Differential modulation of glutamatergic and cholinergic synapses by calcineurin in hippocampal CA1 fast-spiking interneurons

2004 ◽  
Vol 1004 (1-2) ◽  
pp. 125-135 ◽  
Author(s):  
Jin-Hui Wang ◽  
Mei J. Zhang
Keyword(s):  
Differential Modulation ◽  
Cholinergic Synapses ◽  
Hippocampal Ca1 ◽  
Fast Spiking

scholarly journals Emergence of Non-Canonical Parvalbumin-Containing Interneurons in Hippocampus of a Murine Model of Type I Lissencephaly

2020 ◽  
Author(s):  
Tyler G. Ekins ◽  
Vivek Mahadevan ◽  
Yajun Zhang ◽  
James A. D’Amour ◽  
Timothy Petros ◽  
...  
Keyword(s):  
Synapse Formation ◽  
Brain Structures ◽  
Cellular Migration ◽  
Morphological Development ◽  
Type I ◽  
Hippocampal Ca1 ◽  
Migration Disorder ◽  
Fast Spiking ◽  
And Control ◽  
The Impact

ABSTRACTType I lissencephaly is a neuronal migration disorder caused by haploinsuffiency of the LIS1 gene and is characterized in humans by agyria, mislamination of brain structures, developmental delays, and epilepsy. Here, we investigate the impact of LIS1 mutation on the cellular migration, morphophysiology, microcircuitry and genomics of mouse hippocampal CA1 parvalbumin-containing inhibitory interneurons (PV+INTs). We find that WT PV+INTs consist of two physiological subtypes (80% fast-spiking (FS), 20% non-fast-spiking (NFS)) and four morphological subtypes (basket, axo-axonic, bistratified, radiatum-targeting). We also discover that cell-autonomous mutations within interneurons disrupts morphological development of PV+INTs and results in the emergence of a non-canonical “intermediate spiking (IS)” subset of PV+INTs. In the GlobalLis mutant, IS/NFS cells become the dominant PV+INT subtypes (56%) and the percentage of FS cells shrinks to 44%. We also find that IS/NFS cells are prone to entering depolarizing block, causing them to temporarily lose the ability to initiate action potentials and control network excitation, potentially promoting seizures. Finally, single-cell nuclear RNAsequencing of PV+INTs revealed several misregulated genes related to morphogenesis, cellular excitability, and synapse formation.

scholarly journals Mechanisms of Supralinear Calcium Integration in Dendrites of Hippocampal CA1 Fast-Spiking Cells

2018 ◽  
Vol 10 ◽  
Author(s):  
Olivier Camiré ◽  
Ivan Lazarevich ◽  
Tommy Gilbert ◽  
Lisa Topolnik
Keyword(s):  
Hippocampal Ca1 ◽  
Fast Spiking

scholarly journals Diversity of excitatory release sites

2021 ◽  
Author(s):  
Maria Rita Karlocai ◽  
Judit Heredi ◽  
Tünde Benedek ◽  
Noemi Holderith ◽  
Andrea Lorincz ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Pyramidal Cells ◽  
Molecular Heterogeneity ◽  
Glutamatergic Synapses ◽  
Large Variability ◽  
Ca1 Pyramidal Cells ◽  
Hippocampal Ca1 ◽  
Quantal Analysis ◽  
Fast Spiking ◽  
Active Zones

AbstractThe molecular mechanisms underlying the diversity of cortical glutamatergic synapses is still only partially understood. Here, we tested the hypothesis that presynaptic active zones (AZs) are constructed from molecularly uniform, independent release sites (RSs), the number of which scales linearly with the AZ size. Paired recordings between hippocampal CA1 pyramidal cells and fast-spiking interneurons followed by quantal analysis demonstrate large variability in the number of RSs (N) at these connections. High resolution molecular analysis of functionally characterized synapses reveals highly variable Munc13-1 content of AZs that possess the same N. Replica immunolabeling also shows a 3-fold variability in the Munc13-1 content of AZs of identical size. Munc13-1 is clustered within the AZs; cluster size and density are also variable. Our results provide evidence for quantitative molecular heterogeneity of RSs and support a model in which the AZ is built up from variable numbers of molecularly heterogeneous, but independent RSs.

