Stress-induced expression pattern of glutamate signaling genes associated with anhedonia

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Stress-induced expression pattern of glutamate signaling genes associated with anhedonia. / Dygalo, Nikolay N.; Kalinina, Tatyana S.; Shishkina, Galina T.

In: Stress, Vol. 23, No. 6, 01.09.2020, p. 700-707.

Research output: Contribution to journal › Article › peer-review

BibTeX

@article{2187489f9a7b4ac98ed3fdb2da1c7758,

title = "Stress-induced expression pattern of glutamate signaling genes associated with anhedonia",

abstract = "Chronic stress can predispose vulnerable individuals to mood disorders, including depression. Glutamate, one of the key participants in this process, may exert both pathological and therapeutic psycho-emotional effects. However, the role of expression of genes encoding proteins that provide glutamatergic signal is still unclear. In this study, we attempted to distinguish changes in expression of glutamatergic genes associated with stress-induced anhedonia, a core symptom of depression, from those related to other stress-related effects. For this, expression of genes was compared between rats after a short-term stress, which did not yet cause depressive-like symptoms, and animals exposed chronically to different stressors that produce anhedonia-like responses. The changes in gene expression induced by chronic restraint or forced swimming concomitantly with anhedonia development demonstrated similar for both stressors patterns. Main features of the expression patterns include the decrease in mRNA levels for AMPA and NMDA subunits in the midbrain and hippocampus that is consistent with the hypothesis that “monoamine (serotonin)-Glutamate/GABA long neural circuit” involved in mood regulation. The decrease in expression of these subunits in the midbrain may attenuate glutamatergic drive on the serotonergic neurons promoting a shift of excitation/inhibition balance between glutamate and GABA in the forebrain regions resulting in anhedonia. In general, changes in expression of multiple genes involved in glutamatergic neurotransmission in the forebrain and brainstem regions suggest that stress-induced anhedonia may result from the network dysfunction of this neurotransmitter system.",

keywords = "AMPA receptor subunits, chronic stress, depressive-like state, gene expression, NMDA receptor subunits, Short-term stress, DEPRESSION, ACTIVATION, BEHAVIOR, RECEPTOR EXPRESSION, MECHANISMS, MODEL, PREFRONTAL CORTEX, TRANSMISSION, MESSENGER-RNA, BRAIN",

author = "Dygalo, {Nikolay N.} and Kalinina, {Tatyana S.} and Shishkina, {Galina T.}",

year = "2020",

month = sep,

day = "1",

doi = "10.1080/10253890.2020.1812574",

language = "English",

volume = "23",

pages = "700--707",

journal = "Stress",

issn = "1025-3890",

publisher = "Informa Healthcare",

number = "6",

}

RIS

TY - JOUR

T1 - Stress-induced expression pattern of glutamate signaling genes associated with anhedonia

AU - Dygalo, Nikolay N.

AU - Kalinina, Tatyana S.

AU - Shishkina, Galina T.

PY - 2020/9/1

Y1 - 2020/9/1

N2 - Chronic stress can predispose vulnerable individuals to mood disorders, including depression. Glutamate, one of the key participants in this process, may exert both pathological and therapeutic psycho-emotional effects. However, the role of expression of genes encoding proteins that provide glutamatergic signal is still unclear. In this study, we attempted to distinguish changes in expression of glutamatergic genes associated with stress-induced anhedonia, a core symptom of depression, from those related to other stress-related effects. For this, expression of genes was compared between rats after a short-term stress, which did not yet cause depressive-like symptoms, and animals exposed chronically to different stressors that produce anhedonia-like responses. The changes in gene expression induced by chronic restraint or forced swimming concomitantly with anhedonia development demonstrated similar for both stressors patterns. Main features of the expression patterns include the decrease in mRNA levels for AMPA and NMDA subunits in the midbrain and hippocampus that is consistent with the hypothesis that “monoamine (serotonin)-Glutamate/GABA long neural circuit” involved in mood regulation. The decrease in expression of these subunits in the midbrain may attenuate glutamatergic drive on the serotonergic neurons promoting a shift of excitation/inhibition balance between glutamate and GABA in the forebrain regions resulting in anhedonia. In general, changes in expression of multiple genes involved in glutamatergic neurotransmission in the forebrain and brainstem regions suggest that stress-induced anhedonia may result from the network dysfunction of this neurotransmitter system.

AB - Chronic stress can predispose vulnerable individuals to mood disorders, including depression. Glutamate, one of the key participants in this process, may exert both pathological and therapeutic psycho-emotional effects. However, the role of expression of genes encoding proteins that provide glutamatergic signal is still unclear. In this study, we attempted to distinguish changes in expression of glutamatergic genes associated with stress-induced anhedonia, a core symptom of depression, from those related to other stress-related effects. For this, expression of genes was compared between rats after a short-term stress, which did not yet cause depressive-like symptoms, and animals exposed chronically to different stressors that produce anhedonia-like responses. The changes in gene expression induced by chronic restraint or forced swimming concomitantly with anhedonia development demonstrated similar for both stressors patterns. Main features of the expression patterns include the decrease in mRNA levels for AMPA and NMDA subunits in the midbrain and hippocampus that is consistent with the hypothesis that “monoamine (serotonin)-Glutamate/GABA long neural circuit” involved in mood regulation. The decrease in expression of these subunits in the midbrain may attenuate glutamatergic drive on the serotonergic neurons promoting a shift of excitation/inhibition balance between glutamate and GABA in the forebrain regions resulting in anhedonia. In general, changes in expression of multiple genes involved in glutamatergic neurotransmission in the forebrain and brainstem regions suggest that stress-induced anhedonia may result from the network dysfunction of this neurotransmitter system.

KW - AMPA receptor subunits

KW - chronic stress

KW - depressive-like state

KW - gene expression

KW - NMDA receptor subunits

KW - Short-term stress

KW - DEPRESSION

KW - ACTIVATION

KW - BEHAVIOR

KW - RECEPTOR EXPRESSION

KW - MECHANISMS

KW - MODEL

KW - PREFRONTAL CORTEX

KW - TRANSMISSION

KW - MESSENGER-RNA

KW - BRAIN

UR - http://www.scopus.com/inward/record.url?scp=85090147873&partnerID=8YFLogxK

U2 - 10.1080/10253890.2020.1812574

DO - 10.1080/10253890.2020.1812574

M3 - Article

C2 - 32814471

AN - SCOPUS:85090147873

VL - 23

SP - 700

EP - 707

JO - Stress

JF - Stress

SN - 1025-3890

IS - 6

ER -

ID: 25300969