scholarly journals TRPC1 Regulates the Activity of a Voltage-Dependent Nonselective Cation Current in Hippocampal CA1 Neurons

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 459 ◽  
Author(s):  
Frauke Kepura ◽  
Eva Braun ◽  
Alexander Dietrich ◽  
Tim D. Plant
Keyword(s):  
Metabotropic Glutamate Receptor ◽  
Dendritic Morphology ◽  
Current Increase ◽  
Ca1 Neurons ◽  
Cation Current ◽  
Hippocampal Ca1 Neurons ◽  
Group I ◽  
Hippocampal Ca1 ◽  
Voltage Dependent ◽  
Nonselective Cation Current

The cation channel subunit TRPC1 is strongly expressed in central neurons including neurons in the CA1 region of the hippocampus where it forms complexes with TRPC4 and TRPC5. To investigate the functional role of TRPC1 in these neurons and in channel function, we compared current responses to group I metabotropic glutamate receptor (mGluR I) activation and looked for major differences in dendritic morphology in neurons from TRPC1+/+ and TRPC1−/− mice. mGluR I stimulation resulted in the activation of a voltage-dependent nonselective cation current in both genotypes. Deletion of TRPC1 resulted in a modification of the shape of the current-voltage relationship, leading to an inward current increase. In current clamp recordings, the percentage of neurons that responded to depolarization in the presence of an mGluR I agonist with a plateau potential was increased in TRPC1−/− mice. There was also a small increase in the minor population of CA1 neurons that have more than one apical dendrite in TRPC1−/− mice. We conclude that TRPC1 has an inhibitory effect on receptor-operated nonselective cation channels in hippocampal CA1 neurons probably as a result of heterotetramer formation with other TRPC isoforms, and that TRPC1 deletion has only minor effects on dendritic morphology.

Weak excitation and simultaneous inhibition induce long-term depression in hippocampal CA1 neurons

1994 ◽  
Vol 71 (4) ◽  
pp. 1586-1590 ◽  
Author(s):  
X. D. Yang ◽  
J. A. Connor ◽  
D. S. Faber
Keyword(s):  
Receptor Antagonist ◽  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
High Frequency Stimulation ◽  
Long Term Depression ◽  
Ca1 Neurons ◽  
Metabotropic Glutamate ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1

1. Weak excitation to rat hippocampal CA1 neurons via Schaffer collaterals at a frequency of 0.1 or 0.2 Hz accompanied by repeated brief exposures to the inhibitory transmitter gamma-amino-butyric acid (GABA) causes a long-term depression (LTD, up to 90% of the control) of the stimulated pathway. This depression can be reversed by high-frequency stimulation. 2. Although inhibition is necessary for the induction of this LTD, the depression can be produced with either the GABAA or the GABAB receptor agonists. 3. This conjunctive LTD could not be blocked by the N-methyl-D-aspartate receptor antagonist, 2-amino-5-phosphonovaleric acid. 4. It was, however, blocked by the metabotropic glutamate receptor antagonist L-2-amino-3-phosphonopropionic acid and (RS)-alpha-methyl-4-carboxyphenylglycine, indicating that activation of a metabotropic glutamate receptor is necessary for the LTD. Induction also appeared to require an intracellular Ca2+ increase. 5. Because GABAergic inhibition often modulates glutamatergic transmission in the brain, we propose that this form of synaptic modification is of potential importance for neural plasticity.

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.

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