A critical role for CaMKII in behavioral timescale synaptic plasticity in hippocampal CA1 pyramidal neurons

Xiao, Kuo; Li, Yiding; Chitwood, Raymond A.; Magee, Jeffrey C.

doi:10.1101/2023.04.18.537377

Cited by 5 publications

(2 citation statements)

References 32 publications

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“…It was recently confirmed that BTSP is expressed by changes in synaptic efficacy between CA3 and CA1 neurons in vivo 42 . BTSP also requires CaMKIIa signaling, suggesting that canonical LTP expression mechanisms may underlie BTSP 48,49 . Our work extends these findings and demonstrates that full expression of BTSP may require specific membrane fusion proteins implicated in regulated GluA1(+) AMPAR exocytosis.…”

Section: Enriching and Stabilizing Hippocampal Place Codes Through St...mentioning

confidence: 99%

“…Second, sequences of place cells that were active during exploration are stabilized through plasticity during offline reactivation events referred to as sharp-wave ripples (SWRs) -high frequency local field potential (LFP) events in which the same sequences of place cells are reactivated at highly compressed speeds [45][46][47] . Though the molecular underpinnings of BTSP and SWR-induced plasticity are a topic of increasing interest, the mechanisms for expressing either form of plasticity remain a mystery 38,[48][49][50][51][52] .…”

Section: Introductionmentioning

confidence: 99%

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Hippocampal place code plasticity in CA1 requires postsynaptic membrane fusion

Plitt,

Kaganovsky,

Südhof

et al. 2023

Preprint

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SummaryRapid delivery of glutamate receptors to the postsynaptic membrane via vesicle fusion is a central component of synaptic plasticity. However, it is unknown how this process supports specific neural computations during behavior. To bridge this gap, we combined conditional genetic deletion of a component of the postsynaptic membrane fusion machinery, Syntaxin3 (Stx3), in hippocampal CA1 neurons of mice with populationin vivocalcium imaging. This approach revealed that Stx3 is necessary for forming the neural dynamics that support novelty processing, spatial reward memory and offline memory consolidation. In contrast, CA1 Stx3 was dispensable for maintaining aspects of the neural code that exist presynaptic to CA1 such as representations of context and space. Thus, manipulating postsynaptic membrane fusion identified computations that specifically require synaptic restructuring via membrane trafficking in CA1 and distinguished them from neural representation that could be inherited from upstream brain regions or learned through other mechanisms.

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Section: Enriching and Stabilizing Hippocampal Place Codes Through St...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Hippocampal place code plasticity in CA1 requires postsynaptic membrane fusion

Plitt,

Kaganovsky,

Südhof

et al. 2023

Preprint

View full text Add to dashboard Cite

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A Biochemical Description of Postsynaptic Plasticity – with Timescales Ranging from Milliseconds to Seconds

McLaughlin

Peskin

2023

Preprint

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Synaptic plasticity (long term potentiation/depression (LTP/D)), is a cellular mechanism underlying learning. Two distinct types of early LTP/D (E-LTP/D), acting on very different time scales, have been observed experimentally -- spike timing dependent plasticity (STDP), on time scales of tens of ms; and behavioral time scale plasticity(BTSP), on time scales of seconds. BTSP is a candidate for the mechanism for rapid learning of spatial location by hippocampal place cells. Here a computational model of the induction of E-LTP/D at a spine head of a synapse of a hippocampal pyramidal neuron is developed. The single compartment model represents two interacting biochemical pathways for the activation (phosphorylation) of the kinase (CaMKII) with a phosphatase, with Ion inflow described by NMDAR, CaV1, and Na channels. The biochemical reactions are represented by a deterministic system of differential equations. This single model captures realistic responses (temporal profiles with the differing timescales) of STDP and BTSP and their asymmetries for each (STDP or BTSP) signaling protocol. The simulations detail several mechanisms underlying both STDP and BTSP, including i) the flow of Ca^2+ through NMDAR vs CaV1 channels, and ii) the origin of several time scales in the activation of CaMKII. The model also realizes a priming mechanism for E-LTP that is induced by Ca^2+ flow through CaV1.3 channels. Once in the spine head, this small additional Ca^2+ opens the compact state of CaMKII, placing CaMKII "in the ready" for subsequent induction of LTP.

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Neuronal calcium spikes enable vector inversion in theDrosophilabrain

Ishida,

Sethi,

Mohren

et al. 2023

Preprint

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SummaryA typical neuron signals to downstream cells when it is depolarized and firing sodium spikes. Some neurons, however, also fire calcium spikes when hyperpolarized. The function of such bidirectional signaling remains unclear in most circuits. Here we show how a neuron class that participates in vector computation in the fly central complex employs hyperpolarization-elicited calcium spikes to invert two-dimensional mathematical vectors. When cells switch from firing sodium to calcium spikes, this leads to a ∼180° realignment between the vector encoded in the neuronal population and the fly’s internal heading signal, thus inverting the vector. We show that the calcium spikes rely on the T-type calcium channel Ca-a1T, and argue, via analytical and experimental approaches, that these spikes enable vector computations in portions of angular space that would otherwise be inaccessible. These results reveal a seamless interaction between molecular, cellular and circuit properties for implementing vector math in the brain.

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A critical role for CaMKII in behavioral timescale synaptic plasticity in hippocampal CA1 pyramidal neurons

Cited by 5 publications

References 32 publications

Hippocampal place code plasticity in CA1 requires postsynaptic membrane fusion

Hippocampal place code plasticity in CA1 requires postsynaptic membrane fusion

A Biochemical Description of Postsynaptic Plasticity – with Timescales Ranging from Milliseconds to Seconds

Neuronal calcium spikes enable vector inversion in theDrosophilabrain

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