scholarly journals Cholinergic Modulation of CA1 Pyramidal Cells via M1 Muscarinic Receptor Activation: A Computational Study at Physiological and Supraphysiological Levels

2018 ◽  
Author(s):  
Adam R. Mergenthal ◽  
Jean-Marie C. Bouteiller ◽  
Theodore W. Berger
Keyword(s):  
Muscarinic Receptor ◽  
Computational Study ◽  
Pyramidal Cells ◽  
Receptor Activation ◽  
Cholinergic Modulation ◽  
Ca1 Pyramidal Cells ◽  
M1 Muscarinic

scholarly journals Rapid and reversible formation of spine head filopodia in response to muscarinic receptor activation in CA1 pyramidal cells

2011 ◽  
Vol 589 (17) ◽  
pp. 4353-4364 ◽  
Author(s):  
Philipp Schätzle ◽  
Jeanne Ster ◽  
David Verbich ◽  
R. Anne McKinney ◽  
Urs Gerber ◽  
...  
Keyword(s):  
Muscarinic Receptor ◽  
Pyramidal Cells ◽  
Receptor Activation ◽  
Ca1 Pyramidal Cells ◽  
Spine Head ◽  
Reversible Formation

Cannabinoid receptor activation in CA1 pyramidal cells in adult rat hippocampus

2000 ◽  
Vol 863 (1-2) ◽  
pp. 120-131 ◽  
Author(s):  
M.Todd Kirby ◽  
Robert E Hampson ◽  
Sam A Deadwyler
Keyword(s):  
Cannabinoid Receptor ◽  
Pyramidal Cells ◽  
Receptor Activation ◽  
Rat Hippocampus ◽  
Adult Rat ◽  
Ca1 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.

Excitatory effects of ACPD receptor activation in the hippocampus are mediated by direct effects on pyramidal cells and blockade of synaptic inhibition

1991 ◽  
Vol 66 (1) ◽  
pp. 40-52 ◽  
Author(s):  
M. A. Desai ◽  
P. J. Conn
Keyword(s):  
Pyramidal Cells ◽  
Receptor Activation ◽  
Field Population ◽  
Phosphoinositide Hydrolysis ◽  
Initial Slope ◽  
Synaptic Inhibition ◽  
Direct Effects ◽  
Ca1 Pyramidal Cells ◽  
Population Spikes ◽  
Area Ca1

1. Phosphoinositide hydrolysis-linked excitatory amino acid (EAA) receptors (ACPD receptors) are selectively activated by the glutamate analogue trans-1-amino-1,3-cyclopentanedicarboxylic acid (trans-ACPD). Regional analysis of trans-ACPD-induced phosphoinositide hydrolysis indicates that this response is greater in the hippocampus than in other brain regions. Therefore we designed a series of studies aimed at testing the hypothesis that activation of this receptor modulates synaptic function in the hippocampal region. 2. We report that trans-ACPD dramatically altered field population spikes at each of the three major synapses in the hippocampal trisynaptic circuit at concentrations that are effective in activating phosphoinositide hydrolysis. At the perforant path-dentate gyrus synapse, bath application of trans-ACPD resulted in a decrease in the amplitude of field population spikes. In contrast, trans-ACPD markedly enhanced field population spike amplitude at the mossy fiber-CA3 synapse and the Schaffer collateral-CA1 synapse. In area CA1, but not area CA3, trans-ACPD also induced generation of multiple population spikes. 3. Simultaneous field potential recordings from the s. pyramidale and s. radiatum in area CA1 revealed that the effect of trans-ACPD on population spikes in this region was not accompanied by an increase in the initial slope of the field EPSP. This suggests that the effect of trans-ACPD was not mediated by a presynaptic action but must be mediated by direct effects on CA1 pyramidal cells or by a decrease in synaptic inhibition. 4. trans-ACPD had a number of direct excitatory effects on CA1 pyramidal cells. These included 1) cell depolarization (with an increase in input resistance), 2) inhibition of the slow afterhyperpolarization, and 3) blockade of spike frequency adaptation. trans-ACPD also had effects on CA1 pyramidal cells that were not excitatory in nature. These included an increase in the threshold for initiation of calcium spikes and an increase in interspike interval during prolonged current injection. None of these effects were mimicked by an ACPD analogue that does not activate the ACPD receptor (trans-methanoglutamate), nor were they blocked by kynurenate, a nonselective EAA receptor antagonist that does not block the ACPD receptor.(ABSTRACT TRUNCATED AT 400 WORDS)

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