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

Transcription Factors in Long-Term Memory and Synaptic Plasticity DOI
Cristina M. Alberini

Physiological Reviews, Journal Year: 2009, Volume and Issue: 89(1), P. 121 - 145

Published: Jan. 1, 2009

Transcription is a molecular requisite for long-term synaptic plasticity and memory formation. Thus, in the last several years, one main interest of neuroscience has been identification families transcription factors that are involved both these processes. highly regulated process involves combined interaction function chromatin many other proteins, some which essential basal transcription, while others control selective activation or repression specific genes. These interactions ultimately allow sophisticated response to multiple environmental conditions, as well spatial temporal differences gene expression. Evidence based on correlative changes expression, genetic mutations, targeted inhibition expression have shed light This review provides brief overview experimental work showing factors, including CREB, C/EBP, Egr, AP-1, Rel, functions The results this suggest patterns regulation represent signatures

Language: Английский

Citations

955

Neurobiological mechanisms in major depressive disorder DOI Creative Commons
Marije aan het Rot, Sanjay J. Mathew, Dennis S. Charney

et al.

Canadian Medical Association Journal, Journal Year: 2009, Volume and Issue: 180(3), P. 305 - 313

Published: Feb. 2, 2009

Nearly 1 in 5 people will experience a major depressive episode at some point their lives.[1][1] In this review, we discuss data describing how genes, psychosocial adversity childhood, and ongoing or recent stress may impact multiple neurobiological systems relevant to

Language: Английский

Citations

452

Stress Hormone Regulation: Biological Role and Translation into Therapy DOI
Herta Flor, Marcus Ising

Annual Review of Psychology, Journal Year: 2009, Volume and Issue: 61(1), P. 81 - 109

Published: Dec. 4, 2009

Stress is defined as a state of perturbed homeostasis following endangerment that evokes manifold adaptive reactions, which are summarized the stress response. In case mental stress, response follows perception endangerment. Different peptides, steroids, and biogenic amines operate within brain also after they have been released into circulation. We focus in this review on biological roles corticosteroids, corticotrophin-releasing hormone (CRH), arginine vasopressin (AVP), we evaluate effects treatments directed against actions these hormones. CRH AVP central drivers system, but act neuromodulators brain, affecting higher functions including emotion, cognition, behavior. When toward pituitary, neuropeptides elicit corticotrophin periphery, activates corticosteroid release from adrenal cortex. These hormones essential for adequate adaptation to can evoke severe clinical conditions once persistently hypersecreted. Depression anxiety disorders prominent examples stress-related associated with an impaired regulation summarize drugs acting at specific targets axis, discuss their potential use next-generation antidepressant medications. Such require identification patients will optimally benefit such interventions. could be first step personalized medicine using tailored pathology patients.

Language: Английский

Citations

444

Striatal microRNA controls cocaine intake through CREB signalling DOI

Jonathan A. Hollander,

Heh‐In Im, Antonio L. Amelio

et al.

Nature, Journal Year: 2010, Volume and Issue: 466(7303), P. 197 - 202

Published: July 1, 2010

Language: Английский

Citations

381

Therapeutic Potential of Mood Stabilizers Lithium and Valproic Acid: Beyond Bipolar Disorder DOI

Chi‐Tso Chiu,

Zhifei Wang, Joshua Hunsberger

et al.

Pharmacological Reviews, Journal Year: 2013, Volume and Issue: 65(1), P. 105 - 142

Published: Jan. 1, 2013

The mood stabilizers lithium and valproic acid (VPA) are traditionally used to treat bipolar disorder (BD), a severe mental illness arising from complex interactions between genes environment that drive deficits in cellular plasticity resiliency. therapeutic potential of these drugs other central nervous system diseases is also gaining support. This article reviews the various mechanisms action VPA gleaned animal models neurologic, neurodegenerative, neuropsychiatric disorders. Clinical evidence included when available provide comprehensive perspective field acknowledge some limitations treatments. First, review describes how at drugs' primary targets—glycogen synthase kinase-3 for histone deacetylases VPA—induces transcription expression neurotrophic, angiogenic, neuroprotective proteins. Cell survival signaling cascades, oxidative stress pathways, protein quality control may further underlie VPA's beneficial actions. ability cotreatment augment neuroprotection enhance stem cell homing migration discussed, as microRNAs new targets. Finally, preclinical findings have shown benefits agents facilitate anti-inflammation, angiogenesis, neurogenesis, blood-brain barrier integrity, disease-specific neuroprotection. These can be compared with dysregulated disease suggest core molecular disturbances identifiable by specific risk biomarkers. Future clinical endeavors warranted determine across spectrum diseases, particular emphasis on personalized medicine approach toward treating

Language: Английский

Citations

369

Resilience in mental health: linking psychological and neurobiological perspectives DOI Creative Commons
Bart P. F. Rutten,

Caroline Hammels,

Nicole Geschwind

et al.

