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Andrei Molosh

Lauren M Federici, Izabela Facco Caliman, Andrei I Molosh, Stephanie D Fitz, William A Truitt, Pascal Bonaventure, Janet S Carpenter, Anantha Shekhar, Philip L Johnson
No abstract text is available yet for this article.
November 2016: Psychoneuroendocrinology
Lauren M Federici, Izabela Facco Caliman, Andrei I Molosh, Stephanie D Fitz, William A Truitt, Pascal Bonaventure, Janet S Carpenter, Anantha Shekhar, Philip L Johnson
Distressing symptoms such as hot flashes and sleep disturbances affect over 70% of women approaching menopause for an average of 4-7 years, and recent large cohort studies have shown that anxiety and stress are strongly associated with more severe and persistent hot flashes and can induce hot flashes. Although high estrogen doses alleviate symptoms, extended use increases health risks, and current non-hormonal therapies are marginally better than placebo. The lack of effective non-hormonal treatments is largely due to the limited understanding of the mechanisms that underlie menopausal symptoms...
March 2016: Psychoneuroendocrinology
Philip L Johnson, Andrei Molosh, Stephanie D Fitz, Dave Arendt, Gerald A Deehan, Lauren M Federici, Cristian Bernabe, Eric A Engleman, Zachary A Rodd, Christopher A Lowry, Anantha Shekhar
The basolateral and lateral amygdala nuclei complex (BLC) is implicated in a number of emotional responses including conditioned fear and social anxiety. Based on previous studies demonstrating that enhanced serotonin release in the BLC leads to increased anxiety and fear responses, we hypothesized that pharmacologically depleting serotonin in the BLC using 5,7-dihydroxytryptamine (5,7-DHT) injections would lead to diminished anxiety and disrupted fear conditioning. To test this hypothesis, 5,7-DHT(a serotonin-depleting agent) was bilaterally injected into the BLC...
November 2015: Pharmacology, Biochemistry, and Behavior
Andrei I Molosh, Philip L Johnson, John P Spence, David Arendt, Lauren M Federici, Cristian Bernabe, Steven P Janasik, Zaneer M Segu, Rajesh Khanna, Chirayu Goswami, Weiguo Zhu, Su-Jung Park, Lang Li, Yehia S Mechref, D Wade Clapp, Anantha Shekhar
Children with neurofibromatosis type 1 (NF1) are increasingly recognized as having a high prevalence of social difficulties and autism spectrum disorders (ASDs). We demonstrated a selective social learning deficit in mice with deletion of a single Nf1 allele (Nf1(+/-)), along with greater activation of the mitogen-activated protein kinase pathway in neurons from the amygdala and frontal cortex, structures that are relevant to social behaviors. The Nf1(+/-) mice showed aberrant amygdala glutamate and GABA neurotransmission, deficits in long-term potentiation and specific disruptions in the expression of two proteins that are associated with glutamate and GABA neurotransmission: a disintegrin and metalloprotease domain 22 (Adam22) and heat shock protein 70 (Hsp70), respectively...
November 2014: Nature Neuroscience
Karl R Koehler, Andrew M Mikosz, Andrei I Molosh, Dharmeshkumar Patel, Eri Hashino
The inner ear contains sensory epithelia that detect head movements, gravity and sound. It is unclear how to develop these sensory epithelia from pluripotent stem cells, a process that will be critical for modelling inner ear disorders or developing cell-based therapies for profound hearing loss and balance disorders. So far, attempts to derive inner ear mechanosensitive hair cells and sensory neurons have resulted in inefficient or incomplete phenotypic conversion of stem cells into inner-ear-like cells. A key insight lacking from these previous studies is the importance of the non-neural and preplacodal ectoderm, two critical precursors during inner ear development...
