NDLI: From Gene to Behavior: L-Type Calcium Channel Mechanisms Underlying Neuropsychiatric Symptoms

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NeuroRX : Volume 14

NeuroRX : Volume 14, Issue 4, October 2017

NeuroRX : Volume 14, Issue 3, July 2017

Moving Beyond Serendipity to Mechanism-Driven Psychiatric Therapeutics

Evidence-Based Psychotherapy: Advantages and Challenges

Acceptance and Commitment Therapy: A Transdiagnostic Behavioral Intervention for Mental Health and Medical Conditions

Virtual Reality-Enhanced Extinction of Phobias and Post-Traumatic Stress

Genetic Approaches to Understanding Psychiatric Disease

Genomics of Lithium Action and Response

From Gene to Behavior: L-Type Calcium Channel Mechanisms Underlying Neuropsychiatric Symptoms

Emerging Treatments in Eating Disorders

Role of DISC1 in Neuronal Trafficking and its Implication in Neuropsychiatric Manifestation and Neurotherapeutics

Targeting Adult Neurogenesis to Optimize Hippocampal Circuits in Aging

Modulation of Aversive Memory by Adult Hippocampal Neurogenesis

Targeting Neural Hyperactivity as a Treatment to Stem Progression of Late-Onset Alzheimer’s Disease

Neural Substrates of Depression and Resilience

Reward Circuitry in Addiction

HCN Channel Targets for Novel Antidepressant Treatment

Vagal Nerve Stimulation for Treatment-Resistant Depression

Antidepressant Actions of Ketamine Mediated by the Mechanistic Target of Rapamycin, Nitric Oxide, and Rheb

Potential Therapeutic Effects of Psilocybin

Why Psychiatry Needs 3,4-Methylenedioxymethamphetamine: A Child Psychiatrist’s Perspective

Clozapine as a Model for Antipsychotic Development

Enhanced Bulbar Function in Amyotrophic Lateral Sclerosis: The Nuedexta Treatment Trial

Boundary Cap Neural Crest Stem Cells Promote Survival of Mutant SOD1 Motor Neurons

Cilostazol Use Is Associated with Reduced Risk of Dementia: A Nationwide Cohort Study

The Therapeutic Effectiveness of Delayed Fetal Spinal Cord Tissue Transplantation on Respiratory Function Following Mid-Cervical Spinal Cord Injury

Abstracts from the ASENT 19th Annual Meeting

Erratum to: Regulation of Caveolin-1 and Junction Proteins by bFGF Contributes to the Integrity of Blood–Spinal Cord Barrier and Functional Recovery

Erratum to: Enhanced Bulbar Function in Amyotrophic Lateral Sclerosis: The Nuedexta Treatment Trial

NeuroRX : Volume 14, Issue 2, April 2017

NeuroRX : Volume 14, Issue 1, January 2017

From Gene to Behavior: L-Type Calcium Channel Mechanisms Underlying Neuropsychiatric Symptoms

Content Provider	Springer Nature Link
Author	Kabir, Zeeba D. Martínez Rivera, Arlene Rajadhyaksha, Anjali M.
Copyright Year	2017
Abstract	The L-type calcium channels (LTCCs) Ca$_{v}$1.2 and Ca$_{v}$1.3, encoded by the CACNA1C and CACNA1D genes, respectively, are important regulators of calcium influx into cells and are critical for normal brain development and plasticity. In humans, CACNA1C has emerged as one of the most widely reproduced and prominent candidate risk genes for a range of neuropsychiatric disorders, including bipolar disorder (BD), schizophrenia (SCZ), major depressive disorder, autism spectrum disorder, and attention deficit hyperactivity disorder. Separately, CACNA1D has been found to be associated with BD and autism spectrum disorder, as well as cocaine dependence, a comorbid feature associated with psychiatric disorders. Despite growing evidence of a significant link between CACNA1C and CACNA1D and psychiatric disorders, our understanding of the biological mechanisms by which these LTCCs mediate neuropsychiatric-associated endophenotypes, many of which are shared across the different disorders, remains rudimentary. Clinical studies with LTCC blockers testing their efficacy to alleviate symptoms associated with BD, SCZ, and drug dependence have provided mixed results, underscoring the importance of further exploring the neurobiological consequences of dysregulated Ca$_{v}$1.2 and Ca$_{v}$1.3. Here, we provide a review of clinical studies that have evaluated LTCC blockers for BD, SCZ, and drug dependence-associated symptoms, as well as rodent studies that have identified Ca$_{v}$1.2- and Ca$_{v}$1.3-specific molecular and cellular cascades that underlie mood (anxiety, depression), social behavior, cognition, and addiction.
Starting Page	588
Ending Page	613
Page Count	26
File Format	PDF
ISSN	19337213
Journal	NeuroRX
Volume Number	14
Issue Number	3
e-ISSN	18787479
Language	English
Publisher	Springer US
Publisher Date	2017-05-11
Publisher Institution	American Society for Experimental NeuroTherapeutics
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Ca$_{v}$1.2 Ca$_{v}$1.3 CACNA1C CACNA1D Mood Social Addiction Neurosciences Neurology Neurosurgery Neurobiology
Content Type	Text
Resource Type	Article
Subject	Neurology (clinical) Pharmacology Pharmacology (medical)

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1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
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3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
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9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

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