Michal Bajo

ORCID: 0000-0003-1102-2689
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About
Contact & Profiles
Research Areas
  • Stress Responses and Cortisol
  • Tryptophan and brain disorders
  • Neurotransmitter Receptor Influence on Behavior
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Neuroscience and Neuropharmacology Research
  • Memory and Neural Mechanisms
  • Neuropeptides and Animal Physiology
  • Cannabis and Cannabinoid Research
  • Receptor Mechanisms and Signaling
  • Hormonal Regulation and Hypertension
  • Adipose Tissue and Metabolism
  • Sleep and Wakefulness Research
  • Biochemical effects in animals
  • Anesthesia and Neurotoxicity Research
  • Ion channel regulation and function
  • Winter Sports Injuries and Performance
  • Biochemical Analysis and Sensing Techniques
  • Eating Disorders and Behaviors
  • Nicotinic Acetylcholine Receptors Study
  • Immune Response and Inflammation
  • Pain Mechanisms and Treatments
  • Neurological Disease Mechanisms and Treatments
  • Peroxisome Proliferator-Activated Receptors
  • Cardiovascular, Neuropeptides, and Oxidative Stress Research
  • Regulation of Appetite and Obesity

Scripps Research Institute
2015-2024

Torrey Pines Institute For Molecular Studies
2011-2022

Scripps (United States)
2022

Scripps Institution of Oceanography
2022

Dieting to control body weight involves cycles of deprivation from palatable food that can promote compulsive eating. The present study shows rats withdrawn intermittent access exhibit overeating upon renewed and an affective withdrawal-like state characterized by corticotropin-releasing factor-1 (CRF(1)) receptor antagonist-reversible behaviors, including hypophagia, motivational deficits obtain less food, anxiogenic-like behavior. Withdrawal was accompanied increased CRF expression CRF(1)...

10.1073/pnas.0908789106 article EN Proceedings of the National Academy of Sciences 2009-11-10

In the central amygdala (CeA), ethanol acts via corticotrophin-releasing factor (CRF) type 1 receptors to enhance GABA release. Amygdala CRF mediates anxiety associated with stress and drug dependence, it regulates intake. Because mutant mice that lack PKCε exhibit reduced anxiety-like behavior alcohol consumption, we investigated whether lies downstream of in CeA. Compared +/+ CeA neurons, −/− neurons showed increased GABAergic tone due enhanced stimulated release CeA, but not A...

10.1073/pnas.0802302105 article EN Proceedings of the National Academy of Sciences 2008-06-10

Toll-like receptor 4 (TLR4) is a critical component of innate immune signaling and has been implicated in alcohol responses preclinical clinical models. Members the Integrative Neuroscience Initiative on Alcoholism (INIA-Neuroimmune) consortium tested hypothesis that TLR4 mediates excessive ethanol drinking using following models: (1) Tlr4 knock-out (KO) rats, (2) selective knockdown mRNA mouse nucleus accumbens (NAc), (3) injection antagonist (+)-naloxone mice. Lipopolysaccharide (LPS)...

10.1523/jneurosci.2002-16.2016 article EN cc-by-nc-sa Journal of Neuroscience 2016-12-16

Abstract Background and Purpose Chronic pain is considered a key factor contributing to alcohol use disorder (AUD). The mechanisms responsible for chronic associated with consumption are unknown. We evaluated the development of in mouse model dependence investigate role neuroinflammation. Experimental Approach chronic‐intermittent ethanol two‐bottle choice CIE‐2BC paradigm generates three groups: alcohol‐dependent escalating intake, nondependent (moderate drinking) alcohol‐naïve control male...

10.1111/bph.16091 article EN cc-by-nc British Journal of Pharmacology 2023-04-13

Post-traumatic stress disorder (PTSD) and alcohol use (AUD) are often comorbid. Few treatments exist to reduce comorbid PTSD/AUD. Elucidating the mechanisms underlying their comorbidity could reveal new avenues for therapy. Here, we employed a model of PTSD/AUD, in which rats were subjected stressful shock familiar context followed by drinking. We then examined fear overgeneralization irritability these rats. Familiar elevated drinking, increased overgeneralization, alcohol-related...

