Neuromodulation of Hippocampal Cells and Circuits

Lawrence, J. Josh; Cobb, Stuart

doi:10.1007/978-3-319-99103-0_7

Cited by 3 publications

(1 citation statement)

References 688 publications

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“…Neuromodulation exerts a profound influence on the modification of neural responses and synaptic plasticity (1), and allows for the adaptation and reconfiguration of neuronal circuits in response to changing external stimuli and transitions in behavioural states (2). Neuromodulatory systems in the brain influence how attention and experience regulate hippocampal representational stability and hippocampal memory formation (3-5). Activity-dependent modifications in synaptic strength such as long-term potentiation (LTP) or long-term depression (LTD) create highly coupled neuronal ensembles in the hippocampus that encode information and form memories, and are regulated by the action of neuromodulators (1).…”

Section: Introductionmentioning

confidence: 99%

Metaplastic reinforcement of long-term potentiation in rat hippocampal area CA2 by cholinergic receptor activation

Benoy

Ibrahim

Behnisch

et al. 2020

Preprint

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Hippocampal CA2, an inconspicuously positioned area between the well-studied CA1 and CA3 subfields, has captured research interest in recent years due to its role in the formation of social memory. The effects of synaptic depression for subsequent long-term potentiation (LTP) of synaptic transmission at entorhinal cortical (EC)-CA2 and Schaffer collateral (SC)-CA2 synapses have not been previously explored. Here we show that cholinergic receptor activation with the non-selective cholinergic agonist carbachol (CCh) triggers a long-term synaptic depression (CCh-LTD) of field excitatory postsynaptic potentials at EC- and SC-CA2 synapses in the hippocampus of adult rats. The activation of muscarinic acetylcholine receptors (mAChRs) is critical for the induction of an early phase (<100 min) of CCh-LTD, with a strong dependency upon M3 mAChR activation and a weaker one by M1 mAChRs. Interestingly, muscarinic M2 and nicotinic receptor activation are crucially involved in the late phase (>100 min) of CCh-LTD. Importantly, CCh priming lowers the threshold, in a protein synthesis-dependent manner, for the late maintenance of LTP that can be subsequently induced by high-frequency electrical stimulation at EC- or SC-CA2 pathways. The results demonstrate that CA2 synaptic learning rules are modified in a metaplastic manner, wherein synaptic modifications triggered by cholinergic stimulation can dictate the outcome of future plasticity events. Moreover, the observed enabling of late LTP at EC inputs to CA2 following the priming stimulus co-exists with concurrent sustained CCh-LTD at SC-CA2 and is dynamically scaled by modulation of SC-CA2 synaptic transmission.

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Section: Introductionmentioning

confidence: 99%

Metaplastic reinforcement of long-term potentiation in rat hippocampal area CA2 by cholinergic receptor activation

Benoy

Ibrahim

Behnisch

et al. 2020

Preprint

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Robust Resting-State Dynamics in a Large-Scale Spiking Neural Network Model of Area CA3 in the Mouse Hippocampus

et al. 2022

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Vagus nerve stimulation modulates hippocampal inflammation caused by continuous stress in rats

Namgung

Kim

et al. 2022

J Neuroinflammation

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Background Previous studies have shown that vagus nerve stimulation (VNS) can attenuate inflammatory responses in peripheral tissues and also improve some neurological disorders and cognitive function in the brain. However, it is not clear how VNS is involved in neuropathological processes in brain tissues. Here, we investigated the regulatory effects of VNS on the production of proinflammatory cytokines in the hippocampus of an animal model of continuous stress (CS). Methods CS was induced by placing rats in cages immersed with water, and acute or chronic electrical stimulation was applied to the cervical vagus nerve of CS animals. Protein levels in the gastric and hippocampal tissues were measured by western blotting and protein signals analyzed by immunofluorescence staining. von Frey test and forced swimming test were performed to assess pain sensitivity and depressive-like behavior in rats, respectively. Results Levels of TNF-α, IL-1β, and IL-6 in the gastric and hippocampal tissues were significantly increased in CS animals compared to the untreated control and downregulated by acute VNS (aVNS). Iba-1-labeled microglial cells in the hippocampus of CS animals revealed morphological features of activated inflammatory cells and then changed to a normal shape by VNS. VNS elevated hippocampal expression of α7 nicotinic acetylcholine receptors (α7 nAChR) in CS animals, and pharmacological blockade of α7 nAChR increased the production of TNF-α, IL-1β, and IL-6, thus suppressing cholinergic anti-inflammatory activity that was mediated by VNS. Chronic VNS (cVNS) down-regulated the hippocampal production of active form of caspase 3 and 5-HT1A receptors and also decreased levels of TNF-α, IL-1β, and IL-6 in the gastric and hippocampal tissues of CS animals. Pain sensitivity and depressive-like behavior, which were increased by CS, were improved by cVNS. Conclusions Our data suggest that VNS may be involved in modulating pathophysiological processes caused by CS in the brain.

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Neuromodulation of Hippocampal Cells and Circuits

Cited by 3 publications

References 688 publications

Metaplastic reinforcement of long-term potentiation in rat hippocampal area CA2 by cholinergic receptor activation

Metaplastic reinforcement of long-term potentiation in rat hippocampal area CA2 by cholinergic receptor activation

Robust Resting-State Dynamics in a Large-Scale Spiking Neural Network Model of Area CA3 in the Mouse Hippocampus

Vagus nerve stimulation modulates hippocampal inflammation caused by continuous stress in rats

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