Christopher Pittenger

ORCID: 0000-0003-2117-9321
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About
Contact & Profiles
Research Areas
  • Obsessive-Compulsive Spectrum Disorders
  • Autism Spectrum Disorder Research
  • Neurotransmitter Receptor Influence on Behavior
  • Anxiety, Depression, Psychometrics, Treatment, Cognitive Processes
  • Neuroscience and Neuropharmacology Research
  • Memory and Neural Mechanisms
  • Functional Brain Connectivity Studies
  • Psychedelics and Drug Studies
  • Mast cells and histamine
  • Treatment of Major Depression
  • Tryptophan and brain disorders
  • Receptor Mechanisms and Signaling
  • Body Image and Dysmorphia Studies
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Neural and Behavioral Psychology Studies
  • Eating Disorders and Behaviors
  • Neuroendocrine regulation and behavior
  • Attention Deficit Hyperactivity Disorder
  • Stress Responses and Cortisol
  • Neural dynamics and brain function
  • Chemical synthesis and alkaloids
  • Genetics and Neurodevelopmental Disorders
  • Neurogenesis and neuroplasticity mechanisms
  • Genetic Associations and Epidemiology
  • Olfactory and Sensory Function Studies

Yale University
2016-2025

Multidisciplinary Association for Psychedelic Studies
2023

ORCID
2022

Massachusetts General Hospital
2014-2020

University at Buffalo, State University of New York
2020

New Haven Public Schools
2019

National Center for PTSD
2018

The University of Texas Health Science Center at Houston
2017

Michigan Medicine
2017

Michigan United
2017

Significance This study identified elevated global brain signal variability in schizophrenia, but not bipolar illness. was related to schizophrenia symptoms. A commonly used analytic procedure neuroimaging, regression, attenuated clinical effects and altered inferences. Furthermore, local voxel-wise variance increased independent of regression. Finally, neurobiologically grounded computational modeling suggests a putative mechanism, whereby overall connection strength may underlie observed...

10.1073/pnas.1405289111 article EN Proceedings of the National Academy of Sciences 2014-05-05
Lea K. Davis Dongmei Yu Clare L. Keenan Eric R. Gamazon Anuar Konkashbaev and 95 more Eske M. Derks Benjamin M. Neale Jian Yang Sang Lee Patrick Evans Cathy L. Barr Laura Bellodi Fortu Benarroch Gabriel Bedoya Berrío O. Joseph Bienvenu Michael H. Bloch Rianne M. Blom Ruth D. Bruun Cathy L. Budman Beatríz Camarena Desmond Campbell Carolina Cappi Julio César Cardona Silgado Daniëlle C. Cath Maria Cristina Cavallini Denise A. Chavira Sylvain Chouinard David V. Conti Edwin H. Cook Vladimir Coric Bernadette Cullen Dieter Deforce Richard Delorme Yves Dion Christopher K. Edlund Karin Egberts Peter Falkai Thomas Fernandez Patience Gallagher Helena Garrido Daniel Geller Simon Girard Hans J. Grabe Marco A. Grados Benjamin D. Greenberg Varda Gross‐Tsur Stephen A. Haddad Gary A. Heiman Sian Hemmings Ana Gabriela Hounie Cornelia Illmann Joseph Jankovic Michael A. Jenike James L. Kennedy Robert A. King Bárbara Kremeyer Roger Kurlan Nuria Lanzagorta Marion Leboyer James F. Leckman Leonhard Lennertz Chunyu Liu Christine Löchner Thomas L. Lowe Fabìo Macciardi James T. McCracken Lauren M. McGrath Sandra Catalina Mesa Restrepo Rainald Moessner Jubel Morgan Heike Müller Dennis L. Murphy Allan L. Naarden William Cornejo Ochoa Roel A. Ophoff Lisa Osiecki A.J. Pakstis Michele T. Pato Carlos N. Pato John Piacentini Christopher Pittenger Yehuda Pollak Scott L. Rauch Tobias Renner Victor I. Reus Margaret A. Richter Mark A. Riddle Mary M. Robertson Roxana Romero Maria Conceição do Rosário David Rosenberg Guy A. Rouleau Stephan Ruhrmann Andrés Ruiz‐Linares Aline S. Sampaio Jack Samuels Paul Sandor Brooke Sheppard Harvey S. Singer Jan Smit

The direct estimation of heritability from genome-wide common variant data as implemented in the program Genome-wide Complex Trait Analysis (GCTA) has provided a means to quantify attributable all interrogated variants. We have quantified variance liability disease explained by SNPs for two phenotypically-related neurobehavioral disorders, obsessive-compulsive disorder (OCD) and Tourette Syndrome (TS), using GCTA. Our analysis yielded point estimate 0.58 (se = 0.09, p 5.64e-12) TS, 0.37...

10.1371/journal.pgen.1003864 article EN cc-by PLoS Genetics 2013-10-24

Abstract A subanesthetic dose of ketamine causes acute psychotomimetic symptoms and sustained antidepressant effects. In prefrontal cortex, the prevailing disinhibition hypothesis posits that N-methyl-d-aspartate receptor (NMDAR) antagonists such as act preferentially on GABAergic neurons. However, cortical interneurons are heterogeneous. particular, somatostatin-expressing (SST) selectively inhibit dendrites regulate synaptic inputs, yet their response to systemic NMDAR antagonism is...

10.1038/s41467-019-13809-8 article EN cc-by Nature Communications 2020-01-07

We have constructed a strain of Saccharomyces cerevisiae with deletion the YKL510 open reading frame, which was initially identified in chromosome XI as homolog RAD2 nucleotide excision repair gene (A. Jacquier, P. Legrain, and B. Dujon, Yeast 8:121-132, 1992). The mutant exhibits increased sensitivity to UV light alkylating agent methylmethane sulfonate but not ionizing radiation. renamed frame RAD27 gene, keeping accepted nomenclature for radiation-sensitive yeast mutants. Epistasis...

10.1128/jb.177.2.364-371.1995 article EN Journal of Bacteriology 1995-01-01

Anxiety is a core human emotion but can become pathologically dysregulated. We used functional magnetic resonance imaging (fMRI) neurofeedback (NF) to noninvasively alter patterns of brain connectivity, as measured by resting-state fMRI, and reduce contamination anxiety. Activity region the orbitofrontal cortex associated with anxiety was in real time provided subjects significant subclinical NF signal, permitting them learn modulate target region. altered network connectivity regions...

10.1038/tp.2013.24 article EN cc-by Translational Psychiatry 2013-04-30
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