ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
CRF-R2 and the heterosynaptic regulation of VTA glutamate during reinstatement of cocaine seeking.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 58 citations in OpenAlex.
- Translating stress systems: corticotropin releasing factor, its receptors, and the dopamine system in nonhuman primate models.Genomic psychiatry : advancing science from genes to society · 2025Article
- Cdk5-dependent rapid formation and stabilization of dendritic spines by corticotropin-releasing factor.Translational psychiatry · 2024Article
- Corticotropin releasing factor in the nucleus basalis of Meynert impairs attentional performance and reduces levels of glutamate and taurine in male and female rats.Neuropharmacology · 2022Article
- Corticotropin releasing factor and drug seeking in substance use disorders: Preclinical evidence and translational limitations.Addiction neuroscience · 2022Article
- Tripartite extended amygdala-basal ganglia CRH circuit drives locomotor activation and avoidance behavior.Science advances · 2022Article
- A subpopulation of oxytocin neurons initiate expression of CRF receptor 1 (CRFR1) in females post parturition.Psychoneuroendocrinology · 2022Article
- Type 1 Corticotropin-Releasing Factor Receptor Differentially Modulates Neurotransmitter Levels in the Nucleus Accumbens of Juvenile versus Adult Rats.International journal of molecular sciences · 2022Article
- Repeated cocaine or methamphetamine treatment alters astrocytic CRF2 and GLAST expression in the ventral midbrain.Addiction biology · 2022Article
- GABACurrent topics in behavioral neurosciences · 2022Article
- Chronic stress-induced synaptic changes to corticotropin-releasing factor-signaling in the bed nucleus of the stria terminalis.Frontiers in behavioral neuroscience · 2022Review
- Anatomy and Function of Ventral Tegmental Area Glutamate Neurons.Frontiers in neural circuits · 2022Review
- Social isolation of adolescent male rats increases anxiety and KThe European journal of neuroscience · 2021Article
- Neurochemical mechanisms and neurocircuitry underlying the contribution of stress to cocaine seeking.Journal of neurochemistry · 2021Review
- Functional Interplay of Type-2 Corticotrophin Releasing Factor and Dopamine Receptors in the Basolateral Amygdala-Medial Prefrontal Cortex Circuitry.The international journal of neuropsychopharmacology · 2021Article
- Cocaine experience abolishes the motivation suppressing effect of CRF in the ventral midbrain.Addiction biology · 2021Article
- Neurological correlates of brain reward circuitry linked to opioid use disorder (OUD): Do homo sapiens acquire or have a reward deficiency syndrome?Journal of the neurological sciences · 2020Review
- Inhibitory Control of Basolateral Amygdalar Transmission to the Prefrontal Cortex by Local Corticotrophin Type 2 Receptor.The international journal of neuropsychopharmacology · 2020Article
- Differential effects of novel kappa opioid receptor antagonists on dopamine neurons using acute brain slice electrophysiology.PloS one · 2020Article
- Alterations in effort-related decision-making induced by stimulation of dopamine DPsychopharmacology · 2019Article
- Urocortin 3 signalling in the auditory brainstem aids recovery of hearing after reversible noise-induced threshold shift.The Journal of physiology · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Stress can reinstate cocaine seeking through an interaction between the stress hormone corticotropin releasing factor (CRF) and glutamate release onto dopamine neurons in the ventral tegmental area (VTA). To better understand the underlying causes, synaptic mechanisms were investigated in brain slices from rats. In control tissue, EPSCs displayed concentration-dependent, bimodal responses to CRF potentiation at low concentrations (3-100 nm) and attenuation at higher concentrations (300 nm). EPSC potentiation and attenuation were mediated by CRF-R1 and CRF-R2 receptor subtypes, respectively, localized to presynaptic terminals. The CRF-R2 attenuation was blocked by the GABA-B receptor antagonist CGP55843. Additional recordings of GABA-A IPSCs showed CRF-R2 activation-facilitated presynaptic release of GABA, suggesting that CRF-R2 may regulate glutamate release via heterosynaptic facilitation of GABA synapses. After chronic cocaine self-administration and extinction training, the sensitivity of glutamate and GABA receptors was unchanged. However, the ability of CRF-R2 agonists to depress EPSCs and potentiate IPSCs was diminished. After yohimbine plus cue reinstatement, the actions of CRF-R2 on GABA and glutamate release were reversed. CRF-R2 activation increased EPSCs as a result of a reduction of tonic GABA-dependent inhibition. After reinstatement, application of the A1 adenosine antagonist 1,3-dipropyl-8-cyclopentylxanthine increased GABA tone to inhibit the CRF-R2 action. Blockade of GABA-B receptors prevented both the CRF-R2 increase in EPSCs and the attenuation produced by 1,3-dipropyl-8-cyclopentylxanthine. These studies demonstrate that presynaptic CRF-R1/R2 tightly regulate glutamate transmission in the VTA via a concerted, heterosynaptic manner that may become altered by stress-related pathologies, such as addiction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.