Acta Psychiatrica Scandinavica, Journal Year: 2013, Volume and Issue: 128(1), P. 3 - 20

Published: March 14, 2013

To review the literature on psychological and biological findings resilience (i.e. successful adaptation swift recovery after experiencing life adversities) at level of individual, to integrate from animal human studies.Electronic manual search MEDLINE, EMBASE PSYCHINFO, using a range terms around factors influencing as observed in experimental studies, complemented by articles cross-references.The term is used for different phenomena ranging prevention mental health disturbance adversities, may also include post-traumatic growth. Secure attachment, positive emotions having purpose are three important building blocks resilience. Overlap between most apparent topic stress sensitivity, although recent results suggest crucial role reward experience resilience.Improving understanding links genetic endowment, environmental impact gene-environment interactions with developmental psychology biology elucidating neurobiological underpinnings

Language: Английский

Citations

362

Neurobiology of depression, fibromyalgia and neuropathic pain DOI Open Access

Vladimir Maletic

Frontiers in bioscience, Journal Year: 2009, Volume and Issue: 14(1), P. 5291 - 5291

Published: Jan. 1, 2009

This article synthesizes recent data suggesting that the high rates of comorbidity observed between major depression, fibromyalgia and neuropathic pain likely result from fact these disorders share multiple biological environmental underpinnings. perspective suggests biologically complex conditions similar genetic vulnerabilities interacting with adversity. Shared determinants include poorly functional alleles regulating monoaminergic, glutamatergic, neurotrophic, opioid inflammatory cytokine signaling. Chief among risk factors are psychosocial stress illness, both which promote, in vulnerable individuals, relative resistance to glucocorticoids, increased sympathetic/decreased parasympathetic activity production release proinflamnmatory mediators. Dysregulation stress/inflammatory pathways promotes alterations brain circuitry modulates mood, response. Over time, changes promote disruptions neurotrophic support disturbances glia-neuronal communication. These changes, turn, have been associated related processes central sensitization "kindling" may account for progressive self-perpetuating nature disorders, especially when inadequately treated.

Language: Английский

Citations

344

Mechanisms involved in the neurotoxic, cognitive, and neurobehavioral effects of alcohol consumption during adolescence DOI
Consuelo Guerri, María Pascual

Alcohol, Journal Year: 2010, Volume and Issue: 44(1), P. 15 - 26

Published: Jan. 1, 2010

Language: Английский

Citations

341

Natural rewards, neuroplasticity, and non-drug addictions DOI
Christopher M. Olsen

Neuropharmacology, Journal Year: 2011, Volume and Issue: 61(7), P. 1109 - 1122

Published: April 9, 2011

Language: Английский

Citations

320

Repeated alcohol administration during adolescence causes changes in the mesolimbic dopaminergic and glutamatergic systems and promotes alcohol intake in the adult rat DOI
María Pascual, Jordi Boix, Vicente Felipo

et al.

Journal of Neurochemistry, Journal Year: 2008, Volume and Issue: 108(4), P. 920 - 931

Published: Dec. 11, 2008

Adolescence is a developmental period which the risk of drug and alcohol abuse increases. Since mesolimbic dopaminergic system undergoes changes during adolescence, this involved in rewarding effects drugs abuse, we addressed hypothesis that ethanol exposure juvenile/adolescent over-activates inducing adaptations can trigger long-term enduring behavioural abuse. We treated or adult rats with (3 g/kg) for two-consecutive days at 48-h intervals over 14-day period. Here show intermittent treatment juvenile/adolescence alters subsequent intake. In vivo microdialysis demonstrates elicits similar prolonged dopamine response nucleus accumbens both adolescent animals pre-treated multiple doses ethanol, although basal levels were higher ethanol-treated adolescents than adult-treated animals. Repeated administration also down-regulates expression DRD2 NMDAR2B phosphorylation prefrontal cortex animals, but not rats. Finally, adolescence acetylation histones H3 H4 frontal cortex, striatum, suggesting chromatin remodelling changes. summary, our findings demonstrate sensitivity brain to on glutamatergic neurotransmission, suggest abnormal plasticity reward-related processes epigenetic mechanisms could contribute vulnerability addiction.

Language: Английский

Citations

315