Ethanol concentration-dependent effects and the role of stress on ethanol drinking in corticotropin-releasing factor type 1 and double type 1 and 2 receptor knockout mice.

Rationale: Exposure to stressors promotes ethanol (EtOH) consumption and enhances drug craving during abstinence. Corticotropin-releasing factor (CRF), and in particular, CRF actions via type 1 CRF receptors (CRF(1)) are critical in behavioral responses to stressors. CRF(1) play a role in EtOH-induced behavioral neuroadaptation, in binge-like EtOH consumption, and in heightened EtOH consumption in dependent animals.

A comparison of the physiological exercise intensity differences between shod and barefoot submaximal deep-water running at the same cadence.

The purpose of this investigation was to identify whether physiological exercise intensity differed with the use of aquatic training shoes (ATS) during deep-water running (DWR) compared to using a barefoot condition. Eight male intercollegiate (National Collegiate Athletic Association Division III [NCAA III]) varsity distance runners were videotaped from the right sagittal view while running on a treadmill (TR) and while barefoot in deep water at 60-70% of their TR VO2max for 30 minutes. Based on the stride rate of the barefoot DWR trial, a subsequent 30-minute session was completed while wearing ATS.

Corticotropin-releasing factor-1 receptor involvement in behavioral neuroadaptation to ethanol: a urocortin1-independent mechanism.

A common expression of neuroadaptations induced by repeated exposure to addictive drugs is a persistent sensitized behavioral response to their stimulant properties. Neuroplasticity underlying drug-induced sensitization has been proposed to explain compulsive drug pursuit and consumption characteristic of addiction. The hypothalamic-pituitary-adrenal (HPA) axis-activating neuropeptide, corticotropin-releasing factor (CRF), may be the keystone in drug-induced neuroadaptation.

Endotoxin preconditioning protects against the cytotoxic effects of TNFalpha after stroke: a novel role for TNFalpha in LPS-ischemic tolerance.

Lipopolysaccharide (LPS) preconditioning provides neuroprotection against subsequent cerebral ischemic injury. Tumor necrosis factor-alpha (TNFalpha) is protective in LPS-induced preconditioning yet exacerbates neuronal injury in ischemia. Here, we define dual roles of TNFalpha in LPS-induced ischemic tolerance in a murine model of stroke and in primary neuronal cultures in vitro, and show that the cytotoxic effects of TNFalpha are attenuated by LPS preconditioning.

Mice deficient in corticotropin-releasing factor receptor type 2 exhibit normal ethanol-associated behaviors.

Background: Stress is believed to influence alcohol use and relapse in alcoholics. Animal studies suggest an interaction between corticotropin-releasing factor (CRF) and its receptors and the behavioral effects and consumption of alcohol. The objective of these studies was to examine the effect of corticotropin-releasing factor receptor type 2 (CRF2) on ethanol consumption, conditioned taste aversion, sedation, and hypothermia.

Corticotropin-releasing factor overexpression decreases ethanol drinking and increases sensitivity to the sedative effects of ethanol.

Rationale: Corticotropin-releasing factor (CRF) may play a significant role in drug and alcohol abuse.

Objective: To evaluate the role of CRF in these processes, we examined several ethanol (EtOH) related behaviors in mice that carry a transgene that causes overexpression of CRF.

Methods: We examined voluntary EtOH drinking, loss of the righting reflex (LORR), EtOH-induced conditioned taste aversion (CTA), and EtOH clearance in littermate transgenic (TG) and non-transgenic (non-TG) mice.

Activation of the CRF 2 receptor modulates skeletal muscle mass under physiological and pathological conditions.

Two receptors activated by the corticotropin-releasing factor (CRF) family of peptides have been identified, the CRF 1 receptor (CRF1R) and the CRF 2 receptor (CRF2R). Of these, the CRF2R is expressed in skeletal muscle. To understand the role of the CRF2R in skeletal muscle, we utilized CRFR knockout mice and CRF2R-selective agonists to modulate nerve damage and corticosteroid- and disuse-induced skeletal muscle atrophy in mice.

Corticotropin-releasing hormone-related peptides and receptors: emergent regulators of cardiovascular adaptations to stress.

Since its discovery 2 decades ago, potent effects of corticotropin-releasing hormone (CRH) on the heart and vasculature have been consistently observed. The recent discoveries of novel CRH-related peptides residing in the heart and a distinct cardiac CRH receptor (CRH-R2), have renewed interest in the role of the CRH family on cardiovascular function. This review highlights the emerging view of a peripheral, cardiac CRH system and its potential relevance in mediating the adaptive response of the heart to stress.