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.

Dietary Prenatal Choline Supplementation Alters Postnatal Hippocampal Structure and Function

2004 ◽  
Vol 91 (4) ◽  
pp. 1545-1555 ◽  
Author(s):  
Qiang Li ◽  
Shirley Guo-Ross ◽  
Darrell V. Lewis ◽  
Dennis Turner ◽  
Aaron M. White ◽  
...  
Keyword(s):  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Prenatal Development ◽  
Structure And Function ◽  
Cellular Mechanisms ◽  
Ca1 Pyramidal Cells ◽  
Term Potentiation ◽  
Hippocampal Ca1 ◽  
Essential Nutrient ◽  
And Function

Choline, a compound present in many foods, has recently been classified as an essential nutrient for humans. Studies with animal models indicate that the availability of choline during the prenatal period influences neural and cognitive development. Specifically, prenatal choline supplementation has been shown to enhance working memory and hippocampal long-term potentiation (LTP) in adult offspring. However, the cellular mechanisms underlying these effects remain unclear. Here we report that choline supplementation, during a 6-day gestational period, results in greater excitatory responsiveness, reduced slow afterhyperpolarizations (sAHPs), enhanced afterdepolarizing potentials (ADPs), larger somata, and greater basal dendritic arborization among hippocampal CA1 pyramidal cells studied postnatally in juvenile rats (20–25 days of age). These data indicate that dietary supplementation with a single nutrient, choline, during a brief, critical period of prenatal development, alters the structure and function of hippocampal pyramidal cells.

scholarly journals Long-term potentiation at single fiber inputs to hippocampal CA1 pyramidal cells.

1996 ◽  
Vol 93 (16) ◽  
pp. 8710-8715 ◽  
Author(s):  
J. T. Isaac ◽  
G. O. Hjelmstad ◽  
R. A. Nicoll ◽  
R. C. Malenka
Keyword(s):  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Single Fiber ◽  
Ca1 Pyramidal Cells ◽  
Term Potentiation ◽  
Hippocampal Ca1

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.

Distribution of Slow AHP Channels on Hippocampal CA1 Pyramidal Neurons

2000 ◽  
Vol 83 (3) ◽  
pp. 1756-1759 ◽  
Author(s):  
John M. Bekkers
Keyword(s):  
Action Potentials ◽  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Apical Dendrite ◽  
Ca1 Pyramidal Cells ◽  
Ca1 Pyramidal Neurons ◽  
Basal Dendrites ◽  
Hippocampal Ca1 ◽  
Cell Current ◽  
Whole Cell Current

This work was designed to localize the Ca2+-activated K+ channels underlying the slow afterhyperpolarization (sAHP) in hippocampal CA1 pyramidal cells. Cell-attached patches on the proximal 100 μm of the apical dendrite contained K+ channels, but not sAHP channels, activated by backpropagating action potentials. Amputation of the apical dendrite ∼30 μm from the soma, while simultaneously recording the sAHP whole cell current at the soma, depressed the sAHP amplitude by only ∼30% compared with control. Somatic cell-attached and nucleated patches did not contain sAHP current. Amputation of the axon ≥20 μm from the soma had little effect on the amplitude of the sAHP recorded in cortical pyramidal cells. By this process of elimination, it is suggested that sAHP channels may be concentrated in the basal dendrites of CA1 pyramids.

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.

Sign in / Sign up

Export Citation Format

Share Document