Juan Marcos Alarcón

ORCID: 0000-0002-3936-806X
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Memory and Neural Mechanisms
  • Genetics and Neurodevelopmental Disorders
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Receptor Mechanisms and Signaling
  • Neural dynamics and brain function
  • RNA Research and Splicing
  • Single-cell and spatial transcriptomics
  • Neurogenesis and neuroplasticity mechanisms
  • RNA and protein synthesis mechanisms
  • Nerve injury and regeneration
  • RNA regulation and disease
  • Ion channel regulation and function
  • Folate and B Vitamins Research
  • Cannabis and Cannabinoid Research
  • Nuclear Receptors and Signaling
  • Vagus Nerve Stimulation Research
  • Lipid Membrane Structure and Behavior
  • Autism Spectrum Disorder Research
  • Alzheimer's disease research and treatments
  • Protein Kinase Regulation and GTPase Signaling
  • Lysosomal Storage Disorders Research
  • Microtubule and mitosis dynamics
  • Neurological diseases and metabolism
  • Heart Rate Variability and Autonomic Control

SUNY Downstate Health Sciences University
2016-2025

State University of New York
2014-2024

Marine Biological Laboratory
2017-2019

Columbia University
2002-2008

University of Massachusetts Chan Medical School
2004-2008

Kavli Institute for Theoretical Sciences
2007

Columbia University Irving Medical Center
2006

University of Chile
2000-2005

Howard Hughes Medical Institute
2004

To investigate the role of CREB-mediated gene expression on excitability CA1 pyramidal neurons, we obtained intracellular recordings from neurons transgenic mice expressing a constitutively active form CREB, VP16–CREB, in regulated and restricted manner. We found that transgene increased neuronal inhibited slow medium afterhyperpolarization currents. These changes may contribute to reduced threshold for LTP observed these mice. When strong was turned prolonged period time, also showed...

10.1523/jneurosci.3850-07.2007 article EN cc-by-nc-sa Journal of Neuroscience 2007-12-12

CPEB-1 is a sequence-specific RNA binding protein that stimulates the polyadenylation-induced translation of mRNAs containing cytoplasmic polyadenylation element (CPE). Although was identified originally in Xenopus oocytes, it has also been found at postsynaptic sites hippocampal neurons where, response to N -methyl-D-aspartate receptor activation, thought induce and αCaMKII perhaps other CPE-containing mRNAs. Because some forms synaptic modification appear be influenced by local (synaptic)...

10.1101/lm.72704 article EN Learning & Memory 2004-05-01

Reference memory characterizes the long-term storage of information acquired through numerous trials. In contrast, working represents short-term acquisition trial-unique information. A number studies in rodent hippocampus have focused on contribution synaptic potentiation (LTP) to reference memory. little is known about plasticity correlates hippocampal-based components Here, we described a mouse with selective expression dominant-negative mutant regulatory subunit protein kinase (PKA) only...

10.1523/jneurosci.1330-09.2010 article EN cc-by-nc-sa Journal of Neuroscience 2010-03-10

Cytoplasmic polyadenylation element binding protein 1 (CPEB-1) resides at postsynaptic sites in hippocampal neurons which it controls polyadenylation-induced translation. CPEB-1 knock-out (KO) mice display defects some forms of synaptic plasticity and hippocampal-dependent memories. To identify CPEB-1-regulated mRNAs, we used proteomics to compare polypeptides wild-type (WT) KO hippocampus. Growth hormone (GH) was reduced the hippocampus, as were GH signaling molecules phospho-JAK2...

10.1523/jneurosci.1756-08.2008 article EN cc-by-nc-sa Journal of Neuroscience 2008-08-20

Abstract Previously, our metabolomic, transcriptomic, and genomic studies characterized the ceramide/sphingomyelin pathway as a therapeutic target in Alzheimer’s disease, we demonstrated that FTY720, sphingosine-1-phospahate receptor modulator approved for treatment of multiple sclerosis, recovers synaptic plasticity memory APP/PS1 mice. To further investigate how FTY720 rescues pathology, performed metabolomic analysis brain, plasma, liver trained wild-type mice showed area-specific brain...

10.1101/2025.01.17.633452 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2025-01-18

Studies in the rodent hippocampus have demonstrated that when late phase of long-term potentiation (L-LTP) is induced a set synapses by suprathreshold stimulation, L-LTP can also be expressed other receiving subthreshold phenomenon usually referred as “capture L-LTP.” Because pyramidal neurons mammalian both apical and basal dendrites, we now investigated whether capture L-LTP, previously described only within dendritic compartment, take place basilar compartment and, if so, accomplished...

