Tallie Z. Baram

The paper identifies sex-dependent roles of paraventricular thalamus neurons in mediating the effects of early-life adversity on adult reward behaviors in mice.

The paper identifies disrupted CRH signaling as a cause of reward deficits after early-life stress and shows CRHR2 activation can reverse anhedonia-like behaviors.

This study shows early-life unpredictability affects decision-making under uncertainty by increasing discounting and overharvesting, distinct from lifelong stress effects.

This study examines how anhedonia and early-life unpredictability interact to influence threat-reward decision-making in humans.

The paper investigates how early-life adversity affects reward behaviors through peptide signaling in the paraventricular thalamus and identifies CRHR1 as a molecular target for intervention.

The paper investigates sex differences in memory vulnerability to acute traumatic stress, finding that estrogen and its receptors play a role in both males and females.

This study shows that early life stress in mice leads to social behavior deficits and altered stress biomarkers in adolescence, with effects persisting across generations.

The paper investigates sex- and stress-dependent plasticity of a CRH/GABA projection from the BLA to NAc, showing differential effects on reward behaviors in males and females.

The paper defines a histology-informed MRI mask for the human paraventricular nucleus of the thalamus, showing spatial overlap with existing masks but with additional posterior voxels and consistent functional connectivity patterns.

This study examines how early-life unpredictability affects hippocampal and amygdala responses to novelty in adolescents, finding sex-specific differences in brain activation and functional connectivity.

The paper validates a novel Crhr1-FlpO mouse that selectively targets CRHR1-expressing neurons for genetic manipulation.

This study shows that deleting PTEN in adult dentate gyrus neurons leads to hyperexcitable circuits and spontaneous seizures without neuron death.

This paper identifies DNA methylation changes in children linked to early-life adversity and shows their correlation with later executive function, with sex-dependent effects.

The paper identifies a novel stress-sensitive CRH GABA projection from the basolateral amygdala to the nucleus accumbens that contributes to reward behavior disruption following early-life adversity.

The paper identifies the thalamic paraventricular nucleus (PVT) as a region selectively activated by early-life adversity (ELA) in mice, linking it to long-term reward-related behavioral deficits.

The paper shows that early-life adversity impairs microglial pruning of excitatory synapses on CRH-expressing hypothalamic neurons, leading to heightened stress responses later in life.

The paper identifies acute vascular topological changes in the cortex and basolateral amygdala following experimental febrile status epilepticus in rats, which may underlie an MRI signal predictive of future epilepsy.

This study uses single-cell RNA sequencing to identify lasting transcriptional changes in hypothalamic CRH-expressing neurons after early-life adversity, linking these changes to long-term stress responses.

This study shows that early life adversity in male mice alters reward circuit connectivity and leads to anhedonia in adulthood.

This study investigates how early-life adversity affects vulnerability to opioid addiction in rats, finding that it leads to addiction-like behaviors and altered reward circuitry.

Blocking CRH receptor type 1 in adulthood mitigates age-related memory impairments caused by early-life adversity in rats, but not all memory functions.

The paper uses intra-individual DNA methylation analysis in rat buccal cells to show that early-life adversity alters methylation patterns predictive of gene repression and upregulation of inflammation and cell-fate pathways.

This paper introduces a novel diffusion tensor imaging (DTI) method to accurately delineate the rat basolateral amygdala (BLA) and validates it against histological techniques.

The paper investigates how augmented maternal care affects DNA methylation, gene expression, and miRNA levels in the developing hypothalamus, identifying genes linked to stress resilience.

The paper investigates whether NRSF-Sin3 interaction is required for NRSF-mediated repression of target genes in developing hypothalamus and finds that blocking this interaction does not prevent repression.