Tallie Z. Baram

ORCID: 0000-0003-0771-8616
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About
Contact & Profiles
Research Areas
  • Stress Responses and Cortisol
  • Neuroscience and Neuropharmacology Research
  • Neuroendocrine regulation and behavior
  • Epilepsy research and treatment
  • Neonatal and fetal brain pathology
  • Tryptophan and brain disorders
  • Ion channel regulation and function
  • Child and Adolescent Psychosocial and Emotional Development
  • Birth, Development, and Health
  • Anesthesia and Neurotoxicity Research
  • Maternal Mental Health During Pregnancy and Postpartum
  • Early Childhood Education and Development
  • Hormonal Regulation and Hypertension
  • Neurogenesis and neuroplasticity mechanisms
  • Memory and Neural Mechanisms
  • Infectious Encephalopathies and Encephalitis
  • Adrenal Hormones and Disorders
  • Pharmacological Effects and Toxicity Studies
  • Child Abuse and Trauma
  • Mitochondrial Function and Pathology
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Functional Brain Connectivity Studies
  • Neural dynamics and brain function
  • Genetics and Neurodevelopmental Disorders
  • Glioma Diagnosis and Treatment

University of California, Irvine
2016-2025

Institute of Neurobiology
1996-2020

Chapman University
2018

University of Denver
2018

Pediatrics and Genetics
2002-2016

C3J Therapeutics (United States)
2012

Brewster Place
2012

RELX Group (United Kingdom)
2007

Singer (United States)
2007

Royal Children's Hospital
2004

Chronic early-life stress (ES) exerts profound acute and long-lasting effects on the hypothalamic-pituitary-adrenal system, with relevance to cognitive function affective disorders. Our ability determine molecular mechanisms underlying these should benefit greatly from appropriate mouse models because would enable use of powerful transgenic methods. Therefore, we have characterized a model chronic ES, which was provoked in pups by abnormal, fragmented interactions dam. Dam-pup interaction...

10.1210/en.2008-0633 article EN Endocrinology 2008-06-19

Progressive cognitive deficits that emerge with aging are a result of complex interactions genetic and environmental factors. Whereas much has been learned about the underpinnings these disorders, nature “acquired” contributing factors, mechanisms by which they promote progressive learning memory dysfunction, remain largely unknown. Here, we demonstrate period early-life “psychological” stress causes late-onset, selective deterioration both behavior synaptic plasticity: two forms involving...

10.1523/jneurosci.2281-05.2005 article EN cc-by-nc-sa Journal of Neuroscience 2005-10-12

Fever can provoke "febrile" seizures (FS). Because complex FS may promote development of temporal lobe epilepsy, understanding their mechanisms is clinically important. Using an immature rodent model and transgenic technology, we examined the role interleukin-1beta, (IL-1beta), a pyrogenic, proinflammatory cytokine, in FS. IL-1beta receptor-deficient mice were resistant to experimental This resistance appeared independent genetic background was attributed lack signaling, because exogenous...

10.1002/ana.20358 article EN Annals of Neurology 2004-12-27

Chronic stress impairs learning and memory in humans rodents disrupts long-term potentiation (LTP) animal models. These effects are associated with structural changes hippocampal neurons, including reduced dendritic arborization. Unlike the generally reversible of chronic on adult rat hippocampus, we have previously found that early-life endure worsen during adulthood, yet mechanisms for these clinically important sequelae poorly understood. Stress promotes secretion neuropeptide...

10.1523/jneurosci.1784-10.2010 article EN cc-by-nc-sa Journal of Neuroscience 2010-09-29

The immediate and long-term effects of exposure to early life stress (ELS) have been documented in humans animal models. Even relatively brief periods during the first 10 days rodents can impact later behavioral regulation vulnerability develop adult pathologies, particular an impairment cognitive functions neurogenesis, but also modified social, emotional, conditioned fear responses. development preclinical models ELS allows examination mechanisms testing therapeutic approaches that are not...

10.1080/10253890.2017.1343296 article EN Stress 2017-06-15

Whether long febrile seizures (FSs) can cause epilepsy in the absence of genetic or acquired predisposing factors is unclear. Having established causality between FSs and limbic an animal model, we studied here if duration inciting influenced probability developing subsequent severity spontaneous seizures. We evaluated interictal epileptifom activity and/or elevation hippocampal T2 signal on magnetic resonance image (MRI) provided predictive biomarkers for epileptogenesis, inflammatory...

10.1523/jneurosci.0551-10.2010 article EN cc-by-nc-sa Journal of Neuroscience 2010-06-02

Stress affects the hippocampus, a brain region crucial for memory. In rodents, acute stress may reduce density of dendritic spines, location postsynaptic elements excitatory synapses, and impair long-term potentiation Steroid hormones neurotransmitters have been implicated in underlying mechanisms, but role corticotropin-releasing hormone (CRH), hypothalamic also released during within has not elucidated. addition, causal relationship spine loss memory defects after is unclear. We used...

10.1073/pnas.1003825107 article EN Proceedings of the National Academy of Sciences 2010-07-06

Abstract Vulnerability to emotional disorders including depression derives from interactions between genes and environment, especially during sensitive developmental periods. Across evolution, maternal care is a key source of environmental sensory signals the developing brain, vast body work has linked quantitative qualitative aspects outcome in children animals. However, fundamental properties signals, that promote advantageous vs pathological outcomes offspring, are unknown have been topic...

10.1038/tp.2015.200 article EN cc-by Translational Psychiatry 2016-01-05

Significance The receipt of high-quality maternal care is an established promoter optimal neurodevelopment, but the processes by which influences development remain unclear. Using a cross-species approach, we probe possibility that predictability sensory signals from mother process behavior cognitive circuits within developing brain. This in accord with roles patterns information organization visual and auditory systems brain during sensitive periods. Our data support argument degree affects...

10.1073/pnas.1703444114 article EN Proceedings of the National Academy of Sciences 2017-09-11

Information about the adverse effects of COVID-19 pandemic on adolescent and adult mental health is growing, yet impacts preschool children are only emerging. Importantly, environmental factors that augment or protect from multidimensional stressful influences emotional development young poorly understood.Depressive symptoms in 169 (mean age 4.1 years) were assessed with Preschool Feelings Checklist during a state-wide stay-at-home order Southern California. Mothers (46% Latinx) also...

10.1016/j.ynstr.2020.100291 article EN cc-by-nc-nd Neurobiology of Stress 2021-01-10

Several mental illnesses, characterized by aberrant stress reactivity, often arise after early-life adversity (ELA). However, it is unclear how ELA affects stress-related brain circuit maturation, provoking these enduring vulnerabilities. We find that increases functional excitatory synapses onto stress-sensitive hypothalamic corticotropin-releasing hormone (CRH)-expressing neurons, resulting from disrupted developmental synapse pruning adjacent microglia. Microglial process dynamics and...

10.1016/j.celrep.2022.110600 article EN cc-by-nc-nd Cell Reports 2022-03-01

Objective. To compare the efficacy of corticotropin (ACTH) (150 U/m2/day) and prednisone (2 mg/kg/day), given for 2 weeks, in suppressing clinical spasms hypsarrhythmic electroencephalogram (EEG) infantile (IS). ACTH are standard treatments IS. at high doses causes severe dose- duration-dependent side effects, but may be superior to prednisone, based on retrospective or uncontrolled studies. Blinded prospective studies have shown equal low-dose ACTH, low versus high-dose ACTH. Design. A...

10.1542/peds.97.3.375 article EN PEDIATRICS 1996-03-01
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