Inhibition of the NMDA and AMPA receptor channels by antidepressants and antipsychotics

Barygin, Oleg I.; Nagaeva, Elina; Tikhonov, Denis B.; Belinskaya, Darya A.; Ванчакова, Н. П.; Shestakova, N. N.

doi:10.1016/j.brainres.2017.01.028

Cited by 57 publications

(45 citation statements)

References 58 publications

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“…Sodium channel blockers inhibit ectopic discharges occurring when there is nerve damage, thereby inhibiting neuropathic pain [ 85 , 86 ]. Second, some antidepressants act as NMDA receptor antagonists [ 87 , 88 ]. NMDA receptors, which are expressed in the neurons of the dorsal horn of the spinal cord, induce wind-up and central sensitization result in contribute to the onset and maintenance of neuropathic pain [ 89 , 90 ].…”

Section: Other Actionsmentioning

confidence: 99%

Analgesic Mechanisms of Antidepressants for Neuropathic Pain

Obata

2017

IJMS

295

203

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Tricyclic antidepressants and serotonin noradrenaline reuptake inhibitors are used to treat chronic pain, such as neuropathic pain. Why antidepressants are effective for treatment of neuropathic pain and the precise mechanisms underlying their effects, however, remain unclear. The inhibitory effects of these antidepressants for neuropathic pain manifest more quickly than their antidepressive effects, suggesting different modes of action. Recent studies of animal models of neuropathic pain revealed that noradrenaline is extremely important for the inhibition of neuropathic pain. First, increasing noradrenaline in the spinal cord by reuptake inhibition directly inhibits neuropathic pain through α2-adrenergic receptors. Second, increasing noradrenaline acts on the locus coeruleus and improves the function of an impaired descending noradrenergic inhibitory system. Serotonin and dopamine may reinforce the noradrenergic effects to inhibit neuropathic pain. The mechanisms of neuropathic pain inhibition by antidepressants based mainly on experimental findings from animal models of neuropathic pain are discussed in this review.

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Section: Other Actionsmentioning

confidence: 99%

Analgesic Mechanisms of Antidepressants for Neuropathic Pain

Obata

2017

IJMS

295

203

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“…Furthermore, the cluster analysis showed that the pattern of relationships between MBP expression and plasticity markers measure in a previous study was changed by fluoxetine. Fluoxetine is known to regulate NMDA and AMPA receptors (Szasz et al, 2007;Kiss et al, 2012;Vizi et al, 2013;Barygin et al, 2017) and both receptors are found on oligodendroglia where they participate in myelination (Káradóttir and Attwell, 2007;Kougioumtzidou et al, 2017). Thus, fluoxetine could have a direct effect on the regulation of MBP in adult V1 separate from the effects on synaptic plasticity mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Experience-Dependent Changes in Myelin Basic Protein Expression in Adult Visual and Somatosensory Cortex

Murphy

Mancini

Clayworth

et al. 2020

Front. Cell. Neurosci.

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An experience-driven increase in oligodendrocytes and myelin in the somatosensory cortex (S1) has emerged as a new marker of adult cortical plasticity. That finding contrasts with the view that myelin is a structural brake on plasticity, and that contributes to ending the critical period (CP) in the visual cortex (V1). Despite the evidence that myelin-derived signaling acts to end CP in V1, there is no information about myelin changes during adult plasticity in V1. To address this, we quantified the effect of three manipulations that drive adult plasticity (monocular deprivation (MD), fluoxetine treatment or the combination of MD and fluoxetine) on the expression of myelin basic protein (MBP) in adult rat V1. In tandem, we validated that environmental enrichment (EE) increased cortical myelin by measuring MBP in adult S1. For comparison with the MBP measurements, three plasticity markers were also quantified, the spine markers drebrin E and drebrin A, and a plasticity maintenance marker Ube3A. First, we confirmed that EE increased MBP in S1. Next, that expression of the plasticity markers was affected in S1 by EE and in V1 by the visual manipulations. Finally, we found that after adult MD, MBP increased in the non-deprived V1 hemisphere, but it decreased in the deprived hemisphere, and those changes were not influenced by fluoxetine. Together, the findings suggest that modulation of myelin expression in adult V1 may reflect the levels of visually driven activity rather than synaptic plasticity caused by adult plasticity.

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“…The increased probability of onset of Parkinson's disease in post-menopausal women (Wooten et al, 2004) The dihydropyridine and non-dihydropyridine calcium channel blockers and the farnesol-like sesquiterpenoids may both be affecting mitochondrial calcium homeostasis. Phenothiazines have polypharmacology but could also be affecting ion homeostasis (Barygin et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

Drug repurposing for mitochondrial diseases using a pharmacological model of complex I deficiency in the yeastYarrowia lipolytica

Perlstein¹

2020

Preprint

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Mitochondrial diseases affect 1 in 5,000 live births around the world. They are caused by inherited or de novo mutations in over 350 nuclear-encoded and mtDNA-encoded genes. There is no approved treatment to stop the progression of any mitochondrial disease despite the enormous global unmet need. Affected families often self-compound cocktails of over-the-counter vitamins and generally recognized as safe nutritional supplements that have not received regulatory approval for efficacy. Finding a new use for an approved drug is called repurposing, an attractive path for mitochondrial diseases because of the reduced safety risks, low costs and fast timelines to a clinic-ready therapy or combination of therapies. Here I describe the first-ever drug repurposing screen for mitochondrial diseases involving complex I deficiency, e.g., Leigh syndrome, using the yeast Yarrowia lipolytica as a model system. Unlike the more commonly used yeast Saccharomyces cerevisiae but like humans, Yarrowia lipolytica has a functional and metabolically integrated respiratory complex I and is an obligate aerobe. In 384-well-plate liquid culture format without shaking, Yarrowia lipolytica cells grown in either glucose-containing media or acetate-containing media were treated with a half-maximal inhibitory concentration (3µM and 6µM, respectively) of the natural product and complex I inhibitor piericidin A. Out of 2,560 compounds in the Microsource Spectrum collection, 24 suppressors of piercidin A reached statistical significance in one or both media conditions. The suppressors include calcium channel blockers nisoldipine, amiodarone and tetrandrine as well as the farnesol-like sesquiterpenoids parthenolide, nerolidol and bisabolol, which may all be modulating mitochondrial calcium homeostasis. Estradiols and synthetic estrogen receptor agonists are the largest class of suppressors that rescue growth of piericidin-A-treated Yarrowia lipolytica cells in both glucose-containing and acetate-containing media. Analysis of structure-activity relationships suggests that estrogens may enhance bioenergetics by evolutionarily conserved interactions with mitochondrial membranes that promote mitochondrial filamentation and mitochondrial DNA replication.

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Inhibition of the NMDA and AMPA receptor channels by antidepressants and antipsychotics

Cited by 57 publications

References 58 publications

Analgesic Mechanisms of Antidepressants for Neuropathic Pain

Analgesic Mechanisms of Antidepressants for Neuropathic Pain

Experience-Dependent Changes in Myelin Basic Protein Expression in Adult Visual and Somatosensory Cortex

Drug repurposing for mitochondrial diseases using a pharmacological model of complex I deficiency in the yeastYarrowia lipolytica

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