Bi-directional interplay between proximal and distal inputs to CA2 pyramidal neurons

Nasrallah, Kaoutsar; Piskorowski, Rebecca A.; Chevaleyre, Vivien

doi:10.1016/j.nlm.2016.06.024

Cited by 13 publications

(11 citation statements)

References 24 publications

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“…According to this model, enkephalin expressing neurons integrate appropriately timed EC LII stellate cell and SC inputs to generate a large postsynaptic response required to release enkephalin. The large postsynaptic response can also be elicited by strong tetanic stimulation of either pathway alone, explaining the observed induction of iLTD with unpaired strong EC or SC activation (Nasrallah et al, 2015, 2016; Piskorowski and Chevaleyre, 2013). As we observed ENK + terminals apposed to CA2 PNs and PV soma (Figure 7), enkephalin could be released directly onto PV + basket cell terminals to produce a long-lasting presynaptic inhibition of GABA release.…”

Section: Discussionmentioning

confidence: 93%

“…As robust iLTD in CA2 PNs can be induced by tetanic stimulation of the SC or EC inputs to CA2 (Nasrallah et al, 2015; Nasrallah et al, 2016; Piskorowski and Chevaleyre, 2013), we examined the role of iLTD in CA2 ITDP. Application of GABA A and GABA B receptor antagonist (2 µM SR 95531 and 1 µM CGP 55845, respectively) throughout the experiment fully blocked ITDP at both the SC (PSP remained at 102 ± 8 % of baseline, n=8; Wilcoxon test, p=0.9 compared to baseline) and EC inputs (PSP remained at 107 ± 23 % of baseline, n=7; Wilcoxon test, p=0.9 compared to baseline; Figure 2A and C).…”

Section: Resultsmentioning

confidence: 99%

“…The mechanism underlying ITDP in CA2 resembles δ-opioid receptor-dependent iLTD induced by unpaired high-frequency tetanic stimulation of CA2 SC inputs (Nasrallah et al, 2015; Piskorowski and Chevaleyre, 2013) or EC inputs (Nasrallah et al, 2016). Similarly, the mechanism underlying the iLTD component of ITDP in CA1 (Basu et al, 2013) resembles CB1R-dependent iLTD induced by high-frequency tetanic stimulation of the CA1 SC inputs (Chevaleyre and Castillo, 2004).…”

Section: Discussionmentioning

confidence: 99%

“…As 1 Hz stimulation of SC or EC inputs alone fails to elicit iLTD (97 ± 9 %, n=5; Wilcoxon test, p=0.1 compared to baseline for EC stimulation; see Piskorowski and Chevaleyre (2013) for SC 1 Hz stimulation), enkephalin release appears to require strong synaptic activation, either through paired stimulation of EC and SC pathways, which occurs during ITDP induction, or through higher frequency unpaired SC (Piskorowski and Chevaleyre, 2013) or EC (Nasrallah et al, 2016) stimulation. Indeed neuropeptide release generally requires higher levels of presynaptic activity than does release of classical neurotransmitters (van den Pol, 2012).…”

Section: Discussionmentioning

confidence: 99%

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Input-Timing-Dependent Plasticity in the Hippocampal CA2 Region and Its Potential Role in Social Memory

Leroy

Brann

Meira

et al. 2017

Neuron

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Summary Input-timing dependent plasticity (ITDP) is a circuit-based synaptic learning rule whereby precisely timed, paired activation of direct entorhinal cortex (EC) and Schaffer collateral (SC) inputs to hippocampal CA1 pyramidal neurons (PNs) produces a long-term enhancement of CA1 SC excitation, which has been linked to specificity of contextual memory. We report that paired activation of EC and SC inputs also increases SC excitation of CA2 PNs, which are important for social memory. However, whereas CA1 ITDP depends on endocannabinoid CB1 receptor-dependent long-term depression of feedforward inhibition (iLTD) mediated by cholecystokinin-positive interneurons, CA2 ITDP depends on δ-opioid receptor-dependent iLTD of parvalbumin-positive interneuron inhibition. Blockade of CA2 δ-opioid receptors blocked ITDP and impaired social memory whereas a social encounter with a novel animal decreased CA2 feedforward inhibition and occluded ITDP. Thus, ITDP may provide a more general synaptic learning rule for distinct forms of hippocampal-dependent memory through its recruitment by distinct hippocampal regions.

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Section: Discussionmentioning

confidence: 93%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Input-Timing-Dependent Plasticity in the Hippocampal CA2 Region and Its Potential Role in Social Memory

Leroy

Brann

Meira

et al. 2017

Neuron

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“…In turn, precise timing of distal and proximal inputs, called input-timing-dependent plasticity (ITDP) (Leroy et al, 2017), and low-frequency stimulation can reduce feedforward inhibition (Nasrallah et al, 2015). Interestingly, plasticity induced by vasopressin (Pagani et al, 2015), oxytocin (Pagani et al, 2015), substance P (Dasgupta et al, 2017), iLTD (Nasrallah et al, 2015(Nasrallah et al, , 2016 and ITDP (Leroy et al, 2017) share similar dynamics. Net excitation increases slowly and peaks after around 20 minutes, roughly doubling the excitatory drive.…”

Section: Neuromodulation and Synaptic Plasticity In Ca2mentioning

confidence: 99%

Selective neuromodulation and mutual inhibition within the CA3-CA2 system can prioritize sequences for replay

Stöber¹,

Lehr²,

Hafting³

et al. 2020

Preprint

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To make optimal use of previous experiences, important neural activity sequences must be prioritized during hippocampal replay. Integrating insights about the interplay between CA3 and CA2, we propose a conceptual framework that allows the two regions to control which sequences are reactivated. We show that neuromodulatory-gated plasticity and mutual inhibition enable discrete assembly sequences in both regions to support each other while suppressing competing sequences. This perspective provides a coherent interpretation for a variety of seemingly disconnected functional properties of CA2 and paves the way for a more general understanding of CA2.

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Selective neuromodulation and mutual inhibition within the CA3–CA2 system can prioritize sequences for replay

et al. 2020

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To make optimal use of previous experiences, important neural activity sequences must be prioritized during hippocampal replay. Integrating insights about the interplay between CA3 and CA2, we propose a conceptual framework that allows the two regions to control which sequences are reactivated. We suggest that neuromodulatory-gated plasticity and mutual inhibition enable discrete assembly sequences in both regions to support each other while suppressing competing sequences. This perspective provides a coherent interpretation for a variety of seemingly disconnected functional properties of CA2 and paves the way for a more general understanding of CA2.

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Bi-directional interplay between proximal and distal inputs to CA2 pyramidal neurons

Cited by 13 publications

References 24 publications

Input-Timing-Dependent Plasticity in the Hippocampal CA2 Region and Its Potential Role in Social Memory

Input-Timing-Dependent Plasticity in the Hippocampal CA2 Region and Its Potential Role in Social Memory

Selective neuromodulation and mutual inhibition within the CA3-CA2 system can prioritize sequences for replay

Selective neuromodulation and mutual inhibition within the CA3–CA2 system can prioritize sequences for replay

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