Abstract
Vasoactive intestinal peptide (VIP) is an important modulatory peptide throughout the CNS acting as a neurotransmitter, neurotrophic or neuroprotective factor. In the hippocampus, a brain area implicated in learning and memory processes, VIP has a crucial role in the control of GABAergic transmission and pyramidal cell activity in response to specific network activity by either VIP-containing basket cells or interneuron-selective (IS) interneurons and this appears to have a differential impact in hippocampal-dependent cognition. At the cellular level, VIP regulates synaptic transmission by either promoting disinhibition, through activation of VPAC1 receptors, or enhancing pyramidal cell excitability, through activation of VPAC2 receptors. These actions also control several important synaptic plasticity phenomena such as long-term potentiation (LTP) and long-term depression (LTD). This paper reviews the current knowledge on the activation and multiple functions of VIP expressing cells in the hippocampus and their role in controlling synaptic transmission, synaptic plasticity and learning and memory processes, discussing also the role of VPAC1 and VPAC2 VIP receptors in the regulation of these different processes. Furthermore, we address the current knowledge regarding changes in VIP mediated neurotransmission in epileptogenesis and mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS), and discuss the therapeutic opportunities of using selective VIP receptor ligands to prevent epileptogenesis and cognitive decline in MTLE-HS.
Highlights
Vasoactive intestinal peptide (VIP), a 28 amino-acid residue peptide originally isolated from porcine duodenum by Mutt and Said (1974), owes its name to its powerful ability to cause vasodilatation (Said and Mutt, 1970), by promoting vascular smooth muscle relaxation in the gastrointestinal tract when released by peripheral nerves of the sympathetic nervousVIP Receptors in Cognition and mesial temporal lobe epilepsy (MTLE) Prevention system (Said and Rosenberg, 1976)
This paper reviews the multiple roles of VIP in synaptic transmission, synaptic plasticity and hippocampal-dependent learning and memory processes, the role of VIP in hippocampal and cognitive disfunction in mesial temporal lobe epilepsy (MTLE) and the therapeutic opportunities that this presents
VIP is an important regulator of hippocampal activity through both direct actions on pyramidal cell excitability (Haas and Gähwiler, 1992) and by regulating synaptic transmission and synaptic plasticity to pyramidal cell dendrites through disinhibition (Cunha-Reis et al, 2004, 2010, 2014; CunhaReis and Carmo, 2011; Luo et al, 2020), actions that have a major impact on hippocampal-dependent learning and memory formation (Turi et al, 2019)
Summary
Vasoactive intestinal peptide (VIP), a 28 amino-acid residue peptide originally isolated from porcine duodenum by Mutt and Said (1974), owes its name to its powerful ability to cause vasodilatation (Said and Mutt, 1970), by promoting vascular smooth muscle relaxation in the gastrointestinal tract when released by peripheral nerves of the sympathetic nervousVIP Receptors in Cognition and MTLE Prevention system (Said and Rosenberg, 1976). No study has to date identified VPAC1 receptors in hippocampal interneurons, yet the fact that VIP enhancement of synaptic transmission to CA1 pyramidal cells involves inhibition of GABAergic interneurons that control
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