Vitamin D and Depression: Cellular and Regulatory Mechanisms DOI Open Access

Michael J. Berridge

Pharmacological Reviews, Journal Year: 2017, Volume and Issue: 69(2), P. 80 - 92

Published: Feb. 15, 2017

Depression is caused by a change in neural activity resulting from an increase glutamate that drives excitatory neurons and may be responsible for the decline number of GABAergic inhibitory neurons. This imbalance between contribute to onset depression. At cellular level there concentration intracellular Ca2+ within driven entry through NMDA receptors (NMDARs) activation phosphoinositide signaling pathway generates inositol trisphosphate (InsP3) releases internal stores. The importance these two pathways driving elevation supported fact depression can alleviated ketamine inhibits NMDARs scopolamine M1 drive InsP3/Ca2+ pathway. not only contributes but it also explain why individuals with have strong likelihood developing Alzheimer's disease. enhanced levels stimulate formation Aβ initiate progression Alzheimer9s Just how vitamin D acts reduce unclear. phenotypic stability hypothesis argues reducing increased neuronal are action depends on its function maintain expression pumps buffers levels, which

Language: Английский

AMPA receptor plasticity in the nucleus accumbens after repeated exposure to cocaine DOI
Marina E. Wolf, Carrie R. Ferrario

Neuroscience & Biobehavioral Reviews, Journal Year: 2010, Volume and Issue: 35(2), P. 185 - 211

Published: Jan. 29, 2010

Language: Английский

Citations

266

Cellular Plasticity Cascades in the Pathophysiology and Treatment of Bipolar Disorder DOI Open Access

Robert J. Schloesser,

Jian Huang, Peter S. Klein

et al.

Neuropsychopharmacology, Journal Year: 2007, Volume and Issue: 33(1), P. 110 - 133

Published: Oct. 3, 2007

Language: Английский

Citations

247

Cocaine‐induced neuroadaptations in glutamate transmission DOI
Heath D. Schmidt, R. Christopher Pierce

Annals of the New York Academy of Sciences, Journal Year: 2010, Volume and Issue: 1187(1), P. 35 - 75

Published: Jan. 8, 2010

A growing body of evidence indicates that repeated exposure to cocaine leads profound changes in glutamate transmission limbic nuclei, particularly the nucleus accumbens. This review focuses on preclinical studies cocaine-induced behavioral plasticity, including sensitization, self-administration, and reinstatement seeking. Behavioral, pharmacological, neurochemical, electrophysiological, biochemical, molecular biological associated with plasticity systems are reviewed. The ultimate goal these lines research is identify novel targets for development therapies craving addiction. Therefore, we also outline progress prospects modulators treatment

Language: Английский

Citations

241

Gene-Environment Interplay Between Cannabis and Psychosis DOI Open Access
Cécile Henquet, Marta Di Forti, Paul Morrison

et al.

Schizophrenia Bulletin, Journal Year: 2008, Volume and Issue: 34(6), P. 1111 - 1121

Published: Aug. 20, 2008

Cannabis use is considered a contributory cause of schizophrenia and psychotic illness. However, only small proportion cannabis users develop psychosis. This can partly be explained by the amount duration consumption its strength but also age at which individuals are first exposed to cannabis. Genetic factors, in particular, likely play role short- long-term effects may have on psychosis outcome. review will therefore consider interplay between genes exposure development symptoms schizophrenia. Studies using genetic, epidemiological, experimental, observational techniques discussed investigate gene-environment correlation interaction, higher order interactions within cannabis-psychosis association. Evidence suggests that mechanisms interaction underlie association In this respect, multiple variations genes—rather than single genetic polymorphisms—together with other environmental factors (eg, stress) interact increase risk Further research these needed better understand biological pathway use, some individuals, long term.

Language: Английский

Citations

238

Epigenetic side-effects of common pharmaceuticals: A potential new field in medicine and pharmacology DOI
Antonei B. Csòka, Moshe Szyf

Medical Hypotheses, Journal Year: 2009, Volume and Issue: 73(5), P. 770 - 780

Published: June 6, 2009

Language: Английский

Citations

231

Glutamatergic Modulators: The Future of Treating Mood Disorders? DOI
Carlos A. Zarate, Rodrigo Machado‐Vieira, Ioline D. Henter

et al.

