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Abstract

The chemical hypothesis of depression suggests that mood disorders are caused by a chemical imbalance in the brain, which can be corrected by antidepressant drugs. However, recent evidence indicates that problems in information processing within neural networks, rather than changes in chemical balance, might underlie depression, and that antidepressant drugs induce plastic changes in neuronal connectivity, which gradually lead to improvements in neuronal information processing and recovery of mood.

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Large-scale recording of neuronal ensembles.

György Buzsáki (2004)

How does the brain orchestrate perceptions, thoughts and actions from the spiking activity of its neurons? Early single-neuron recording research treated spike pattern variability as noise that needed to be averaged out to reveal the brain's representation of invariant input. Another view is that variability of spikes is centrally coordinated and that this brain-generated ensemble pattern in cortical structures is itself a potential source of cognition. Large-scale recordings from neuronal ensembles now offer the opportunity to test these competing theoretical frameworks. Currently, wire and micro-machined silicon electrode arrays can record from large numbers of neurons and monitor local neural circuits at work. Achieving the full potential of massively parallel neuronal recordings, however, will require further development of the neuron-electrode interface, automated and efficient spike-sorting algorithms for effective isolation and identification of single neurons, and new mathematical insights for the analysis of network properties.

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Neurobiology of Depression

Eric J. Nestler, Michel Barrot, Ralph DiLeone … (2002)

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Chronic antidepressant treatment increases neurogenesis in adult rat hippocampus.

Eric J. Nestler, J Malberg, Amelia J. Eisch … (2000)

Recent studies suggest that stress-induced atrophy and loss of hippocampal neurons may contribute to the pathophysiology of depression. The aim of this study was to investigate the effect of antidepressants on hippocampal neurogenesis in the adult rat, using the thymidine analog bromodeoxyuridine (BrdU) as a marker for dividing cells. Our studies demonstrate that chronic antidepressant treatment significantly increases the number of BrdU-labeled cells in the dentate gyrus and hilus of the hippocampus. Administration of several different classes of antidepressant, but not non-antidepressant, agents was found to increase BrdU-labeled cell number, indicating that this is a common and selective action of antidepressants. In addition, upregulation of the number of BrdU-labeled cells is observed after chronic, but not acute, treatment, consistent with the time course for the therapeutic action of antidepressants. Additional studies demonstrated that antidepressant treatment increases the proliferation of hippocampal cells and that these new cells mature and become neurons, as determined by triple labeling for BrdU and neuronal- or glial-specific markers. These findings raise the possibility that increased cell proliferation and increased neuronal number may be a mechanism by which antidepressant treatment overcomes the stress-induced atrophy and loss of hippocampal neurons and may contribute to the therapeutic actions of antidepressant treatment.

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PubMed ID:: 15738959

DOI:: 10.1038/nrn1629

ScienceOpen disciplines: Chemistry

Keywords: Affect,physiology,Animals,Biogenic Monoamines,metabolism,Brain Chemistry,Humans,Models, Neurological,Mood Disorders,etiology,Neural Networks (Computer)

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ScienceOpen disciplines: Chemistry

Keywords: Affect, physiology, Animals, Biogenic Monoamines, metabolism, Brain Chemistry, Humans, Models, Neurological, Mood Disorders, etiology, Neural Networks (Computer)

Is mood chemistry?

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A Sustainable Future

Most cited references 52

Large-scale recording of neuronal ensembles.

Neurobiology of Depression

Chronic antidepressant treatment increases neurogenesis in adult rat hippocampus.

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