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Early life stress in fathers impairs synaptic plasticity in the offspring - brain collected after acute swim stress

ABSTRACT: We show that traumatic stress experienced by males in early postnatal life impairs memory in their offspring, blocks long-term potentiation (LTP) and favors long-term depression (LTD). These effects are accompanied by suppression of key molecular pathways involved in neuronal plasticity both at rest and after acute stress.

ORGANISM(S): Mus musculus

PROVIDER: GSE47847 | GEO | 2014/07/01

SECONDARY ACCESSION(S): PRJNA208121

REPOSITORIES: GEO

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Early life stress in fathers impairs synaptic plasticity in the offspring - brain collected at rest

2014-07-01 | GSE47846 | GEO

Early life stress in fathers impairs synaptic plasticity in the offspring - brain collected after acute swim stress

Project description:We show that traumatic stress experienced by males in early postnatal life impairs memory in their offspring, blocks long-term potentiation (LTP) and favors long-term depression (LTD). These effects are accompanied by suppression of key molecular pathways involved in neuronal plasticity both at rest and after acute stress. Male mice were exposed to chronic traumatic stress in early postnatal life and were later bred to naM-CM-/ve females to produce second-generation offspring. Memory performance was evaluated in the offspring, and synaptic plasticity was examined in the hippocampus and the amygdala, brain areas important for memory formation. The two groups tested were 1: offspring of fathers which were stressed (MSUS - maternal separation unpredictable stress) and 2: offspring of non-stressed fathers (control). Genome-wide gene expression in hippocampus of these two groups was assessed at rest and after acute stress (this study).

2014-07-01 | E-GEOD-47847 | biostudies-arrayexpress

Early life stress in fathers impairs synaptic plasticity in the offspring - brain collected at rest

2014-07-01 | E-GEOD-47846 | biostudies-arrayexpress

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Project description:This is a mathematical model describing the formation of long-term potentiation (LTP) at the Schaffer collateral of CA1 pyramidal cell synapse. The model consists of nine ordinary differential equations that denote synaptic states associated with different degrees of LTP, as well as the levels of regulatory proteins involved in the formation and maintenance of LTP.

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Li2019 - Neurogranin stimulates Ca/calmodulin-dependent kinase II by inhibiting Calcineurin

Project description:Calmodulin sits at the center of molecular mechanisms underlying learning and memory. Its complex, and sometimes opposite, influences via the binding to various proteins are yet to be fully understood. Calcium/calmodulin-dependent protein kinase II (CaMKII) and calcineurin (CaN) both bind open calmodulin, favoring Long-term-potentiation (LTP) or depression (LTD) respectively. Neurogranin binds to the closed conformation of calmodulin and its impact on synaptic plasticity is less clear. We set up a mechanistic computational model based on allosteric principles to simulate calmodulin state transitions and its interaction with calcium ions and the three binding partners mentioned above. We simulated calcium spikes at various frequencies and show that neurogranin regulates synaptic plasticity along three modalities. At low spike frequencies, neurogranin inhibits the onset of LTD by limiting CaN activation. At intermediate frequencies, neurogranin limits LTP by precluding binding of CaMKII with calmodulin. Finally, at high spike frequencies, neurogranin promotes LTP by enhancing CaMKII autophosphorylation. While neurogranin might act as a calmodulin buffer, it does not significantly preclude the calmodulin opening by calcium. On the contrary, neurogranin synchronizes the opening of calmodulin's two lobes and promotes their activation at specific frequencies, increasing the chance of CaMKII trans-autophosphorylation. Importantly, the positive effect of neurogranin on CaMKII activation is mediated via CaN, and too few or too much CaN will abolish this effect. Furthermore, the amount of neurogranin itself differentially regulates the levels of CaN and CaMKII activities, as well as the frequencies at which the balance switch from one to the other.

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