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1

Stimulation-dependent changes in oligomeric conformationof serotonin 5-HT receptors

100%
Ponimaskin E.
Acta Neurobiologiae Experimentalis
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2009
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tom 69
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nr 3
An increasing number of G protein-coupled receptors (GPCRs) have been shown to form oligomeric units in the plasma membrane. In many cases there is evidence that this oligomerization can result in altered receptor pharmacology, desensitization and traffi cking. These alterations can consequently result in different effects in intracellular signalling, thus diversifying the functional role of a GPCR. The serotonin (5-HT)1A receptor is a GPCR involved in multiple processes, among which, the regulation of neurogenesis, respiratory control, as well as depression and anxiety states have found the most interest. Biochemical experiments performed in N1E-115 neuroblastoma cells have suggested that 5-HT1A receptors form homooligomers. Acceptor-photobleaching allows for the direct measurement of apparent FRET between the fl uorophores of CFP- and YFP-tagged proteins, further suggesting some specifi c interaction between the receptors. Furthermore, with the use a novel FRET quantifi cation method, we have also been able to discriminate between specifi c and random proteinprotein interaction and to verify dynamics of homo- and heterooligomerization between 5-HT1A and 5-HT7 receptors.
2

Cooperative involvement of serotonergic signalling and MMP-9 in synaptic plasticity

45%
Bijata M., Figiel L., Ponimaskin E., Kaczmarek L., Wlodarczyk J.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
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nr Suppl.1
The brain plasticity is a re-organization of the neuronal and synaptic networks that allows for changes in response to incoming environmental stimuli. Pathological forms of neuronal plasticity underlie the multiple neuropsychiatric disorders like depression. Clinical observations on the efficacy of antidepressants targeting serotonergic system strongly suggest that serotonin and its receptors play a pivotal role in modulation of pathological plasticity. It is known that matrix metalloproteinase-9 is one of the most important biomarker in depression and polymorphism in this protein affect bipolar disorder. We have recently shown that MMP-9, having an established role in synaptic plasticity, influences dendritic morphology in a similar way to that obtained after the 5-HT7 receptor stimulation, e.g. it induces formation of long, thin dendritic spines. It is also known that stimulation of 5-HT7 receptor leads to activation of small Rho GTPase – Cdc42 in fibroblast cell line and in neurons. In this work we investigate whether MMP-9 substrate represents a novel downstream effector of 5-HT7 receptor. Our results indicate that stimulation of the 5-HT7 receptor increases MMP-9 activity toward its synaptic substrates and results in activation of small Rho GTPases.
3

Synaptic remodeling depends on signaling between serotonin receptors and the extracellular matrix

33%
Wlodarczyk J., Bijata M., Labus J., Guseva D., Michaluk P., Rusakov D. A., Dityatev A., Dzwonek J., Ponimaskin E.
Acta Neurobiologiae Experimentalis
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2017
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tom 77
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nr Suppl.1
The rewiring of synaptic circuitry pertinent to memory formation in the brain has often been associated with morphological changes in dendritic spines and extracellular matrix (ECM) remodeling. Here, we linked these processes by uncovering the signaling pathway involving the serotonin 5-HT7 receptors (5 HT7R) the matrix metalloproteinase-9 (MMP-9), the hyaluronan receptor CD44, and the small GTPase Cdc42. We highlight a physical interaction between 5‑HT7R and CD44 (identified as a novel MMP 9 substrate in neurons) on the nanoscale, and find that 5-HT7R stimulation increases local MMP 9 activity triggering dendritic spines remodeling, synaptic pruning and impairment of long-term potentiation (LTP). The underlying molecular machinery involves 5-HT7R-mediated activation of MMP-9, which leads to CD44 cleavage followed by Cdc42 activation. Pharmacological/genetic suppression of this pathway rescues the 5-HT7R-induced synaptic changes and the deficit in LTP. Our results thus reveal causal interactions in a previously unknown molecular mechanism regulating neuronal plasticity. FINANCIAL SUPPORT: The work was supported by the National Science Centre (grant no. DEC-2012/06/M/ NZ3/00163), TANGO1/269352/NCBR/2015, Deutsche Forschungsgemeinschaft (grant no. PO732, excellence cluster REBIRTH), and ERA-NET Neuron/BMBF funding for the TargetECM project to E.P and A.D.
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