10.1038/s41380-024-02514-8 article EN cc-by Molecular Psychiatry 2024-03-21

Neuroinflammation is hypothesized to enhance alcohol consumption and contribute the development of alcoholism. GABAergic transmission in central amygdala (CeA) plays an important role transition dependence. Therefore, we studied effects interleukin-1β (IL-1β), a proinflammatory cytokine mediating ethanol-induced neuroinflammation, its interaction with ethanol on CeA GABAegic B6129SF2/J mice. We also assessed intake Intake unlimited (24 h) access was 9.2-12.7 g/kg (3-15% ethanol), while...

10.3389/fphar.2015.00049 article EN cc-by Frontiers in Pharmacology 2015-03-19

Alcohol use disorder (AUD) is linked to hyperactivity of brain stress systems, leading withdrawal states which drive relapse. AUD differs among the sexes, as men are more likely have than women, but women progress from casual binge and heavy alcohol quickly relapse into repetitive episodes drinking. In dependence animal models AUD, central amygdala (CeA) functions a hub anxiety processing gamma-Aminobutyric acid (GABA)ergic signaling within CeA involved in dependence-induced increases...

10.1093/alcalc/agab034 article EN Alcohol and Alcoholism 2021-04-13

Abstract Prefrontal circuits are thought to underlie aberrant emotion contributing relapse in abstinence; however, the discrete cell-types and mechanisms remain largely unknown. Corticotropin-releasing factor its cognate type-1 receptor, a prominent brain stress system, is implicated anxiety alcohol use disorder (AUD). Here, we tested hypothesis that medial prefrontal cortex CRF1-expressing (mPFC CRF1+ ) neurons comprise distinct population exhibits neuroadaptations following withdrawal from...

10.1038/s41380-022-01642-3 article EN cc-by Molecular Psychiatry 2022-06-06

Excessive serotonin (5-HT) signaling plays a critical role in the etiology of alcohol use disorder. The central nucleus amygdala (CeA) is key player alcohol-dependence associated behaviors. CeA receives dense innervation from dorsal raphe nucleus, major source 5-HT, and expresses 5-HT receptor subtypes (e.g., 5-HT2C 5-HT1A) critically linked to Notably, regulating rat activity dependence poorly investigated. Here, we examined neuroadaptations adult, male Sprague Dawley rats using an...

10.1523/jneurosci.0733-20.2020 article EN Journal of Neuroscience 2020-08-07

The nucleus accumbens (NAcc) and central amygdala (CeA) are parts of the extended amygdala, a complex that plays key role in drug abuse dependence. Our previous studies showed opiates ethanol alter glutamatergic transmission these regions. N-methyl-D-aspartate (NMDA) receptors components likely involved development opiate tolerance In this study we examined effects chronic morphine administration on gene protein expression three major NMDA subunits (NR1, NR2A, NR2B) NAcc CeA. Real-time PCR...

10.1002/jnr.20756 article EN Journal of Neuroscience Research 2006-01-01

The endogenous cannabinoids (eCBs) influence the acute response to ethanol and development of tolerance, dependence relapse. Chronic alcohol exposure alters eCB levels Type 1 cannabinoid receptor (CB1) expression function in brain regions associated with addiction. CB1 inhibits GABA release, GABAergic dysregulation central nucleus amygdala (CeA) is critical transition dependence. We investigated possible disruptions signaling rat CeA transmission following intermittent exposure. In...

10.1111/adb.12256 article EN Addiction Biology 2015-05-05

Several lines of evidence support a critical role TLR4 in the neuroimmune responses associated with alcohol disorders and propose inhibitors signaling as potential treatments for alcoholism. In this work, we investigated effect T5342126 compound, selective inhibitor, on excessive drinking microglial activation ethanol dependence.We used 2BC-CIE (two-bottle choice-chronic intermittent vapor exposure) paradigm to induce dependence mice. After induction dependence, injected (i.p., 57 mg/kg) 14...

10.1093/alcalc/agw026 article EN Alcohol and Alcoholism 2016-05-05
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