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Wildwood Crest, NJ, United States

Badalamenti A.F.,The Nathan Kline Institute
Journal of Religion and Health | Year: 2013

This paper develops an integration of psychoanalytic and wisdom tradition concepts to answer the question as to why nature does not turn off neurosis, The proposed answer is that nature wants a person to exploit the neurosis for two gains, one being the increase in adaptive capacity resulting from releasing it and the second involving the difficulty in the release itself, the latter related to gains proffered by the world's wisdom traditions. These see a movement from the psyche's creation by passive, unconscious means of finite promise rooted in parental love to creation by active, consciously chosen means of unlimited promise involving a direct relationship with nature and the Cosmos. © 2011 Springer Science+Business Media, LLC. Source


McCloskey D.P.,CUNY - College of Staten Island | Scharfman H.E.,The Nathan Kline Institute | Scharfman H.E.,New York University
Epilepsy Research | Year: 2011

Rat hippocampal area CA3 pyramidal cells synchronously discharge in rhythmic bursts of action potentials after acute disinhibition or convulsant treatment in vitro. These burst discharges resemble epileptiform activity, and are of interest because they may shed light on mechanisms underlying limbic seizures. However, few studies have examined CA3 burst discharges in an animal model of epilepsy, because a period of prolonged, severe seizures (status epilepticus) is often used to induce the epileptic state, which can lead to extensive neuronal loss in CA3. Therefore, the severity of pilocarpine-induced status epilepticus was decreased with anticonvulsant treatment to reduce damage. Rhythmic burst discharges were recorded in the majority of slices from these animals, between two weeks and nine months after status epilepticus. The incidence and amplitude of bursts progressively increased with time after status, even after spontaneous behavioral seizures had begun. The results suggest that modifying the pilocarpine models of temporal lobe epilepsy to reduce neuronal loss leads to robust network synchronization in area CA3. The finding that these bursts increase long after spontaneous behavioral seizures begin supports previous arguments that temporal lobe epilepsy exhibits progressive pathophysiology. © 2011 Elsevier B.V. Source


Yang J.,New York Medical College | Harte-Hargrove L.C.,The Nathan Kline Institute | Siao C.-J.,New York Medical College | Marinic T.,New York Medical College | And 11 more authors.
Cell Reports | Year: 2014

Experience-dependent plasticity shapes postnatal development of neural circuits, but the mechanisms that refine dendritic arbors, remodel spines, and impair synaptic activity are poorly understood. Mature brain-derived neurotrophic factor (BDNF) modulates neuronal morphology and synaptic plasticity, including long-term potentiation (LTP) via TrkB activation. BDNF is initially translated as proBDNF, which binds p75NTR. In vitro, recombinant proBDNF modulates neuronal structure and alters hippocampal long-term plasticity, but the actions of endogenously expressed proBDNF are unclear. Therefore, we generated a cleavage-resistant probdnf knockin mouse. Our results demonstrate that proBDNF negatively regulates hippocampal dendritic complexity and spine density through p75NTR. Hippocampal slices from probdnf mice exhibit depressed synaptic transmission, impaired LTP, and enhanced long-term depression (LTD) in area CA1. These results suggest that proBDNF acts in vivo as a biologically active factor that regulates hippocampal structure, synaptic transmission, and plasticity, effects that are distinct from those of mature BDNF. © 2014 The Authors. Source

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