scholarly journals Hippocampal Place Cell Firing Patterns Can Induce Long-Term Synaptic Plasticity In Vitro

2009 ◽  
Vol 29 (21) ◽  
pp. 6840-6850 ◽  
Author(s):  
J. T. R. Isaac ◽  
K. A. Buchanan ◽  
R. U. Muller ◽  
J. R. Mellor
Keyword(s):  
Synaptic Plasticity ◽  
Place Cell ◽  
Firing Patterns ◽  
Cell Firing ◽  
Hippocampal Place Cell

scholarly journals Sharp-Wave Ripples Orchestrate the Induction of Synaptic Plasticity during Reactivation of Place Cell Firing Patterns in the Hippocampus

Cell Reports ◽  
2016 ◽  
Vol 14 (8) ◽  
pp. 1916-1929 ◽  
Author(s):  
Josef H.L.P. Sadowski ◽  
Matthew W. Jones ◽  
Jack R. Mellor
Keyword(s):  
Synaptic Plasticity ◽  
Place Cell ◽  
Firing Patterns ◽  
Sharp Wave ◽  
Cell Firing

scholarly journals Prefrontal Cortex Focally Modulates Hippocampal Place Cell Firing Patterns

2013 ◽  
Vol 33 (8) ◽  
pp. 3443-3451 ◽  
Author(s):  
V. Hok ◽  
E. Chah ◽  
E. Save ◽  
B. Poucet
Keyword(s):  
Prefrontal Cortex ◽  
Place Cell ◽  
Firing Patterns ◽  
Cell Firing ◽  
Hippocampal Place Cell

scholarly journals Dentate gyrus granule cell firing patterns can induce mossy fiber long-term potentiation in vitro

Hippocampus ◽  
2010 ◽  
Vol 21 (11) ◽  
pp. 1157-1168 ◽  
Author(s):  
Rajen Mistry ◽  
Siobhan Dennis ◽  
Matthew Frerking ◽  
Jack R. Mellor
Keyword(s):  
Dentate Gyrus ◽  
Granule Cell ◽  
Mossy Fiber ◽  
Long Term Potentiation ◽  
Firing Patterns ◽  
Term Potentiation ◽  
Cell Firing

scholarly journals Protein kinase D promotes plasticity-induced F-actin stabilization in dendritic spines and regulates memory formation

2015 ◽  
Vol 210 (5) ◽  
pp. 771-783 ◽  
Author(s):  
Norbert Bencsik ◽  
Zsófia Szíber ◽  
Hanna Liliom ◽  
Krisztián Tárnok ◽  
Sándor Borbély ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Protein Kinase ◽  
Dendritic Spines ◽  
Morphological Changes ◽  
Long Term Potentiation ◽  
Memory Formation ◽  
Protein Kinase D

Actin turnover in dendritic spines influences spine development, morphology, and plasticity, with functional consequences on learning and memory formation. In nonneuronal cells, protein kinase D (PKD) has an important role in stabilizing F-actin via multiple molecular pathways. Using in vitro models of neuronal plasticity, such as glycine-induced chemical long-term potentiation (LTP), known to evoke synaptic plasticity, or long-term depolarization block by KCl, leading to homeostatic morphological changes, we show that actin stabilization needed for the enlargement of dendritic spines is dependent on PKD activity. Consequently, impaired PKD functions attenuate activity-dependent changes in hippocampal dendritic spines, including LTP formation, cause morphological alterations in vivo, and have deleterious consequences on spatial memory formation. We thus provide compelling evidence that PKD controls synaptic plasticity and learning by regulating actin stability in dendritic spines.

scholarly journals Altered hippocampal place cell representation and theta rhythmicity following moderate prenatal alcohol exposure

2020 ◽  
Author(s):  
Ryan E. Harvey ◽  
Laura E. Berkowitz ◽  
Daniel D. Savage ◽  
Derek A. Hamilton ◽  
Benjamin J. Clark
Keyword(s):  
Spatial Memory ◽  
Prenatal Alcohol Exposure ◽  
Alcohol Exposure ◽  
Place Cell ◽  
Place Cells ◽  
Spatial Tuning ◽  
Cell Firing ◽  
Prenatal Alcohol ◽  
Ca3 Neurons ◽  
Hippocampal Place Cell

SummaryPrenatal alcohol exposure (PAE) leads to profound deficits in spatial memory and synaptic and cellular alterations to the hippocampus that last into adulthood. Neurons in the hippocampus, called place cells, discharge as an animal enters specific places in an environment, establish distinct ensemble codes for familiar and novel places, and are modulated by local theta rhythms. Spatial memory is thought to critically depend on the integrity of hippocampal place cell firing. We therefore tested the hypothesis that hippocampal place cell firing is impaired after PAE by performing in-vivo recordings from the hippocampi (CA1 and CA3) of moderate PAE and control adult rats. Our results show that hippocampal CA3 neurons from PAE rats have reduced spatial tuning. Secondly, CA1 and CA3 neurons from PAE rats are less likely to orthogonalize their firing between directions of travel on a linear track and between contexts in an open arena compared to control neurons. Lastly, reductions in the number of hippocampal place cells exhibiting significant theta rhythmicity and phase precession were observed which may suggest changes to hippocampal microcircuit function. Together, the reduced spatial tuning and sensitivity to context provides a neural systems-level mechanism to explain spatial memory impairment after moderate PAE.

