Calcium transient of CA1 pyramidal neurons induced by potassium blocker 4-aminopyridine in acute hippocampal slices / 中华神经医学杂志

Objective To investigate the calcium transient of CA1 pyramidal neurons induced by potassium blocker 4-aminopyridine (4-AP) in acute hippocampal slices to explore the relation between potassium channel function and calcium transient, and their mechanism. Methods Fluorescent probe was employed to mark the hippocampai neurons in acute brain slices of rats; confocal microscopy was used to perform calcium imaging to observe the influences of different concentrations of 4-AP and perfusate with/without calcium on calcium transient of CA1 pyramidal neurons. Results The response of [Ca2+]I to lower concentration of 4-AP (<15 mmol/L) was in a dose-dependent manner (r2=0.910, P=0.000); the higher the concentration of 4-AP (20-80 mmol/L), the lower the peak level of calcium transient. The latency and amplitude of calcium transient induced by 4-AP were obviously reduced when the extracellular condition was switched to an absence of calcium, which was significantly different as compared with that with calcium (P<0.05). Conclusion Blockade of potassium channels with 4-AP can increase [Ca2+]I in the hippocampal pyramidal neurons of acute slices. The increase of [Ca2+]1 to 4-AP could be ascribe to calcium release from intracellular stores and calcium influx from extracellular matrix.

Effect of bicuculline on first spike latency of the neurons in the inferior colliculus of mice / 南方医科大学学报

<p><b>OBJECTIVE</b>To evaluate the effect of bicuculline on the first spike latency of the neurons in the inferior colliculus of mice and investigate the role of GABA inhibition in sound signal processing of the neurons.</p><p><b>METHODS</b>In vivo extracellular recording was performed on the inferior colliculus of 13 BALB/c mice (4 to 5 weeks old) to record the neuronal response to pure tones. Bicuculline, a GABA-A receptor antagonist, was applied to the neurons iontophoretically through one channel in the three-barrel glass-pipettes. The first spike latency and other response properties of the characteristic frequency were recorded for analysis.</p><p><b>RESULTS</b>A total of 30 well-isolated single neurons were recorded. Increased spike counts characterized 96% of the neurons, with either increased (40%) or decreased (60%) latency of neuronal responses. Characteristic frequency alterations occurred in 50% of the neurons with increased spike latency, and the minimum threshold showed linear changes.</p><p><b>CONCLUSION</b>GABAergic inhibition may participate in the latency formation and increased frequency selectivity of mouse inferior colliculus neurons by lateral inhibition. The changes in the first spike latency can be indicative of the information integration in GABAergic neurons at the synaptic level.</p>

Immunohistochemical investigation of voltage-gated potassium channel-interacting protein 1 in normal rat brain and Pentylenettrazole-induced seizures / 神经科学通报·英文版

Objective To explore the possible role of voltage-gated potassium channel-interacting protein 1 (KChIP1) in the pathogenesis of epilepsy. Methods Sprague Dawley female adult rats were treated with pentylenettrazole (PTZ) to develop acute and chronic epilepsy models. The approximate coronal sections of normal and epilepsy rat brain were processed for immunohistochemistry. Double-labeling confocal microscopy was used to determine the coexistence of KChIP1 and gamma-aminobutyric acid (GABA). Results KChIP1 was expressed abundantly throughout adult rat brain. KChIP1 is highly co-localize with GABA transmitter in hippocampus and cerebral cortex. In the acute PTZ-induced convulsive rats, the number of KChIP1-postive cells was significantly increased especially in the regions of CA1 and CA3 (P < 0.05); whereas the chronic PTZ-induced convulsive rats were found no changes. The number of GABA-labeled and co-labeled neurons in the hippocampus appeared to have no significant alteration responding to the epilepsy-genesis treatments. Conclusion KChIP1 might be involved in the PTZ-induced epileptogenesis process as a regulator to neuronal excitability through influencing the properties of potassium channels. KChIP1 is preferentially expressed in GABAergic neurons, but its changes did not couple with GABA in the epileptic models.