The Nathan Kline Institute

Orangeburg, NY, United States

The Nathan Kline Institute

Orangeburg, NY, United States

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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.


PubMed | Sloan Kettering Cancer Center, The Nathan Kline Institute, Brown University, New York Medical College and New York University
Type: Journal Article | Journal: 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 p75(NTR). Invitro, recombinant proBDNF modulates neuronal structure and alters hippocampal long-term plasticity, but the actions ofendogenously 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 p75(NTR). 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 invivo as a biologically active factor that regulates hippocampal structure, synaptic transmission, and plasticity, effects that are distinct from those of mature BDNF.


PubMed | The Nathan Kline Institute, Beth Israel Deaconess Medical Center and Cedars Sinai Medical Center
Type: Journal Article | Journal: Journal of Parkinson's disease | Year: 2016

Stimulation of the subthalamic nuclei (STN) is an effective treatment for Parkinsons disease, but complaints of speech difficulties after surgery have been difficult to quantify. Speech measures do not convincingly account for such reports.This study examined STN stimulation effects on vowel production, in order to probe whether DBS affects articulatory posturing. The objective was to compare positioning during the initiation phase with the steady prolongation phase by measuring vowel spaces for three corner vowels at these two time frames.Vowel space was measured over the initial 0.25sec of sustained productions of high front (/i/), high back (/u/) and low vowels (/a/), and again during a 2sec segment at the midpoint. Eight right-handed male subjects with bilateral STN stimulation and seven age-matched male controls were studied based on their participation in a larger study that included functional imaging. Mean values: age=574.6 yrs; PD duration=12.32.7 yrs; duration of DBS=25.621.2 mos, and UPDRS III speech score=1.60.7. STN subjects were studied off medication at their therapeutic DBS settings and again with their stimulators off, counter-balanced order.Vowel space was larger in the initiation phase compared to the midpoint for both the control and the STN subjects off stimulation. With stimulation on, however, the initial vowel space was significantly reduced to the area measured at the mid-point. For the three vowels, the acoustics were differentially affected, in accordance with expected effects of front versus back position in the vocal tract.STN stimulation appears to constrain initial articulatory gestures for vowel production, raising the possibility that articulatory positions normally used in speech are similarly constrained.


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.


Joseph A.M.,The Nathan Kline Institute | Manseau M.W.,New York University | Lalane M.,New York University | Rajparia A.,New York University | Lewis C.F.,New York University
American Journal of Drug and Alcohol Abuse | Year: 2016

Background: Growing evidence of adverse outcomes following synthetic cannabinoid use has engendered interest into populations at risk. The existing literature reports that synthetic cannabinoid use is predominant among young, white males. However, reports from local Departments of Health have found contrary evidence, showing that synthetic cannabinoid use is prevalent in populations other than those of young, white men. Objectives: This study sought to examine sociodemographic characteristics associated with self-reported synthetic cannabinoid use among a clinical psychiatric population within a public hospital in New York City. Methods: A cross-sectional medical record review was conducted on synthetic cannabinoid users and non-users in an emergency psychiatric setting. A total of 948 patients who presented at the emergency psychiatric setting in 2014 were included in this sample, 110 (11.6%) of whom were synthetic cannabinoid users. Logistic regressions were used to determine the sociodemographic correlates of synthetic cannabinoid use. Results: The most prominent correlate of synthetic cannabinoid use was homelessness/residing in a shelter during time of treatment (AOR = 17.77, 95% CI = 9.74–32.5). Male (AOR = 5.37, 95% CI = 2.04–14.1), non-white (AOR = 2.74, 95% CI = 1.36–5.54), and younger age (AOR = .961, 95% CI = .940–.980) were also significant correlates of synthetic cannabinoid use. Conclusion: Synthetic cannabinoid use among the homeless and mentally ill is a growing public health concern, representing a population with unique clinical and social needs. Areas and populations with high rates of homelessness should be targeted for synthetic cannabinoid prevention and treatment efforts, particularly in urban and racial/ethnic minority communities. © 2016 Research Foundation for Mental Hygiene, Inc.


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.


PubMed | The Nathan Kline Institute
Type: Journal Article | Journal: Endocrinology | Year: 2011

Vascular endothelial growth factor (VEGF) is critical to angiogenesis and vascular permeability. It is also important in the endocrine system, in which VEGF mediates the vascular effects of estrogens in target tissues such as the uterus, a response attributed to an estrogen response element on the VEGF gene. Here we asked whether 17-estradiol increases VEGF levels in the brain. We focused on the hippocampus, in which 17-estradiol and VEGF both have important actions, and used immunocytochemistry to evaluate VEGF protein. VEGF immunoreactivity was compared in adult female rats sampled during the estrous cycle when serum levels of 17-estradiol peak (proestrous morning) as well as when they are low (metestrous morning). In addition, adult rats were ovariectomized and compared after treatment with 17-estradiol or vehicle. The results demonstrated that VEGF immunoreactivity was increased when serum levels of 17-estradiol were elevated. Confocal microscopy showed that VEGF immunofluorescence was predominantly nonneuronal, often associated with astrocytes. Glial VEGF labeling was primarily punctate rather than diffuse and labile because glial VEGF immunoreactivity was greatly reduced if tissue sections were left in an aqueous medium overnight. We conclude that VEGF protein in normal female hippocampus is primarily nonneuronal rather than neuronal and suggest that glial VEGF immunoreactivity has been underestimated by past studies with other methods because there is a labile extracellular pool. We suggest that estrogens may exert actions on female hippocampal structure and function by increasing hippocampal VEGF.


PubMed | The Nathan Kline Institute
Type: Journal Article | Journal: 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 worlds wisdom traditions. These see a movement from the psyches 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.


The dentate gyrus is one of two main areas of the mammalian brain where neurons are born throughout adulthood, a phenomenon called postnatal neurogenesis. Most of the neurons that are generated are granule cells (GCs), the major principal cell type in the dentate gyrus. Some adult-born granule cells develop in ectopic locations, such as the dentate hilus. The generation of hilar ectopic granule cells (HEGCs) is greatly increased in several animal models of epilepsy and has also been demonstrated in surgical specimens from patients with intractable temporal lobe epilepsy (TLE). Herein we review the results of our quantitative neuroanatomic analysis of HEGCs that were filled with Neurobiotin following electrophysiologic characterization in hippocampal slices. The data suggest that two types of HEGCs exist, based on a proximal or distal location of the cell body relative to the granule cell layer, and based on the location of most of the dendrites, in the molecular layer or hilus. Three-dimensional reconstruction revealed that the dendrites of distal HEGCs can extend along the transverse and longitudinal axis of the hippocampus. Analysis of axons demonstrated that HEGCs have projections that contribute to the normal mossy fiber innervation of CA3 as well as the abnormal sprouted fibers in the inner molecular layer of epileptic rodents (mossy fiber sprouting). These data support the idea that HEGCs could function as a hub cell in the dentate gyrus and play a critical role in network excitability.

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