Molecular signaling, Circuit Neuroplasticity and the Cognitive Function

A topical collection in Cells (ISSN 2073-4409). This collection belongs to the section "Cells of the Nervous System".

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Editor


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Collection Editor
Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, 1090 Vienna, Austria
Interests: synaptogenesis; synaptic transmission; synaptic plasticity; learning and memory; fear; anxiety; cognition; biopsychology

Topical Collection Information

Dear Colleagues,

What is cognition from a molecular and cellular perspective? How does the plastic rearrangement of synaptic contacts generate specific patterns of neuronal activity so that some—and not other—cognitive functions emerge? Which specific molecular signaling pathways become suppressed in the aged brain to restrain the unleashing of those neuronal skills that make youngsters such efficient learners?

No matter how enigmatic the phenomenon of cognition appears to be, it is nothing but reasonable to conclude that cognition, understood as a property of given nervous systems, is not only a cognoscible phenomenon but also one not exclusive to humans and, moreover, not exclusive to brains. Our approaches to the problem of the physical nature of cognition can thus afford perspectives free of anthropomorphized boundaries. In this regard, the use of animal models and the combination of in vivo and in vitro approaches comprise powerful experimental tools in neuroscience in the search for the structural, molecular, cellular, and functional underpinnings of the cognitive function.

The Cells team is delighted to invite you to contribute with your original research articles and reviews to this Topic Collection addressing molecular, cellular, and neural circuit functional mechanisms of the nervous system that generate and regulate cognitive function (including—but not limited to—attention, emotion, social cognition, and learning and memory) in health and disease.

We look forward to learning about your findings.

Dr. Francisco Monje
Collection Editor

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Keywords

  • synaptogenesis
  • synaptic transmission
  • synaptic plasticity
  • learning and memory
  • fear
  • anxiety
  • cognition

Published Papers (3 papers)

2024

Jump to: 2023, 2022

20 pages, 1615 KiB  
Review
Astrocytic GABAergic Regulation in Alcohol Use and Major Depressive Disorders
by Dina N. Ali, Hossam M. Ali, Matthew R. Lopez, Shinwoo Kang and Doo-Sup Choi
Cells 2024, 13(4), 318; https://doi.org/10.3390/cells13040318 - 09 Feb 2024
Viewed by 1144
Abstract
Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the central nervous system (CNS). Most GABAergic neurons synthesize GABA from glutamate and release it in the synaptic cleft in the CNS. However, astrocytes can also synthesize and release GABA, activating GABA receptors in [...] Read more.
Gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the central nervous system (CNS). Most GABAergic neurons synthesize GABA from glutamate and release it in the synaptic cleft in the CNS. However, astrocytes can also synthesize and release GABA, activating GABA receptors in the neighboring neurons in physiological and pathological conditions. As the primary homeostatic glial cells in the brain, astrocytes play a crucial role in regulating GABA homeostasis and synaptic neurotransmission. Accumulating evidence demonstrates that astrocytic GABA dysregulation is implicated in psychiatric disorders, including alcohol use disorder (AUD) and major depressive disorder (MDD), the most prevalent co-occurring psychiatric disorders. Several current medications and emerging pharmacological agents targeting GABA levels are in clinical trials for treating AUD and MDD. This review offers a concise summary of the role of astrocytic GABA regulation in AUD and MDD. We also provide an overview of the current understanding and areas of debate regarding the mechanisms by which astrocytes regulate GABA in the CNS and their potential significance in the molecular basis of AUD and MDD, paving the way toward future research directions and potential therapeutic target areas within this field. Full article
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Graphical abstract

2023

Jump to: 2024, 2022

12 pages, 294 KiB  
Review
The Role of Oxytocin in Alzheimer’s Disease and Its Relationship with Social Interaction
by Junpei Takahashi, Daisuke Yamada, Wakana Nagano and Akiyoshi Saitoh
Cells 2023, 12(20), 2426; https://doi.org/10.3390/cells12202426 - 10 Oct 2023
Viewed by 1427
Abstract
Alzheimer’s disease (AD)—the most common cause of dementia in the elderly—is characterized by progressive memory loss and β-amyloid protein (Aβ) accumulation in the brain. Recently, loneliness was found to be a high risk factor for AD, and social isolation has become a major [...] Read more.
Alzheimer’s disease (AD)—the most common cause of dementia in the elderly—is characterized by progressive memory loss and β-amyloid protein (Aβ) accumulation in the brain. Recently, loneliness was found to be a high risk factor for AD, and social isolation has become a major cause of AD. AD. Oxytocin (OXT), the main hormone involved in social bonding, has been implicated in social interactions, notably in building trust and relationships. Moreover, social isolation or social enrichment modulates the activation of neurons related to OXT. Recently, we reported that OXT reverses learning and memory impairment in AD animal models. Based on the limited number of studies currently available, OXT might be a therapeutic target for AD. Further studies are necessary in order to better understand the role of oxytocin in AD. In this review, we described the relationships between OXT, AD, and social interaction. Full article

2022

Jump to: 2024, 2023

16 pages, 2609 KiB  
Article
Sustained Activation of the Anterior Thalamic Neurons with Low Doses of Kainic Acid Boosts Hippocampal Neurogenesis
by Farah Chamaa, Batoul Darwish, Rami Arnaout, Ziad Nahas, Elie D. Al-Chaer, Nayef E. Saadé and Wassim Abou-Kheir
Cells 2022, 11(21), 3413; https://doi.org/10.3390/cells11213413 - 28 Oct 2022
Viewed by 1816
Abstract
Adult hippocampal neurogenesis is prone to modulation by several intrinsic and extrinsic factors. The anterior nucleus (AN) of the thalamus has extensive connections with the hippocampus, and stimulation of this region may play a role in altering neurogenesis. We have previously shown that [...] Read more.
Adult hippocampal neurogenesis is prone to modulation by several intrinsic and extrinsic factors. The anterior nucleus (AN) of the thalamus has extensive connections with the hippocampus, and stimulation of this region may play a role in altering neurogenesis. We have previously shown that electrical stimulation of the AN can substantially boost hippocampal neurogenesis in adult rats. Here, we performed selective unilateral chemical excitation of the cell bodies of the AN as it offers a more specific and sustained stimulation when compared to electrical stimulation. Our aim is to investigate the long-term effects of KA stimulation of the AN on baseline hippocampal proliferation of neural stem cells and neurogenesis. Continuous micro-perfusion of very low doses of kainic acid (KA) was administered into the right AN for seven days. Afterwards, adult male rats received 5′-bromo-2′-deoxyuridine (BrdU) injections (200 mg/kg, i.p) and were euthanized at either one week or four weeks post micro-perfusion. Open field and Y-maze tests were performed before euthanasia. The KA stimulation of the AN evoked sustained hippocampal neurogenesis that was associated with improved spatial memory in the Y-maze test. Administering dexamethasone prior to and simultaneously with the KA stimulation decreased both the hippocampal neurogenesis and the improved spatial recognition memory previously seen in the Y-maze test. These results suggest that hippocampal neurogenesis may be a downstream effect of stimulation in general, and of excitation of the cell bodies of the AN in particular, and that stimulation of that area improves spatial memory in rats. Full article
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Figure 1

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