Intracellular QX-314 blocks the hyperpolarization-activated inward current Iq in hippocampal CA1 pyramidal cells

1995 ◽  
Vol 73 (2) ◽  
pp. 911-915 ◽  
Author(s):  
K. L. Perkins ◽  
R. K. Wong
Keyword(s):  
Hippocampal Slice ◽  
Pyramidal Cells ◽  
Cell Voltage ◽  
Oscillatory Activity ◽  
Inward Current ◽  
Ca1 Pyramidal Cells ◽  
Quaternary Derivative ◽  
Hippocampal Ca1 ◽  
Current Activation ◽  
Access Resistance

1. Whole cell voltage-clamp recordings (access resistance < or = 12 M omega) from CA1 pyramidal cells in the guinea pig hippocampal slice revealed a hyperpolarization-activated inward current with an inward tail upon repolarization. The current activation range extended from approximately -50 mV to -130 mV, with half-activation at -86 mV. This current was identified as the q current (Iq). 2. Intracellular QX-314 (5 or 10 mM), a quaternary derivative of lidocaine, blocked Iq completely throughout its activation range. 3. There is a growing realization that Iq may be responsible for the pacemaker depolarization in cells that display rhythmic calcium spikes. Because QX-314 blocks Iq completely, it could be used to test whether Iq is essential to this oscillatory activity.

Zn2+ Blocks the NMDA- and Ca2+-Triggered Postexposure Current I pe in Hippocampal Pyramidal Cells

1998 ◽  
Vol 79 (2) ◽  
pp. 1124-1126 ◽  
Author(s):  
Qiang X. Chen ◽  
Katherine L. Perkins ◽  
Robert K. S. Wong
Keyword(s):  
Divalent Cations ◽  
Pyramidal Cells ◽  
Cell Voltage ◽  
Continuous Growth ◽  
Ca1 Pyramidal Cells ◽  
Cation Current ◽  
Hippocampal Ca1 ◽  
Intracellular Ca ◽  
Hippocampal Pyramidal Cells

Chen, Qiang X., Katherine L. Perkins, and Robert K. S. Wong. Zn2+ blocks the NMDA- and Ca2+-triggered postexposure current I pe in hippocampal pyramidal cells. J. Neurophysiol. 79: 1124–1126, 1998. Whole cell voltage-clamp recordings from acutely isolated hippocampal CA1 pyramidal cells from adult guinea pigs were used to evaluate divalent cations as possible blockers of the postexposure current ( I pe). I pe is a cation current that is triggered by the rise in intracellular Ca2+ concentration that occurs after the application of a toxic level of N-methyl-d-aspartate (NMDA). Once triggered, I pe continues to grow until death of the neuron occurs. I pe may be a critical link between transient NMDA exposure and cell death. I pe was blocked by micromolar concentrations of Zn2+. The Zn2+ effect had an IC50 of 64 μM and saturated at 500 μM. Prolonged Zn2+ block of I pe revealed that the maintenance of a steady I pe is not dependent on I pe-mediated Ca2+ influx but that the continuous growth in I pe is dependent on I pe-mediated Ca2+ influx. The availability of an effective blocker of I pe should facilitate the investigation of the intracellular activation pathway of I pe and the role of I pe in neuronal death.

Histamine decreases calcium-mediated potassium current in guinea pig hippocampal CA1 pyramidal cells

1986 ◽  
Vol 55 (4) ◽  
pp. 727-738 ◽  
Author(s):  
T. C. Pellmar
Keyword(s):  
Potassium Current ◽  
Potassium Conductance ◽  
Outward Current ◽  
Pyramidal Cells ◽  
Slow Inward Current ◽  
Inward Current ◽  
M Current ◽  
Ca1 Pyramidal Cells ◽  
Hippocampal Ca1 ◽  
A Current

