scholarly journals Effect of Extracellular HCO3 − on Na+Channel Characteristics in Hippocampal CA1 Neurons

2000 ◽  
Vol 84 (5) ◽  
pp. 2477-2483 ◽  
Author(s):  
Xiang Q. Gu ◽  
Hang Yao ◽  
Gabriel G. Haddad
Keyword(s):  
Membrane Properties ◽  
Inactivation Kinetics ◽  
Na Channel ◽  
Action Potential Firing ◽  
Patch Clamp Technique ◽  
Ca1 Neurons ◽  
Hippocampal Ca1 Neurons ◽  
Neuronal Membranes ◽  
Recovery From Inactivation ◽  
Hippocampal Ca1

The effect of HCO3 −/CO2 on membrane properties of isolated hippocampal CA1 neurons was studied with the use of the whole cell configuration of the patch-clamp technique. Neurons were acutely dissociated from 21- to 30-day-old mice. In the current-clamp mode, HCO3 −/CO2significantly hyperpolarized CA1 neurons by more than 10 mV and decreased their input resistance. In addition, the overall excitability of these neurons was lower in the presence of HCO3 −/CO2 than in HEPES. Spontaneous and evoked action potential firing frequency was lower in the presence of HCO3 −/CO2 than in its absence. In the voltage-clamp mode, both activation and steady-state inactivation of a fast Na+ current were shifted in the hyperpolarized direction in such a way that the window currents were smaller in HCO3 −/CO2 than in HEPES. Recovery from inactivation and deactivation from the open state of the fast Na+ current was slower in HCO3 −/CO2 than in HEPES. We conclude that HCO3 −/CO2decreases the intrinsic excitability of CA1 neurons by altering not only the passive properties of the neuronal membranes but also by changing several characteristics of the fast Na+current, including activation and inactivation kinetics as well as the recovery from inactivation and deactivation.

1402 Postnatal changes in membrane properties of rat hippocampal CA1 neurons

1997 ◽  
Vol 28 ◽  
pp. S178
Author(s):  
Naoko Fujimura ◽  
Eiichiro Tanaka ◽  
Hideho Higashi
Keyword(s):  
Membrane Properties ◽  
Ca1 Neurons ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1

Effect of metabolic inhibition on the excitability of isolated hippocampal CA1 neurons: developmental aspects

1991 ◽  
Vol 66 (5) ◽  
pp. 1471-1482 ◽  
Author(s):  
T. R. Cummins ◽  
D. F. Donnelly ◽  
G. G. Haddad
Keyword(s):  
Sodium Current ◽  
Potassium Currents ◽  
Patch Clamp Technique ◽  
Ca1 Neurons ◽  
Inward Current ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1 ◽  
Immature Neurons ◽  
Voltage Dependent ◽  
Mature Neurons

1. The effects of brief exposures to hypoxia on the membrane currents of isolated hippocampal CA1 neurons were studied with the use of the whole-cell variation of the patch-clamp technique. Neurons were acutely dissociated from immature (day 2–7) and mature (day 21–43) rats. 2. In the current-clamp mode, Na-cyanide (CN) hyperpolarized both mature and immature neurons. In the voltage-clamp mode, CN decreased the magnitude of the hyperpolarizing holding current in both age groups. 3. CN did not have a consistent effect on the voltage-dependent calcium and potassium currents of immature and mature CA1 neurons but decreased the voltage-dependent inward current of neurons at both ages. This effect was age dependent: the inward current of immature neurons decreased by only 10%, but that of mature neurons decreased by approximately 40%. 4. The decrease in the magnitude of the hyperpolarizing holding current and the depression of the voltage-dependent inward current of mature neurons were observed during brief exposure to N2 (PO2 = 0), indicating that the electroresponses observed with CN were the result of blocking oxidative respiration. 5. The hypoxia-sensitive inward current was blocked by tetrodotoxin (TTX) but was not blocked by cadmium or cesium + tetraethylammonium (TEA). Therefore this current was identified as the voltage-dependent, fast-inactivating sodium current (INa). 6. The isolated sodium current was studied with the use of cadmium to block calcium and TEA + cesium to block potassium currents. In mature neurons, CN left-shifted the steady-state inactivation curve for INa and slowed the deactivation kinetics of INa. CN caused little or no change in INa activation, fast inactivation, recovery from inactivation, or current-voltage (I-V) relationship. 7. We conclude that brief exposures to CN and hypoxia alter the intrinsic excitability of CA1 neurons by at least two mechanisms: 1) alterations in leakage currents and 2) alterations in the fast Na+ conductance that are maturationally dependent. We propose that the alterations in the Na+ conductance may play an adaptive role by reducing O2 demands and thus possibly delaying neuronal injury.

Potentiation of NMDA Receptors by Withania somnifera on Hippocampal CA1 Pyramidal Neurons

2013 ◽  
Vol 41 (03) ◽  
pp. 503-513 ◽  
Author(s):  
Janardhan Prasad Bhattarai ◽  
Soo Joung Park ◽  
Seong Kyu Han
Keyword(s):  
Withania Somnifera ◽  
Pyramidal Neurons ◽  
Glycine Receptor ◽  
Patch Clamp Technique ◽  
Pipette Solution ◽  
Ca1 Neurons ◽  
Ca1 Pyramidal Neurons ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1 ◽  
Dose Dependent

In Ayurveda,Withania somnifera (WS) is used as a medicine to maintain mental and physical health as well as to enhance memory. In this study, the methanolic extract of WS(mWS) was tested for its electrical influence on hippocampal CA1 pyramidal neurons using a patch clamp technique. In current clamp mode under a high chloride pipette solution, mWS (400 ng/μl) induced remarkable membrane depolarization (9.75 ± 2.54 mV, n = 6) of CA1 neurons. The mWS-induced depolarization was dose-dependent, reproducible, and persistent in the presence of 0.5 μM tetrodotoxin (TTX, 10.17 ± 0.04 mV, n = 6). In voltage clamp mode (holding potential = -60 mV), mWS induced a dose-dependent non-desensitizing inward current that persisted in the presence of TTX (0.5 μM), suggesting that the response induced by mWS was purely a postsynaptic event. Interestingly, these inward currents were partially blocked by strychnine, a glycine receptor blocker. Further, mWS potentiated the NMDA response in hippocampal CA1 neurons at low concentrations. Overall, these results suggest that there are compounds in WS with possible glycine mimetic activities, which may be potential targets for inducing memory consolidation in hippocampal CA1 neurons.

Ischemic preconditioning protects the hippocampal CA1 neurons by inhibiting synaptic activity in rat

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S300-S300
Author(s):  
Thomas J Sick ◽  
Ami P Raval ◽  
Isabel Saul ◽  
Kunjan R Dave ◽  
Raul Busto ◽  
...  
Keyword(s):  
Ischemic Preconditioning ◽  
Synaptic Activity ◽  
Ca1 Neurons ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1
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