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.

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.

Synaptically Activated Cl– Accumulation Responsible for Depolarizing GABAergic Responses in Mature Hippocampal Neurons

2003 ◽  
Vol 90 (4) ◽  
pp. 2752-2756 ◽  
Author(s):  
Y. Isomura ◽  
M. Sugimoto ◽  
Y. Fujiwara-Tsukamoto ◽  
S. Yamamoto-Muraki ◽  
J. Yamada ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Critical Role ◽  
Pyramidal Cells ◽  
Receptor Activation ◽  
Patch Clamp Recording ◽  
Gaba A ◽  
Ca1 Pyramidal Cells ◽  
Whole Cell Patch Clamp ◽  
Hippocampal Ca1 ◽  
Temporal Profiles

It is known that GABA, a major inhibitory transmitter in the CNS, acts as an excitatory (or depolarizing) transmitter transiently after intense GABAA receptor activation in adult brains. The depolarizing effect is considered to be dependent on two GABAA receptor-permeable anions, chloride (Cl–) and bicarbonate (HCO3–). However, little is known about their spatial and temporal profiles during the GABAergic depolarization in postsynaptic neurons. In the present study, we show that the amplitude of synaptically induced depolarizing response was correlated with intracellular Cl– accumulation in the soma of mature hippocampal CA1 pyramidal cells, by using whole cell patch-clamp recording and Cl– imaging technique with a Cl– indicator 6-methoxy- N-ethylquinolinium iodide (MEQ). The synaptically activated Cl– accumulation was mediated dominantly through GABAA receptors. Basket cells, a subclass of fast-spiking interneurons innervating the somatic portion of the pyramidal cells, actually fired at high frequency during the Cl– accumulation accompanying the depolarizing responses. These results suggest synaptically activated GABAA-mediated Cl– accumulation may play a critical role in generation of an excitatory GABAergic response in the mature pyramidal cells receiving intense synaptic inputs. This may be the first demonstration of microscopic visualization of intracellular Cl– accumulation during synaptic activation.

Calcium-dependent hyperexcitability of hippocampal CA1 pyramidal cells in an in vitro slice after ethanol withdrawal of the rat

1994 ◽  
Vol 656 (2) ◽  
pp. 432-436 ◽  
Author(s):  
Tomomi Shindou ◽  
Shigenori Watanabe ◽  
Osamu Kamata ◽  
Kenji Yamamoto ◽  
Hiroshi Nakanishi
Keyword(s):  
Pyramidal Cells ◽  
Ethanol Withdrawal ◽  
Calcium Dependent ◽  
Ca1 Pyramidal Cells ◽  
Hippocampal Ca1

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.

Chronic prenatal ethanol exposure-induced decrease of guinea pig hippocampal CA1 pyramidal cell and cerebellar Purkinje cell density

2003 ◽  
Vol 81 (5) ◽  
pp. 476-484 ◽  
Author(s):  
Tara N McGoey ◽  
James N Reynolds ◽  
James F Brien
Keyword(s):  
Purkinje Cell ◽  
Purkinje Cells ◽  
Linear Density ◽  
Time Course ◽  
Pyramidal Cells ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Ca1 Pyramidal Cells ◽  
Hippocampal Ca1 ◽  
Cerebellar Purkinje Cells

The brain is a key target of ethanol teratogenicity, in which ethanol can produce neurodegeneration in selected areas, including the hippocampus and cerebellum. The research objective was to test the hypothesis that chronic prenatal ethanol exposure, via maternal ethanol administration, produces differential time course of decreased linear density of hippocampal CA1 pyramidal cells and cerebellar Purkinje cells. Timed pregnant guinea pigs received chronic oral administration of ethanol, isocaloric-sucrose/pair-feeding, or water throughout gestation (term, about gestational day (GD) 68), and the offspring were studied at GD 62 (near-term fetus), postnatal day (PD) 1 (neonate), PD 5, and PD 12 (early postnatal life). Ethanol treatment, compared with isocaloric-sucrose/pair-feeding and water treatments, decreased brain, hippocampal, and cerebellar weights at GD 62, PD 1, PD 5, and PD 12. Hippocampal CA1 pyramidal cell linear density and cerebellar Purkinje cell linear density were unaffected at GD 62. Ethanol treatment produced 25, 30, and 30% decreases in linear density of hippocampal CA1 pyramidal cells at PD 1, PD 5, and PD 12, respectively, and a 30% decrease in linear density of cerebellar Purkinje cells at PD 12 only. At PD 5, Purkinje cell profile linear density remained unaffected; however, ethanol treatment appeared to increase linear density of apoptotic Purkinje cell nuclei, as determined by a modified TUNEL method. The data demonstrate that chronic prenatal ethanol exposure produces apparent differential time course of decreased linear density of hippocampal CA1 pyramidal cells and cerebellar Purkinje cells in the developing guinea pig.Key words: prenatal ethanol exposure, hippocampal CA1 pyramidal cells, cerebellar Purkinje cells, decreased linear density, differential time course, guinea pig.

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.

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.

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