The action of histamine on CA1 pyramidal cells was studied in a hippocampal slice preparation. In the presence of tetrodotoxin (TTX) and tetraethylammonium (TEA), histamine had little effect on the calcium spikes. Using the single-electrode voltage-clamp technique, the actions of histamine on membrane currents were tested. In TTX, histamine (1 microM) decreased outward current only at potentials more depolarized than approximately -50 mV, where calcium-mediated potassium current is predominant. In the presence of manganese, histamine was without effect. Histamine (10 microM) did not affect the transient outward potassium current (A-current), the inward M-current resulting from small hyperpolarizing steps, or the inward Q-current elicited by larger hyperpolarizing steps. Blocking potassium currents with TEA or replacing calcium with barium revealed a slow inward current normally carried by calcium. With TTX present to block sodium currents, histamine (10 microM) did not reduce the inward current. The outward current reduced by a maximally effective concentration of histamine (10 microM) can be further decreased by manganese. The results support the conclusion that histamine selectively decreases the calcium-mediated potassium conductance in CA1 pyramidal cells of hippocampus. The possibility is raised that there is a component of calcium-mediated potassium current that is insensitive to histamine.

scholarly journals Caffeine-Induced Suppression of GABAergic Inhibition and Calcium-Independent Metaplasticity

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Masako Isokawa
Keyword(s):  
Time Course ◽  
Calcium Release ◽  
Critical Role ◽  
Pyramidal Cells ◽  
Ruthenium Red ◽  
Gabaergic Inhibition ◽  
Inward Current ◽  
Calcium Dependent ◽  
Ca1 Pyramidal Cells ◽  
Hippocampal Ca1

GABAergic inhibition plays a critical role in the regulation of neuron excitability; thus, it is subject to modulations by many factors. Recent evidence suggests the elevation of intracellular calcium ([Ca2+]i) and calcium-dependent signaling molecules underlie the modulations. Caffeine induces a release of calcium from intracellular stores. We tested whether caffeine modulated GABAergic transmission by increasing[Ca2+]i. A brief local puff-application of caffeine to hippocampal CA1 pyramidal cells transiently suppressed GABAergic inhibitory postsynaptic currents (IPSCs) by 73.2 ± 6.98%. Time course of suppression and the subsequent recovery of IPSCs resembled DSI (depolarization-induced suppression of inhibition), mediated by endogenous cannabinoids that require a[Ca2+]irise. However, unlike DSI, caffeine-induced suppression of IPSCs (CSI) persisted in the absence of a[Ca2+]irise. Intracellular applications of BAPTA and ryanodine (which blocks caffeine-induced calcium release from intracellular stores) failed to prevent the generation of CSI. Surprisingly, ruthenium red, an inhibitor of multiple calcium permeable/release channels including those of stores, induced metaplasticity by amplifying the magnitude of CSI independently of calcium. This metaplasticity was accompanied with the generation of a large inward current. Although ionic basis of this inward current is undetermined, the present result demonstrates that caffeine has a robustCa2+-independent inhibitory action on GABAergic inhibition and causes metaplasticity by opening plasma membrane channels.

scholarly journals The Entorhinal Cortical Alvear Pathway Differentially Excites Pyramidal Cells and Interneuron Subtypes in Hippocampal CA1

2020 ◽  
Author(s):  
Karen A Bell ◽  
Rayne Delong ◽  
Priyodarshan Goswamee ◽  
A Rory McQuiston
Keyword(s):  
Brain Slices ◽  
Pyramidal Cells ◽  
Excitatory Input ◽  
Theta Burst Stimulation ◽  
Ca1 Pyramidal Cells ◽  
Whole Cell Patch Clamp ◽  
Hippocampal Ca1 ◽  
Physiological Impact ◽  
Theta Burst ◽  
Synaptic Responses

Abstract The entorhinal cortex alvear pathway is a major excitatory input to hippocampal CA1, yet nothing is known about its physiological impact. We investigated the alvear pathway projection and innervation of neurons in CA1 using optogenetics and whole cell patch clamp methods in transgenic mouse brain slices. Using this approach, we show that the medial entorhinal cortical alvear inputs onto CA1 pyramidal cells (PCs) and interneurons with cell bodies located in stratum oriens were monosynaptic, had low release probability, and were mediated by glutamate receptors. Optogenetic theta burst stimulation was unable to elicit suprathreshold activation of CA1 PCs but was capable of activating CA1 interneurons. However, different subtypes of interneurons were not equally affected. Higher burst action potential frequencies were observed in parvalbumin-expressing interneurons relative to vasoactive-intestinal peptide-expressing or a subset of oriens lacunosum-moleculare (O-LM) interneurons. Furthermore, alvear excitatory synaptic responses were observed in greater than 70% of PV and VIP interneurons and less than 20% of O-LM cells. Finally, greater than 50% of theta burst-driven inhibitory postsynaptic current amplitudes in CA1 PCs were inhibited by optogenetic suppression of PV interneurons. Therefore, our data suggest that the alvear pathway primarily affects hippocampal CA1 function through feedforward inhibition of select interneuron subtypes.

