Publications by authors named "I V Melnick"

Introduction: Hippocampal interneurons (INs) are known to synchronize their electrical activity mechanisms, which are poorly defined due to immense complexity of neural tissue but seem to depend on local cell interactions and intensity of network activity.

Methods: Here, synchronization of INs was studied using paired patch-clamp recordings in a simplified culture model with intact glutamate transmission. The level of network activity was moderately elevated by field electric stimulation, which is probably an analogue of afferent processing .

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Key Points: Central regulation of energy homeostasis and stress are believed to be reciprocally regulated, i.e. excessive food intake suppresses, while prolonged hunger exacerbates, stress responses in vivo.

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One of the main functions of astrocytes is to ensure glutamate homeostasis by glutamate uptake and glutamine synthesis. However, during the past ten years it has become clear that astrocytes may also induce changes in synaptic glutamate release when respective pathways must cope with the consequences of brain damage or other alterations in their functional requirements. The loss of glutamatergic synapses in Parkinson's and Huntington's disease is likely to associate with a continuous redistribution of presynaptic activity within the pool of surviving synapses, and astrocytes may have a role in the maintenance of independent control at individual glutamate release sites.

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With the advent of psychotropic medications and with the deinstitutionalization of psychiatry starting in 1968, patients were prematurely discharged from forensic state hospitals. Due to lack of resources, psychiatric forensic patients ended up in the correctional system or homeless with the reduction of psychiatric beds in forensic and civil state hospitals. Lacking proper training and medication management, the recidivism rate of this population was close to 10% for rearrest and about 35% for revocation of conditional release (CR; Manguno-Mire et al.

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Article Synopsis
  • Huntington's disease (HD) is a genetic neurodegenerative disorder characterized by motor symptoms, particularly the hypokinetic-rigid phenotype, which can be studied using the Q175 mouse model.
  • At one year old, Q175 mice showed significant reductions in spontaneous movements, increased inactivity, and delays in reactions, indicating severe hypokinesia, without notable loss of certain striatal neurons.
  • Findings suggest that decreased dopamine release and impaired cortico-striatal synaptic transmission contribute to hypokinesia in HD, evidenced by changes in synaptic activity and neurotransmitter signaling in the affected mice.
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