scholarly journals Maladaptive striatal plasticity and abnormal reward-learning in cervical dystonia

2019 ◽  
Author(s):  
Tom Gilbertson ◽  
Mark Humphries ◽  
J. Douglas Steele
Keyword(s):  
Synaptic Plasticity ◽  
Reversal Learning ◽  
Cervical Dystonia ◽  
Long Term Potentiation ◽  
Focal Dystonia ◽  
Abnormal Behavior ◽  
Reward Learning ◽  
Learning Behavior

AbstractIn monogenetic generalized forms of dystonia, in vitro neurophysiological recordings have demonstrated direct evidence for abnormal plasticity at the level of the cortico-striatal synapse. It is unclear whether similar abnormalities contribute to the pathophysiology of cervical dystonia, the most common type of focal dystonia. We investigated whether abnormal cortico-striatal synaptic plasticity contributes to abnormal reward-learning behavior in patients with focal dystonia. Forty patients and forty controls performed a reward-gain and loss-avoidance reversal learning task. Participant’s behavior was fitted to a computational model of the basal ganglia incorporating detailed cortico-striatal synaptic learning rules. Model comparisons were performed to assess the ability of four hypothesised receptor specific abnormalities of cortico-striatal long term potentiation (LTP) and Long Term Depression (LTD): increased or decreased D1:LTP/LTD and increased or decreased D2: LTP/LTD to explain abnormal behavior in patients. Patients were selectively impaired in the post-reversal phase of the reward task. Individual learning rates in the reward reversal task correlated with the severity of the patient’s motor symptoms. A model of the striatum with decreased D2:LTP/ LTD best explained the patient’s behavior, suggesting excessive D2 cortico-striatal synaptic depotentiation could underpin biased reward learning in patients with cervical dystonia. Reversal learning impairment in cervical dystonia may be a behavioural correlate of D2 specific abnormalities in cortico-striatal synaptic plasticity. Reinforcement learning tasks with computational modeling could allow the identification of molecular targets for novel treatments based on their ability to restore normal reward-learning behavior in these patients.

scholarly journals Alpha-synuclein is involved in manganese-induced spatial memory and synaptic plasticity impairments via TrkB/Akt/Fyn-mediated phosphorylation of NMDA receptors

2020 ◽  
Vol 11 (10) ◽  
Author(s):  
Zhuo Ma ◽  
Kuan Liu ◽  
Xin-Ru Li ◽  
Can Wang ◽  
Chang Liu ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Spatial Memory ◽  
Long Term Potentiation ◽  
Alpha Synuclein ◽  
Ht22 Cells ◽  
Protein Levels ◽  
Trkb Receptors ◽  
Term Potentiation

Abstract Manganese (Mn) overexposure produces long-term cognitive deficits and reduces brain-derived neurotrophic factor (BDNF) in the hippocampus. However, it remains elusive whether Mn-dependent enhanced alpha-synuclein (α-Syn) expression, suggesting a multifaceted mode of neuronal toxicities, accounts for interference with BDNF/TrkB signaling. In this study, we used C57BL/6J WT and α-Syn knockout (KO) mice to establish a model of manganism and found that Mn-induced impairments in spatial memory and synaptic plasticity were related to the α-Syn protein. In addition, consistent with the long-term potentiation (LTP) impairments that were observed, α-Syn KO relieved Mn-induced degradation of PSD95, phosphorylated CaMKIIα, and downregulated SynGAP protein levels. We transfected HT22 cells with lentivirus (LV)-α-Syn shRNA, followed by BDNF and Mn stimulation. In vitro experiments indicated that α-Syn selectively interacted with TrkB receptors and inhibited BDNF/TrkB signaling, leading to phosphorylation and downregulation of GluN2B. The binding of α-Syn to TrkB and Fyn-mediated phosphorylation of GluN2B were negatively regulated by BDNF. Together, these findings indicate that Mn-dependent enhanced α-Syn expression contributes to further exacerbate BDNF protein-level reduction and to inhibit TrkB/Akt/Fyn signaling, thereby disturbing Fyn-mediated phosphorylation of the NMDA receptor GluN2B subunit at tyrosine. In KO α-Syn mice treated with Mn, spatial memory and LTP impairments were less pronounced than in WT mice. However, the same robust neuronal death was observed as a result of Mn-induced neurotoxicity.

scholarly journals Spatial Navigation and Hippocampal Place Cell Firing: The Problem of Goal Encoding

2004 ◽  
Vol 15 (2) ◽  
Author(s):  
Β. Poucet ◽  
P.P. Lenck-Santini ◽  
V. Hok ◽  
E. Save ◽  
J.P. Banquet ◽  
...  
Keyword(s):  
Spatial Navigation ◽  
Place Cell ◽  
Cell Firing ◽  
Hippocampal Place Cell
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