scholarly journals Neuromodulation of fast-spiking and non-fast-spiking hippocampal CA1 interneurons by human cerebrospinal fluid

2016 ◽  
Vol 594 (4) ◽  
pp. 937-952 ◽  
Author(s):  
Andreas Bjorefeldt ◽  
Pontus Wasling ◽  
Henrik Zetterberg ◽  
Eric Hanse
Keyword(s):  
Cerebrospinal Fluid ◽  
Human Cerebrospinal Fluid ◽  
Hippocampal Ca1 ◽  
Fast Spiking

scholarly journals Variability in the Munc13-1 content of excitatory release site

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Maria Rita Karlocai ◽  
Judit Heredi ◽  
Tünde Benedek ◽  
Noemi Holderith ◽  
Andrea Lorincz ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Release Site ◽  
Pyramidal Cells ◽  
Molecular Heterogeneity ◽  
Glutamatergic Synapses ◽  
Large Variability ◽  
Ca1 Pyramidal Cells ◽  
Adult Mice ◽  
Hippocampal Ca1 ◽  
Fast Spiking

The molecular mechanisms underlying the diversity of cortical glutamatergic synapses is still incompletely understood. Here, we tested the hypothesis that presynaptic active zones (AZs) are constructed from molecularly uniform, independent release sites (RSs), the number of which scales linearly with the AZ size. Paired recordings between hippocampal CA1 pyramidal cells and fast-spiking interneurons in acute slices from adult mice followed by quantal analysis demonstrate large variability in the number of RSs (N) at these connections. High resolution molecular analysis of functionally characterized synapses reveals variability in the content of one of the key vesicle priming factors – Munc13-1 – in AZs that possess the same N. Replica immunolabeling also shows a 3-fold variability in the total Munc13-1 content of AZs of identical size, and a 4-fold variability in the size and density of Munc13-1 clusters within the AZs. Our results provide evidence for quantitative molecular heterogeneity of RSs and support a model in which the AZ is built up from variable numbers of molecularly heterogeneous, but independent RSs.

scholarly journals Emergence of non-canonical parvalbumin-containing interneurons in hippocampus of a murine model of type I lissencephaly

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Tyler G Ekins ◽  
Vivek Mahadevan ◽  
Yajun Zhang ◽  
James A D'Amour ◽  
Gülcan Akgül ◽  
...  
Keyword(s):  
Synapse Formation ◽  
Cellular Migration ◽  
Type I ◽  
Hippocampal Ca1 ◽  
Cellular Excitability ◽  
Neuronal Migration Disorder ◽  
Migration Disorder ◽  
Fast Spiking ◽  
And Control ◽  
The Impact

Type I lissencephaly is a neuronal migration disorder caused by haploinsuffiency of the PAFAH1B1 (mouse: Pafah1b1) gene and is characterized by brain malformation, developmental delays, and epilepsy. Here, we investigate the impact of Pafah1b1 mutation on the cellular migration, morphophysiology, microcircuitry, and transcriptomics of mouse hippocampal CA1 parvalbumin-containing inhibitory interneurons (PV+INTs). We find that WT PV+INTs consist of two physiological subtypes (80% fast-spiking (FS), 20% non-fast-spiking (NFS)) and four morphological subtypes. We find that cell-autonomous mutations within interneurons disrupts morphophysiological development of PV+INTs and results in the emergence of a non-canonical ‘intermediate spiking (IS)’ subset of PV+INTs. We also find that now dominant IS/NFS cells are prone to entering depolarization block, causing them to temporarily lose the ability to initiate action potentials and control network excitation, potentially promoting seizures. Finally, single-cell nuclear RNAsequencing of PV+INTs revealed several misregulated genes related to morphogenesis, cellular excitability, and synapse formation.

Sign in / Sign up

Export Citation Format

Share Document