Modeling Research on Spatiotemporal Dynamics of the Hippocampus

1997 ◽  
Vol 07 (01) ◽  
pp. 187-198 ◽  
Author(s):  
Haijian Sun ◽  
Lin Liu ◽  
Chunhua Feng ◽  
Aike Guo
Keyword(s):  
Pyramidal Cells ◽  
Behavioral Pattern ◽  
Spatiotemporal Dynamics ◽  
Epileptic Focus ◽  
Power Law Distribution ◽  
Ca1 Pyramidal Cells ◽  
Self Organized ◽  
Hippocampal Ca1 ◽  
Self Organized Criticality ◽  
Neurological Insult

The spatiotemporal dynamics of the hippocampus is studied. We first propose a fractal algorithm to model the growth of hippocampal CA1 pyramidal cells, together with an avalanche model for information transmission. Then the optical records of an epileptic focus in the hippocampus are analyzed and simulated. These processes indicate that the hippocampus normally stays in self-organized criticality with a harmonious spatiotemporal behavioral pattern, that is, showing 1/f fluctuation and power law distribution. In case of a neurological insult, the hippocampal system may step into supercriticality and initiate epilepsy.

Distance-Dependent Ni2+-Sensitivity of Synaptic Plasticity in Apical Dendrites of Hippocampal CA1 Pyramidal Cells

2002 ◽  
Vol 87 (2) ◽  
pp. 1169-1174 ◽  
Author(s):  
Yoshikazu Isomura ◽  
Yoko Fujiwara-Tsukamoto ◽  
Michiko Imanishi ◽  
Atsushi Nambu ◽  
Masahiko Takada
Keyword(s):  
Calcium Influx ◽  
Critical Role ◽  
Field Potential ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Apical Dendrite ◽  
Excitatory Postsynaptic Potential ◽  
Distal Dendrite ◽  
Ca1 Pyramidal Cells ◽  
Hippocampal Ca1

Low concentration of Ni2+, a T- and R-type voltage-dependent calcium channel (VDCC) blocker, is known to inhibit the induction of long-term potentiation (LTP) in the hippocampal CA1 pyramidal cells. These VDCCs are distributed more abundantly at the distal area of the apical dendrite than at the proximal dendritic area or soma. Therefore we investigated the relationship between the Ni2+-sensitivity of LTP induction and the synaptic location along the apical dendrite. Field potential recordings revealed that 25 μM Ni2+ hardly influenced LTP at the proximal dendritic area (50 μm distant from the somata). In contrast, the same concentration of Ni2+ inhibited the LTP induction mildly at the middle dendritic area (150 μm) and strongly at the distal dendritic area (250 μm). Ni2+ did not significantly affect either the synaptic transmission at the distal dendrite or the burst-firing ability at the soma. However, synaptically evoked population spikes recorded near the somata were slightly reduced by Ni2+ application, probably owing to occlusion of dendritic excitatory postsynaptic potential (EPSP) amplification. Even when the stimulating intensity was strengthened sufficiently to overcome such a reduction in spike generation during LTP induction, the magnitude of distal LTP was not significantly recovered from the Ni2+-dependent inhibition. These results suggest that Ni2+ may inhibit the induction of distal LTP directly by blocking calcium influx through T- and/or R-type VDCCs. The differentially distributed calcium channels may play a critical role in the induction of LTP at dendritic synapses of the hippocampal pyramidal cells.

scholarly journals Sex and chronic stress alter delta opioid receptor distribution within rat hippocampal CA1 pyramidal cells following behavioral challenges

2020 ◽  
Vol 13 ◽  
pp. 100236
Author(s):  
Batsheva R. Rubin ◽  
Megan A. Johnson ◽  
Jared M. Berman ◽  
Ellen Goldstein ◽  
Vera Pertsovskaya ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
Chronic Stress ◽  
Pyramidal Cells ◽  
Delta Opioid Receptor ◽  
Behavioral Challenges ◽  
Ca1 Pyramidal Cells ◽  
Hippocampal Ca1 ◽  
Receptor Distribution
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