Cited by 404Treatment of Major DepressionStress Responses and CortisolNeurogenesis and neuroplasticity mechanisms

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Neural basis of major depressive disorder: Beyond monoamine hypothesis

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Boku, Shuken, Nakagawa, Shin, Toda, Hiroyuki, Hishimoto, Akitoyo·2018·Psychiatry and Clinical Neurosciences

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Abstract

The monoamine hypothesis has been accepted as the most common hypothesis of major depressive disorder (MDD) for a long period because of its simplicity and understandability. Actually, most currently used antidepressants have been considered to act based on the monoamine hypothesis. However, an important problem of the monoamine hypothesis has been pointed out as follows: it fails to explain the latency of response to antidepressants. In addition, many patients with MDD have remained refractory to currently used antidepressants. Therefore, monoamine-alternate hypotheses are required to explain the latency of response to antidepressants. Such hypotheses have been expected to contribute to identifying hopeful new therapeutic targets for MDD. Past studies have revealed that the volume of the hippocampus is decreased in patients with MDD, which is likely caused by the failure of the hypothalamic-pituitary-adrenal axis and following elevation of glucocorticoids. Two hypotheses have been proposed to explain the volume of the hippocampus: (i) the neuroplasticity hypothesis; and (ii) the neurogenesis hypothesis. The neuroplasticity hypothesis explains how the hippocampal volume is decreased by the morphological changes of hippocampal neurons, such as the shortening length of dendrites and the decreased number and density of spines. The neurogenesis hypothesis explains how the hippocampal volume is decreased by the decrease of neurogenesis in the hippocampal dentate gyrus. These hypotheses are able to explain the latency of response to antidepressants. In this review, we first overview how the neuroplasticity and neurogenesis hypotheses have been developed. We then describe the details of these hypotheses.

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Authors: Boku, S., Nakagawa, S., Toda, H., & Hishimoto, A.
Affiliations: Kobe University (JP)
Hokkaido University (JP)
National Defense Medical College Hospital (JP)
Corresponding author: Boku, Shuken
ORCID: Boku, Shuken
Nakagawa, Shin
Toda, Hiroyuki
Hishimoto, Akitoyo
Venue: Psychiatry and Clinical Neurosciences
Publisher: Wiley
Published: 2017-10-19
Volume: 72
Issue: 1
Pages: 3-12
ISSN: 1323-1316 (ISSN-L)
1440-1819
DOI: 10.1111/pcn.12604
OpenAlex: W2770859047
Cited by: 402
References: 79
Citations by year: 2026: 30 · 2025: 52 · 2024: 61 · 2023: 58 · 2022: 56 · 2021: 72 · 2020: 38 · 2019: 26 · 2018: 9
FWCI: 2.54
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Psychiatry and Clinical Neurosciences (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Keywords: major depressive disorder, monoamine hypothesis, antidepressant resistance, hippocampal volume, hippocampal neurogenesis, dentate gyrus, hypothalamic-pituitary-adrenal axis, glucocorticoids, therapeutic target
MeSH terms: Major Depressive Disorder, Glucocorticoids, Hippocampus, Humans, Hypothalamo-Hypophyseal System, Neuronal Plasticity, Pituitary-Adrenal System, Stress, Psychological, Neurotransmitter Agents, Neurogenesis

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Neural basis of major depressive disorder: Beyond monoamine hypothesis

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