Abstract
Considerable evidence has been provided these last years for the involvement of the GABA-A receptor complex in memory processes. Compounds that enhance the action of GABA, such as benzodiazepines, impair memory processing. On the contrary, compounds that reduce the action of GABA, such as ß-CCM, pentylenetetrazol or picrotoxin, have the opposite action, that is : enhance memory processing. All these actions seem to focus mainly on the acquisition (learning) processes. Depending on the dose, the same compounds also have effects on anxiety and on seizuring. Benzodiazepines are well-known anxiolytic and anticonvulsant agents whereas compounds that reduce the action of GABA have been found to produce anxiogenic and convulsant actions. The GABA-A receptor complex might thus be the location of a possible link between a pathological state (epilepsy) and two normal functions (anxiety and learning). This link is likely to involve common genetic pathways. In the normal subject, these data also emphasize the idea that normal memory processing involves a moderate level of anxiety.
Keywords: gaba receptor complex, pentylenetetrazol, picrotoxin, learning, anxiety, epilepsy
Current Topics in Medicinal Chemistry
Title: GABA-A Receptor Complex and Memory Processes
Volume: 2 Issue: 8
Author(s): Georges Chapouthier and Patrice Venault
Affiliation:
Keywords: gaba receptor complex, pentylenetetrazol, picrotoxin, learning, anxiety, epilepsy
Abstract: Considerable evidence has been provided these last years for the involvement of the GABA-A receptor complex in memory processes. Compounds that enhance the action of GABA, such as benzodiazepines, impair memory processing. On the contrary, compounds that reduce the action of GABA, such as ß-CCM, pentylenetetrazol or picrotoxin, have the opposite action, that is : enhance memory processing. All these actions seem to focus mainly on the acquisition (learning) processes. Depending on the dose, the same compounds also have effects on anxiety and on seizuring. Benzodiazepines are well-known anxiolytic and anticonvulsant agents whereas compounds that reduce the action of GABA have been found to produce anxiogenic and convulsant actions. The GABA-A receptor complex might thus be the location of a possible link between a pathological state (epilepsy) and two normal functions (anxiety and learning). This link is likely to involve common genetic pathways. In the normal subject, these data also emphasize the idea that normal memory processing involves a moderate level of anxiety.
Export Options
About this article
Cite this article as:
Chapouthier Georges and Venault Patrice, GABA-A Receptor Complex and Memory Processes, Current Topics in Medicinal Chemistry 2002; 2 (8) . https://dx.doi.org/10.2174/1568026023393552
DOI https://dx.doi.org/10.2174/1568026023393552 |
Print ISSN 1568-0266 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4294 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
Related Articles
-
Biomarkers of Alzheimer’s Disease: An Overview of the Recent Inventions
Recent Patents on Biomarkers Commentary [Research Highlights (Making Sense Out of Antisense in Huntington’s Disease)]
CNS & Neurological Disorders - Drug Targets PDZ Domain-mediated Protein Interactions: Therapeutic Targets in Neurological Disorders
Current Medicinal Chemistry The Renin-Angiotensin System: New Insight into Old Therapies
Current Medicinal Chemistry Polyphenols Beyond Barriers: A Glimpse into the Brain
Current Neuropharmacology Blood-Brain Barrier Integrity and Glial Support: Mechanisms that can be Targeted for Novel Therapeutic Approaches in Stroke
Current Pharmaceutical Design Editorial
Current Medical Imaging Delayed Cerebral Ischemia after Subarachnoid Hemorrhage: From Vascular Spasm to Cortical Spreading Depolarizations
Current Neurovascular Research Tissue Distribution and Pharmacodynamics: A Complicated Relationship
Current Drug Metabolism RhoGEFs in Cell Motility: Novel Links Between Rgnef and Focal Adhesion Kinase
Current Molecular Medicine Trafficking of Neuronal Two Pore Domain Potassium Channels
Current Neuropharmacology Concurrent Use of Antiretrovirals and Anticonvulsants in Human Immunodeficiency Virus (HIV) Seropositive Patients
Current Pharmaceutical Design GABAA Receptors, Anesthetics and Anticonvulsants in Brain Development
CNS & Neurological Disorders - Drug Targets Upregulated Long Non-coding RNA ALMS1-IT1 Promotes Neuroinflammation by Activating NF-κB Signaling in Ischemic Cerebral Injury
Current Pharmaceutical Design An Update on Drug Interactions with the Herbal Medicine Ginkgo biloba
Current Drug Metabolism Advances in the Understanding of the Gabaergic Neurobiology of FMR1 Expanded Alleles Leading to Targeted Treatments for Fragile X Spectrum Disorder
Current Pharmaceutical Design Complex and Differential Glial Responses in Alzheimer´s Disease and Ageing
Current Alzheimer Research Potassium Channels and CNS Diseases
CNS & Neurological Disorders - Drug Targets Synthesis, Antifungal Activity and Carbonic Anhydrase Inhibitory Properties of Cu (II) Bis (3, 4 Dimethoxybenzoate) Bis (Nicotinamide) Dihydrate
Current Enzyme Inhibition Editorial [Hot Topic: Peripheral Proteins as Drug Targets (Guest Editor: Robert V. Stahelin) ]
Current Drug Targets