Harvard Review of Psychiatry, Journal Year: 2010, Volume and Issue: 18(5), P. 293 - 303

Published: Aug. 1, 2010

Mood disorders such as bipolar disorder and major depressive are common, chronic, recurrent conditions affecting millions of individuals worldwide. Existing antidepressants mood stabilizers used to treat these insufficient for many. Patients continue have low remission rates, delayed onset action, residual subsyndromal symptoms, relapses. New therapeutic agents able exert faster sustained antidepressant or mood-stabilizing effects urgently needed disorders. In this context, the glutamatergic system has been implicated in pathophysiology unique clinical neurobiological ways. addition evidence confirming role modulators riluzole ketamine proof-of-concept system, trials with diverse under way. Overall, holds considerable promise developing next generation novel therapeutics treatment disorder.

Language: Английский

Citations

224

Childhood Stress, Serotonin Transporter Gene and Brain Structures in Major Depression DOI Open Access
Thomas Frodl,

Elena Reinhold,

Nikolaos Koutsouleris

et al.

Neuropsychopharmacology, Journal Year: 2010, Volume and Issue: 35(6), P. 1383 - 1390

Published: Feb. 10, 2010

Language: Английский

Citations

196

Regulation of MiR-124, Let-7d, and MiR-181a in the Accumbens Affects the Expression, Extinction, and Reinstatement of Cocaine-Induced Conditioned Place Preference DOI Open Access
Vijay Chandrasekar, Jean‐Luc Dreyer

Neuropsychopharmacology, Journal Year: 2011, Volume and Issue: 36(6), P. 1149 - 1164

Published: Feb. 9, 2011

Language: Английский

Citations

187

Cellular and molecular mechanisms in the long-term action of antidepressants. DOI Creative Commons
Giorgio Racagni, Maurizio Popoli

Dialogues in Clinical Neuroscience, Journal Year: 2008, Volume and Issue: 10(4), P. 385 - 400

Published: Dec. 31, 2008

The hypotheses on the pathophysiology of depression/mood disorders and antidepressant mechanisms have greatly changed in recent years. classical monoamine hypothesis was revealed to be simplistic, that it could not explain temporal delay therapeutic action antidepressants. Converging lines evidence shown adaptive changes several neuroplasticity are likely cellular molecular correlates effect. In this article, analyzed relation mechanism antidepressants, ranging from gene expression (including neurotrophic mechanisms), synaptic transmission plasticity, neurogenesis. We propose current version simply called "hypothesis neuroplasticity". final section, we also briefly review main novel strategies pharmacology depression new putative targets for with particular emphasis nonmonoaminergic mechanisms.

Language: Английский

Citations

180

Behavior-specific changes in transcriptional modules lead to distinct and predictable neurogenomic states DOI Open Access
Sriram Chandrasekaran, Seth A. Ament, James A. Eddy

et al.

Proceedings of the National Academy of Sciences, Journal Year: 2011, Volume and Issue: 108(44), P. 18020 - 18025

Published: Sept. 29, 2011

Using brain transcriptomic profiles from 853 individual honey bees exhibiting 48 distinct behavioral phenotypes in naturalistic contexts, we report that behavior-specific neurogenomic states can be inferred the coordinated action of transcription factors (TFs) and their predicted target genes. Unsupervised hierarchical clustering these showed three clusters correspond to ecologically important categories: aggression, maturation, foraging. To explore genetic influences potentially regulating states, reconstructed a transcriptional regulatory network (TRN) model. This TRN quantitatively predicts with high accuracy gene expression changes more than 2,000 genes involved behavior, even for on which it was not trained, suggesting there is core set TFs regulates bee brain, other specific particular categories. playing key roles include well-known regulators neural plasticity, e.g., Creb , as well better known biological NF-κB (immunity). Our results reveal insights concerning relationship between behavior. First, behaviors are subserved by brain. Second, underlying different rely upon both shared modules. Third, despite complexity simple linear relationships putative surprisingly prominent feature networks

Language: Английский

Citations

178