scholarly journals Somatic Colocalization of Rat SK1 and D class (Cav 1.2) L-type Calcium Channels in Rat CA1 Hippocampal Pyramidal Neurons

2001 ◽  
Vol 21 (20) ◽  
pp. RC175-RC175 ◽  
Author(s):  
Sarah E. H. Bowden ◽  
Stephanie Fletcher ◽  
David J. Loane ◽  
Neil V. Marrion
Keyword(s):  
Calcium Channels ◽  
Pyramidal Neurons ◽  
Hippocampal Pyramidal Neurons

scholarly journals Somatostatin and parvalbumin inhibitory synapses onto hippocampal pyramidal neurons are regulated by distinct mechanisms

2018 ◽  
Vol 115 (3) ◽  
pp. 589-594 ◽  
Author(s):  
Meryl E. Horn ◽  
Roger A. Nicoll
Keyword(s):  
Calcium Channels ◽  
Brain Function ◽  
Pyramidal Neurons ◽  
Neuronal Firing ◽  
Inhibitory Neurons ◽  
Inhibitory Synapses ◽  
Hippocampal Pyramidal Neurons ◽  
Excitatory Neurons ◽  
Glutamatergic Signaling ◽  
Different Populations

Excitation–inhibition balance is critical for optimal brain function, yet the mechanisms underlying the tuning of inhibition from different populations of inhibitory neurons are unclear. Here, we found evidence for two distinct pathways through which excitatory neurons cell-autonomously modulate inhibitory synapses. Synapses from parvalbumin-expressing interneurons onto hippocampal pyramidal neurons are regulated by neuronal firing, signaling through L-type calcium channels. Synapses from somatostatin-expressing interneurons are regulated by NMDA receptors, signaling through R-type calcium channels. Thus, excitatory neurons can cell-autonomously regulate their inhibition onto different subcellular compartments through their input (glutamatergic signaling) and their output (firing). Separately, while somatostatin and parvalbumin synapses onto excitatory neurons are both dependent on a common set of postsynaptic proteins, including gephyrin, collybistin, and neuroligin-2, decreasing neuroligin-3 expression selectively decreases inhibition from somatostatin interneurons, and overexpression of neuroligin-3 selectively enhances somatostatin inhibition. These results provide evidence that excitatory neurons can selectively regulate two distinct sets of inhibitory synapses.

Q- and L-type calcium channels control the development of calbindin phenotype in hippocampal pyramidal neurons in vitro

2000 ◽  
Vol 12 (6) ◽  
pp. 2068-2078 ◽  
Author(s):  
Hassan Boukhaddaoui ◽  
Victor Sieso ◽  
Frédérique Scamps ◽  
Stephan Vigues ◽  
Anne Roig ◽  
...  
Keyword(s):  
Calcium Channels ◽  
Pyramidal Neurons ◽  
Hippocampal Pyramidal Neurons

Ca2+ Channels Involved in the Generation of the Slow Afterhyperpolarization in Cultured Rat Hippocampal Pyramidal Neurons

2000 ◽  
Vol 83 (5) ◽  
pp. 2554-2561 ◽  
Author(s):  
M. Shah ◽  
D. G. Haylett
Keyword(s):  
Calcium Channels ◽  
Action Potentials ◽  
Calcium Release ◽  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Isolated Cells ◽  
Hippocampal Pyramidal Neurons ◽  
Calcium Induced Calcium Release ◽  
Ca2 Channels ◽  
Hippocampal Pyramidal Cells

The advantages of using isolated cells have led us to develop short-term cultures of hippocampal pyramidal cells, which retain many of the properties of cells in acute preparations and in particular the ability to generate afterhyperpolarizations after a train of action potentials. Using perforated-patch recordings, both medium and slow afterhyperpolarization currents (m I AHP and s I AHP, respectively) could be obtained from pyramidal cells that were cultured for 8–15 days. The s I AHP demonstrated the kinetics and pharmacologic characteristics reported for pyramidal cells in slices. In addition to confirming the insensitivity to 100 nM apamin and 1 mM TEA, we have shown that the s I AHP is also insensitive to 100 nM charybdotoxin but is inhibited by 100 μMd-tubocurarine. Concentrations of nifedipine (10 μM) and nimodipine (3 μM) that maximally inhibit L-type calcium channels reduced the s I AHP by 30 and 50%, respectively. However, higher concentrations of nimodipine (10 μM) abolished the s I AHP, which can be partially explained by an effect on action potentials. Both nifedipine and nimodipine at maximal concentrations were found to reduce the HVA calcium current in freshly dissociated neurons to the same extent. The N-type calcium channel inhibitor, ω-conotoxin GVIA (100 nM), irreversibly inhibited the s I AHP by 37%. Together, ω-conotoxin (100 nM) and nifedipine (10 μM) inhibited the s I AHP by 70%. 10 μM ryanodine also reduced the s I AHP by 30%, suggesting a role for calcium-induced calcium release. It is concluded that activation of the s I AHP in cultured hippocampal pyramidal cells is mediated by a rise in intracellular calcium involving multiple pathways and not just entry via L-type calcium channels.