August 8, 2013: Nature
Andrei I Molosh, Tammy J Sajdyk, William A Truitt, Weiguo Zhu, Gerry S Oxford, Anantha Shekhar
Neuropeptide Y (NPY) administration into the basolateral amygdala (BLA) decreases anxiety-like behavior, mediated in part through the Y1 receptor (Y1R) isoform. Activation of Y1Rs results in G-protein-mediated reduction of cAMP levels, which results in reduced excitability of amygdala projection neurons. Understanding the mechanisms linking decreased cAMP levels to reduced excitability in amygdala neurons is important for identifying novel anxiolytic targets. We studied the intracellular mechanisms of activation of Y1Rs on synaptic transmission in the BLA...
June 2013: Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology
Philip L Johnson, Andrei Molosh, Stephanie D Fitz, William A Truitt, Anantha Shekhar
A panic response is an adaptive response to deal with an imminent threat and consists of an integrated pattern of behavioral (aggression, fleeing, or freezing) and increased cardiorespiratory and endocrine responses that are highly conserved across vertebrate species. In the 1920s and 1940s, Philip Bard and Walter Hess, respectively, determined that the posterior regions of the hypothalamus are critical for a "fight-or-flight" reaction to deal with an imminent threat. Since the 1940s it was determined that the posterior hypothalamic panic area was located dorsal (perifornical hypothalamus: PeF) and dorsomedial (dorsomedial hypothalamus: DMH) to the fornix...
2012: Progress in Brain Research
Elizabeth A Lungwitz, Andrei Molosh, Philip L Johnson, Brian P Harvey, Rachel C Dirks, Amy Dietrich, Pamela Minick, Anantha Shekhar, William A Truitt
The hypothalamic neuropeptide orexin (ORX) has been implicated in anxiety, and anxiety-like behaviors. The purpose of these studies was to determine the role of ORX, specifically orexin-A (ORX-A) in the bed nucleus of the stria terminalis (BNST) on anxiety-like behaviors in rats. Rats injected with ORX-A into the BNST displayed greater anxiety-like measures in the social interaction and elevated plus maze tests compared to vehicle treated controls. Such anxiety-like behaviors were not observed when the ORX-A injections were adjacent to the BNST, in the medial septum...
December 5, 2012: Physiology & Behavior
Joel M Brittain, Liang Chen, Sarah M Wilson, Tatiana Brustovetsky, Xiang Gao, Nicole M Ashpole, Andrei I Molosh, Haitao You, Andy Hudmon, Anantha Shekhar, Fletcher A White, Gerald W Zamponi, Nickolay Brustovetsky, Jinhui Chen, Rajesh Khanna
Neurological disabilities following traumatic brain injury (TBI) may be due to excitotoxic neuronal loss. The excitotoxic loss of neurons following TBI occurs largely due to hyperactivation of N-methyl-d-aspartate receptors (NMDARs), leading to toxic levels of intracellular Ca(2+). The axon guidance and outgrowth protein collapsin response mediator protein 2 (CRMP2) has been linked to NMDAR trafficking and may be involved in neuronal survival following excitotoxicity. Lentivirus-mediated CRMP2 knockdown or treatment with a CRMP2 peptide fused to HIV TAT protein (TAT-CBD3) blocked neuronal death following glutamate exposure probably via blunting toxicity from delayed calcium deregulation...
October 28, 2011: Journal of Biological Chemistry
Dmitry V Zaretsky, Andrei I Molosh, Maria V Zaretskaia, Daniel E Rusyniak, Joseph A DiMicco
Although anesthetic doses of urethane increase plasma levels of ACTH, the exact mechanism through which this occurs is unclear. We theorized that these increases might be a consequence of an increased systemic osmolality owing to the large doses of urethane usually employed. To evaluate this possibility, we measured plasma osmolality and ACTH in a total of six rats after graded infusions of urethane (N=3 rats) or equimolar amounts of mannitol (N=3 rats). Rats received infusions at 15 min intervals up to a cumulative dose equivalent to an anesthetic dose for urethane (1...
July 19, 2010: Neuroscience Letters
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