Inhibitory Feedback Circuit Control of Behavioral Timescale Synaptic Plasticity in Hippocampal Pyramidal Neurons

2021 ◽  
Vol 89 (9) ◽  
pp. S210-S211
Author(s):  
Mohsin Ahmed ◽  
Sebastian Rolotti ◽  
Miklos Szoboszlay ◽  
Heike Blockus ◽  
Kevin Gonzalez ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Pyramidal Neurons ◽  
Feedback Circuit ◽  
Hippocampal Pyramidal Neurons ◽  
Inhibitory Feedback

scholarly journals RGS7/Gβ5/R7BP complex regulates synaptic plasticity and memory by modulating hippocampal GABABR-GIRK signaling

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Olga Ostrovskaya ◽  
Keqiang Xie ◽  
Ikuo Masuho ◽  
Ana Fajardo-Serrano ◽  
Rafael Lujan ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Neuronal Excitability ◽  
Pyramidal Neurons ◽  
Dynamic Range ◽  
Gabab Receptor ◽  
Girk Channels ◽  
Hippocampal Pyramidal Neurons ◽  
Inhibitory Neurotransmitter ◽  
Membrane Anchoring

In the hippocampus, the inhibitory neurotransmitter GABA shapes the activity of the output pyramidal neurons and plays important role in cognition. Most of its inhibitory effects are mediated by signaling from GABAB receptor to the G protein-gated Inwardly-rectifying K+ (GIRK) channels. Here, we show that RGS7, in cooperation with its binding partner R7BP, regulates GABABR-GIRK signaling in hippocampal pyramidal neurons. Deletion of RGS7 in mice dramatically sensitizes GIRK responses to GABAB receptor stimulation and markedly slows channel deactivation kinetics. Enhanced activity of this signaling pathway leads to decreased neuronal excitability and selective disruption of inhibitory forms of synaptic plasticity. As a result, mice lacking RGS7 exhibit deficits in learning and memory. We further report that RGS7 is selectively modulated by its membrane anchoring subunit R7BP, which sets the dynamic range of GIRK responses. Together, these results demonstrate a novel role of RGS7 in hippocampal synaptic plasticity and memory formation.

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.

scholarly journals Early Life Vitamin C Deficiency Does Not Alter Morphology of Hippocampal CA1 Pyramidal Neurons or Markers of Synaptic Plasticity in a Guinea Pig Model

Nutrients ◽  
2018 ◽  
Vol 10 (6) ◽  
pp. 749 ◽  
Author(s):  
Stine Hansen ◽  
Jane Jørgensen ◽  
Jens Nyengaard ◽  
Jens Lykkesfeldt ◽  
Pernille Tveden-Nyborg
Keyword(s):  
Synaptic Plasticity ◽  
Vitamin C ◽  
Guinea Pig ◽  
Early Life ◽  
Pyramidal Neurons ◽  
Pig Model ◽  
Vitamin C Deficiency ◽  
Ca1 Pyramidal Neurons ◽  
Hippocampal Ca1 ◽  
Guinea Pig Model

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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