10.1523/jneurosci.3196-05.2006 article EN cc-by-nc-sa Journal of Neuroscience 2006-01-04

In humans, vitamin B12 deficiency causes peripheral and CNS manifestations. Loss of myelin in the nerves spinal cord (SC) contributes to neuropathy motor deficits. The metabolic basis for demyelination brain disorder is unknown. transcobalamin receptor–knockout mouse (Cd320−/−) develops cobalamin (Cb1) nervous system, with mild anemia. A decreased S-adenosylme-thionine:S-adenosylhomocysteine ratio increased methionine were seen no significant changes neurotransmitter metabolites. structural...

10.1096/fj.201800754rr article EN The FASEB Journal 2018-10-10

Long-term memory (LTM) formation requires new protein synthesis and gene expression. Based on our work in Aplysia, we hypothesized that the rRNA genes, stimulation-dependent targets of enzyme Poly(ADP-ribose) polymerase-1 (PARP-1), are primary effectors activity-dependent changes synaptic function maintain plasticity memory. Using electrophysiology, immunohistochemistry, pharmacology molecular biology techniques, show here, for first time, maintenance forskolin-induced late-phase long-term...

10.1371/journal.pone.0104364 article EN cc-by PLoS ONE 2014-08-04

PKMζ is an autonomously active PKC isoform crucial for the maintenance of synaptic long-term potentiation (LTP) and memory. Unlike other kinases that are transiently stimulated by second messengers, persistently activated through sustained increases in protein expression kinase. Therefore, visualizing during memory storage might reveal sites its persistent action thus location memory-associated LTP brain. Using quantitative immunohistochemistry validated lack staining PKMζ-null mice, we...

10.1111/ejn.15137 article EN European Journal of Neuroscience 2021-02-08

Phencyclidine (PCP) causes psychosis, is abused with increasing frequency, and was extensively used in antipsychotic drug discovery. PCP discoordinates hippocampal ensemble action potential discharge impairs cognitive control rats, but how this uncompetitive NMDA receptor (NMDAR) antagonist cognition remains unknown.

10.1016/j.bpsgos.2023.04.009 article EN cc-by Biological Psychiatry Global Open Science 2023-05-31

Vitamin B12 (cobalamin) deficiency is prevalent worldwide and causes megaloblastic anemia neurologic deficits. While the can be treated, deficits become refractive to treatment as disease progresses. Therefore, timely intervention critical for a favorable outcome. Moreover, metabolic basis neuro-pathologic changes role of cobalamin in pathology still remains unexplained. Using transcobalamin receptor / CD320 knockout mouse that lacks cellular uptake bound cobalamin, we aimed determine...

10.1371/journal.pone.0177156 article EN cc-by PLoS ONE 2017-05-18

The hippocampal CA1 field processes spatial information, but the relative importance of intra- versus extra-hippocampal sources input into for behavior is unclear. To characterize roles these two input, originating in CA3 and medial entorhinal cortex (MEC), we studied effects discrete neurotoxic lesions or MEC on concurrent nonspatial navigation tasks, synaptic transmission afferents to CA1. Lesions regions that abolished CA3-CA1, reduced MEC-CA1 transmission, respectively, impaired...

10.3389/fnbeh.2014.00292 article EN cc-by Frontiers in Behavioral Neuroscience 2014-08-28

Information arriving at a neuron via anatomically defined pathways undergoes spatial and temporal encoding. A proposed mechanism by which temporally spatially segregated information is encoded the cellular level based on interactive properties of synapses located within across functional dendritic compartments. We examined cooperative interfering interactions between long-term synaptic potentiation (LTP) depression (LTD), two forms plasticity thought to be key in encoding brain. Two...

10.1371/journal.pone.0029865 article EN cc-by PLoS ONE 2012-01-17

Abstract Accumulating evidence links dysfunction in the endocannabinoid system (ECS) with pathology of neurodevelopmental disorders, particularly autism spectrum disorder (ASD). Variants ECS genes CNR1 and DAGLA are associated neurological phenotypes humans. The endocannabinoids (eCBs), 2‐AG AEA, which act at primary cannabinoid receptor (CB1), mediate behaviors relevant to disorders. overlap between these eCBs is poorly understood. Most studies have focused on stress responses, anxiety,...

10.1002/aur.2520 article EN Autism Research 2021-04-21
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