially mimicked the effect of BMI on AHPs. The shapes of RBs were altered by a selective CaMKII inhibitor KN-62, but not by an inactive analog KN-04.
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Lit.: 34
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- $a Lit.: 34
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- $a Whole cell patch-clamp recordings from GABAergic cells of thalamic reticular nucleus (RTN) in thalamocortical slices made from postnatal day 6 (P6) to 10 (P10) were used to investigate the pattern of rebound bursts (RBs) triggered by an injection of hyperpolarizing current into RTN cells. The number of RBs in the RTN and the overlying Na+/K+ spikes changed in an agedependent manner. The generation of RBs depended largely on the amplitude of the after-hyperpolarizations (AHPs). RB patterns in response to hyperpolarizing current injection into relay cells were markedly different from RB patterns in RTN cells with an after-depolarization. GABAA receptor antagonist bicuculline methiodide (BMI) changed burst firing patterns, increasing the duration of RB and decreasing the amplitude of AHP in RTN cells. Furthermore, local puffs of NMDA in the presence of BMI induced RBs. K+ channel blocker 4-aminopyridine partially mimicked the effect of BMI on AHPs. The shapes of RBs were altered by a selective CaMKII inhibitor KN-62, but not by an inactive analog KN-04.
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