Lateralized hippocampal effects of vasoactive intestinal peptide on learning and memory in rats in a model of depression

Ivanova, Margarita; Belcheva, S.; Belcheva, Iren; Negrev, Negrin; Tashev, Roman

doi:10.1007/s00213-011-2600-1

Cited by 14 publications

(9 citation statements)

References 71 publications

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“…Finally, we found no statistically significant change in CCK or VIP mRNA levels in the PFC or HPC. This was in contrast with the reported increased in CCK levels in the cortex 94,95 and decreased VIP expression in specific sub-regions of the HPC 96 following chronic stress.…”

Section: Discussioncontrasting

confidence: 99%

Characterization of GABAergic Marker Expression in the Chronic Unpredictable Stress Model of Depression

et al. 2017

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Evidence continues to build suggesting that the GABAergic neurotransmitter system is altered in brains of patients with major depressive disorder. However, there is little information available related to the extent of these changes or the potential mechanisms associated with these alterations. As stress is a well-established precipitant to depressive episodes, we sought to explore the impact of chronic stress on GABAergic interneurons. Using western blot analyses and quantitative real-time PCR (qPCR) we assessed the effects of five-weeks of chronic unpredictable stress (CUS) exposure on the expression of GABA-synthesizing enzymes (GAD65 and GAD67), calcium-binding proteins (calbindin (CB), parvalbumin (PV) and calretinin (CR)), and neuropeptides co-expressed in GABAergic neurons (somatostatin (SST), neuropeptide Y (NPY), vasoactive intestinal peptide (VIP) and cholecystokinin (CCK)) in the prefrontal cortex (PFC) and hippocampus (HPC) of rats. We also investigated the effects of corticosterone (CORT) and dexamethasone (DEX) exposure on these markers in vitro in primary cortical and hippocampal cultures. We found that CUS induced significant reductions of GAD67 protein levels in both the PFC and HPC of CUS-exposed rats, but did not detect changes in GAD65 protein expression. Similar protein expression changes were found in vitro in cortical neurons. In addition, our results provide clear evidence of reduced markers of interneuron population(s), namely SST and NPY, in the PFC, suggesting these cell types may be selectively vulnerable to chronic stress. Together, this work highlights that chronic stress induces regional and cell type-selective effects on GABAergic interneurons in rats. These findings provide additional supporting evidence that stress-induced GABA neuron dysfunction and cell vulnerability play critical roles in the pathophysiology of stress-related illnesses, including major depressive disorder.

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Section: Discussioncontrasting

confidence: 99%

Characterization of GABAergic Marker Expression in the Chronic Unpredictable Stress Model of Depression

et al. 2017

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“…VIP participates in the pathophysiology of several neurological disorders associated with cognitive disfunction, like depression (Ivanova et al, 2012), autism spectrum disorders, Alzheimer's disease (AD), Parkinson's disease (PD) and epilepsy (de Lanerolle et al, 1995;Hill, 2007;White et al, 2010). Due to its anti-apoptotic, anti-inflammatory and neuroprotective actions, VIP and its receptors constitute promising therapeutic targets in many of these pathologies (Gozes, 2001;Delgado et al, 2002;Yu et al, 2017).…”

Section: Vip In Cognitive Processesmentioning

confidence: 99%

VIP Modulation of Hippocampal Synaptic Plasticity: A Role for VIP Receptors as Therapeutic Targets in Cognitive Decline and Mesial Temporal Lobe Epilepsy

Cunha‐Reis

Caulino-Rocha

2020

Front. Cell. Neurosci.

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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.

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“…The alteration of VIP release and/or the VIP binding receptors could be potentially implicated in multiple pathophysiological conditions. It has been shown that the VIP peptide has a significant role in regulating neuronal activity, and the selective loss of this peptide is associated with several pathological disorders such as depression ( Ivanova et al, 2012 ), Parkinson’s disease, and epilepsy ( Hill, 2007 ; White et al, 2010 ). Indeed, in human temporal lobe epilepsy brains, the receptors for the VIP peptide are increased in expression in the focus of the seizure.…”

Section: The Role Of Vip-expressing Neurons In Cortical Dysfunctionmentioning

confidence: 99%

VIP-Expressing GABAergic Neurons: Disinhibitory vs. Inhibitory Motif and Its Role in Communication Across Neocortical Areas

Apicella

Marchionni

2022

Front. Cell. Neurosci.

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GABAergic neurons play a crucial role in shaping cortical activity. Even though GABAergic neurons constitute a small fraction of cortical neurons, their peculiar morphology and functional properties make them an intriguing and challenging task to study. Here, we review the basic anatomical features, the circuit properties, and the possible role in the relevant behavioral task of a subclass of GABAergic neurons that express vasoactive intestinal polypeptide (VIP). These studies were performed using transgenic mice in which the VIP-expressing neurons can be recognized using fluorescent proteins and optogenetic manipulation to control (or regulate) their electrical activity. Cortical VIP-expressing neurons are more abundant in superficial cortical layers than other cortical layers, where they are mainly studied. Optogenetic and paired recordings performed in ex vivo cortical preparations show that VIP-expressing neurons mainly exert their inhibitory effect onto somatostatin-expressing (SOM) inhibitory neurons, leading to a disinhibitory effect onto excitatory pyramidal neurons. However, this subclass of GABAergic neurons also releases neurotransmitters onto other GABAergic and non-GABAergic neurons, suggesting other possible circuit roles than a disinhibitory effect. The heterogeneity of VIP-expressing neurons also suggests their involvement and recruitment during different functions via the inhibition/disinhibition of GABAergic and non-GABAergic neurons locally and distally, depending on the specific local circuit in which they are embedded, with potential effects on the behavioral states of the animal. Although VIP-expressing neurons represent only a tiny fraction of GABAergic inhibitory neurons in the cortex, these neurons’ selective activation/inactivation could produce a relevant behavioral effect in the animal. Regardless of the increasing finding and discoveries on this subclass of GABAergic neurons, there is still a lot of missing information, and more studies should be done to unveil their role at the circuit and behavior level in different cortical layers and across different neocortical areas.

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Lateralized hippocampal effects of vasoactive intestinal peptide on learning and memory in rats in a model of depression

Abstract: Our results point to a lateralized modulatory effect of VIP injected in the hippocampal CA1 area on the avoidance deficits in OBX rats. The right CA1 area was predominantly involved in the positive effect of VIP on learning and memory. A possible role of the PAC1 receptors is suggested.

Cited by 14 publications

References 71 publications

Characterization of GABAergic Marker Expression in the Chronic Unpredictable Stress Model of Depression

Characterization of GABAergic Marker Expression in the Chronic Unpredictable Stress Model of Depression

VIP Modulation of Hippocampal Synaptic Plasticity: A Role for VIP Receptors as Therapeutic Targets in Cognitive Decline and Mesial Temporal Lobe Epilepsy

VIP-Expressing GABAergic Neurons: Disinhibitory vs. Inhibitory Motif and Its Role in Communication Across Neocortical Areas

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