Maria (Masha) Ryazantseva

Maria (Masha) Ryazantseva
University of Helsinki | HY · Helsinki Institute of Life Science (HiLIFE)

PhD
Academy of Finland Postdoctoral Researcher

About

27
Publications
2,495
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327
Citations
Additional affiliations
February 2010 - October 2014
Russian Academy of Sciences
Position
  • Impaired activity of calcium channeles in neurons and Alzheimer's disease
January 2008 - June 2010
Russian Academy of Sciences
Position
  • Homer proteins regulation of native calcium channels
Description
  • Homer proteins, store-operated calcium channels,
Education
October 2011
September 2009 - June 2011
Saint-Peterburg State University
Field of study
September 2005 - June 2009
Saint-Peterburg State University
Field of study

Publications

Publications (27)
Article
Full-text available
Early life stress (ELS) is a well-characterized risk factor for mood and anxiety disorders. GABAergic microcircuits in the amygdala are critically implicated in anxiety; however, whether their function is altered after ELS is not known. Here we identify a novel mechanism by which kainate receptors (KARs) modulate feedforward inhibition in the later...
Article
Full-text available
Elevated states of brain plasticity typical for critical periods of early postnatal life can be reinstated in the adult brain through interventions, such as antidepressant treatment and environmental enrichment, and induced plasticity may be critical for the antidepressant action. Parvalbumin-positive (PV) interneurons regulate the closure of devel...
Article
Kainate receptors (KARs) are highly expressed in the immature brain and have unique developmentally regulated functions that may be important in linking neuronal activity to morphogenesis during activity-dependent fine-tuning of the synaptic connectivity. Altered expression of KARs in the developing neural network leads to changes in glutamatergic...
Preprint
Full-text available
Activation state of Parvalbumin (PV) interneurons regulates neuronal plasticity, driving the closure of developmental critical periods and alternating between high and low plasticity states in response to experience in adulthood. We now show that PV plasticity states are regulated through the activation of TrkB neurotrophin receptors. Activation of...
Article
Full-text available
Perturbed information processing in the amygdala has been implicated in developmentally originating neuropsychiatric disorders. However, little is known on the mechanisms that guide formation and refinement of intrinsic connections between amygdaloid nuclei. We demonstrate that in rodents the glutamatergic connection from basolateral to central amy...
Preprint
Full-text available
Perturbed information processing in the amygdala has been implicated in developmentally originating neuropsychiatric disorders. However, little is known on the mechanisms that guide formation and refinement of intrinsic connections between amygdaloid nuclei. We demonstrate that the glutamatergic connection from basolateral to central amygdala (BLA-...
Article
Familial Alzheimer’s disease is a severe neurodegenerative disorder. Mutations in the presenilin-1 (PS1) gene account for most familial Alzheimer’s disease cases. Normally, PS1 is cleaved to 2 terminal fragments to form an enzyme center of the γ-secretase complex. A significant number of mutations in the gene of PS1 protein leads to impairment of i...
Article
Store-operated channels activated in response to intracellular calcium store depletion represent the main pathway of calcium entry from the extracellular space in nonelectroexcitable cells. Adapter proteins organize the components of this system into integral complex. We studied the influence of adapter proteins of the Homer family on endogenous st...
Article
Full-text available
Presenilins regulate calcium homeostasis in the endoplasmic reticulum, and dysregulation of intracellular calcium has been implicated in the pathogenesis of Alzheimer disease. Elevated presenilin-1 (PS1) holoprotein levels have been detected in postmortem brains of patients carrying familial Alzheimer disease (FAD) PS1 mutations. This study examine...
Article
Full-text available
A brief burst-suppressing isoflurane anesthesia has been shown to rapidly alleviate symptoms of depression in a subset of patients, but the neurobiological basis of these observations remains obscure. We show that a single isoflurane anesthesia produces antidepressant-like behavioural effects in the learned helplessness paradigm and regulates molec...
Preprint
Full-text available
A brief burst-suppressing isoflurane anesthesia has been shown to rapidly alleviate symptoms of depression in a subset of patients, but the neurobiological basis of these observations remains obscure. We show that a single isoflurane anesthesia produces antidepressant-like behavioural effects in the learned helplessness paradigm and regulates molec...
Article
Full-text available
Background Huntington’s disease (HD) is an incurable hereditary neurodegenerative disorder, which manifests itself as a loss of GABAergic medium spiny (GABA MS) neurons in the striatum and caused by an expansion of the CAG repeat in exon 1 of the huntingtin gene. There is no cure for HD, existing pharmaceutical can only relieve its symptoms. Resul...
Article
Presenilins have been reported to regulate calcium homeostasis in the endoplasmic reticulum, and dysregulation of intracellular calcium has been implicated in the pathogenesis of Alzheimer's disease (AD). Reduced endoproteolysis levels of presenilin-1 (PS1) have been detected in postmortem brains of patients carrying familial Alzheimer's disease PS...
Article
Full-text available
We have shown that the expression of full-length mutated huntingtin in human neuroblastoma cells (SK-N-SH) leads to an abnormal increase in calcium entry through store-operated channels. In this paper, the expression of the N-terminal fragment of mutated huntingtin (Htt138Q-1exon) is shown to be enough to provide an actual model for Huntington's di...
Article
Alzheimer's disease (AD) is a neurodegenerative disorder that leads to neuron death and synapse loss in the hippocampus and cortex, with consequent cognitive disability and dementia. Mutations in the presenilin-1 (PS1) gene lead to familial Alzheimer's disease (FAD). Here, we report that the expression of FAD-linked PS1 M146V mutant affects store-o...
Conference Paper
Familial Alzheimer's disease (FAD) is caused by mutations in presenilin-1 (PS1) gene in approximately 50% of cases. It was found that FAD PS1 mutants disrupt calcium homeostasis in hippocampal neurons disrupting Ca2+ storage in the lumen of endoplasmic reticulum (ER). Recently calcium sensors of ER STIM1 were found to negatively regulate the activi...
Article
Full-text available
The mouse hippocampal cell line HT22 is an excellent model for studying the consequences of endogenous oxidative stress. Addition of extracellular glutamate depletes the cells of glutathione (GSH) by blocking the glutamate-cystine antiporter system x(c)(-). GSH is the main antioxidant in neurons and its depletion induces a well-defined program of c...
Article
Homers are adapter proteins that play a significant role in the organization of calcium signaling protein complexes. Previous functional studies linked Homer proteins to calcium influx in nonexcitable cells. These studies utilized calcium imaging or whole-cell current recordings. Because of limited resolution of these methods, an identity of Homer-...
Article
Full-text available
Store-operated channels are major calcium influx pathways in nonexitable cells. Homer scaffold proteins are well known for their role in regulating calcium signaling. Here we report on a detailed single-channel level characterization of native store-operated channels regulated by Homer scaffold proteins in A431 carcinoma cells. By applying the sing...

Projects

Project (1)
Project
One of the most common and distressing co-occurring mental health issues in people with Autism spectrum disorder (ASD) is anxiety. Anxiety disorders are present in at least 50% of people with ASD significantly affecting their quality of life. The role of amygdala dysfunction is increasingly being recognized as one of the major contributing factors for disturbances in processing of emotions connected with ASD as well as with anxiety. The project aims to study molecular mechanisms behind the pathological development of amygdala. State-of-the-art molecular and genetic toolsets, imaging and electrophysiological methods in addition to behavioral studies in animal models will be combined to understand ASD related pathophysiology. The identification of specific molecules involved in regulation of pathological development leading abnormal behaviors or responses to environmental cues will provide potential approaches to targeted therapy.