scholarly journals Prenatal treatment with rapamycin restores enhanced hippocampal mGluR-LTD and mushroom spine size in a Down’s syndrome mouse model

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Jesús David Urbano-Gámez ◽  
Juan José Casañas ◽  
Itziar Benito ◽  
María Luz Montesinos
Keyword(s):  
Intellectual Disability ◽  
Pyramidal Neurons ◽  
Metabotropic Glutamate Receptor ◽  
Therapeutic Potential ◽  
Mammalian Target Of Rapamycin ◽  
Memory Deficits ◽  
Prenatal Treatment ◽  
Hippocampal Pyramidal Neurons ◽  
Metabotropic Glutamate ◽  
Mushroom Spines

AbstractDown syndrome (DS) is the most frequent genetic cause of intellectual disability including hippocampal-dependent memory deficits. We have previously reported hippocampal mTOR (mammalian target of rapamycin) hyperactivation, and related plasticity as well as memory deficits in Ts1Cje mice, a DS experimental model. Here we characterize the proteome of hippocampal synaptoneurosomes (SNs) from these mice, and found a predicted alteration of synaptic plasticity pathways, including long term depression (LTD). Accordingly, mGluR-LTD (metabotropic Glutamate Receptor-LTD) is enhanced in the hippocampus of Ts1Cje mice and this is correlated with an increased proportion of a particular category of mushroom spines in hippocampal pyramidal neurons. Remarkably, prenatal treatment of these mice with rapamycin has a positive pharmacological effect on both phenotypes, supporting the therapeutic potential of rapamycin/rapalogs for DS intellectual disability.

The effects of 4-aminopyridine on spike adaptation in hippocampal pyramidal neurons

1985 ◽  
Vol 1 ◽  
pp. S148
Author(s):  
Yoshihiro Matsuda ◽  
Shigeru Yoshida ◽  
Koichi Fujimura ◽  
Minoru Nakamura
Keyword(s):  
Pyramidal Neurons ◽  
Hippocampal Pyramidal Neurons

scholarly journals Age- and location-dependent differences in store depletion-induced h-channel plasticity in hippocampal pyramidal neurons

2014 ◽  
Vol 111 (6) ◽  
pp. 1369-1382 ◽  
Author(s):  
Ann M. Clemens ◽  
Daniel Johnston
Keyword(s):  
Pyramidal Neurons ◽  
Cyclopiazonic Acid ◽  
Neural Basis ◽  
Adult Rats ◽  
Hippocampal Pyramidal Neurons ◽  
Store Depletion ◽  
Whole Cell Patch Clamp ◽  
Age Dependent ◽  
Adaptive Processes ◽  
Cellular Dysfunction

Disruptions of endoplasmic reticulum (ER) Ca2+ homeostasis are heavily linked to neuronal pathology. Depletion of ER Ca2+ stores can result in cellular dysfunction and potentially cell death, although adaptive processes exist to aid in survival. We examined the age and region dependence of one postulated, adaptive response to ER store-depletion (SD), hyperpolarization-activated cation-nonspecific ( h)-channel plasticity in neurons of the dorsal and ventral hippocampus (DHC and VHC, respectively) from adolescent and adult rats. With the use of whole-cell patch-clamp recordings from the soma and dendrites of CA1 pyramidal neurons, we observed a change in h-sensitive measurements in response to SD, induced by treatment with cyclopiazonic acid, a sarcoplasmic reticulum/ER Ca2+-ATPase blocker. We found that whereas DHC and VHC neurons in adolescent animals respond to SD with a perisomatic expression of SD h plasticity, adult animals express SD h plasticity with a dendritic and somatodendritic locus of plasticity in DHC and VHC neurons, respectively. Furthermore, SD h plasticity in adults was dependent on membrane potential and on the activation of L-type voltage-gated Ca2+ channels. These results suggest that cellular responses to the impairment of ER function, or ER stress, are dependent on brain region and age and that the differential expression of SD h plasticity could provide a neural basis for region- and age-dependent disease vulnerabilities.

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