Environmental enrichment reverses proulcerogenic action of social isolation on the gastric mucosa and positively influences pain sensitivity and work capacity.

The aim of the study was to investigate the effects of rat housing conditions-standard conditions, social isolation, environmental enrichment-and the subsequent reversal of these conditions on the vulnerability of the gastric mucosa to ulcerogenic stimuli, somatic pain sensitivity, and treadmill work capacity. Rats, aged 30 days, were placed in standard conditions (SC), social isolation (Is), and environmental enrichment (EE) for 4 weeks. Then half of each group underwent a reversal of housing conditions: SC rats were moved to Is, Is rats were placed in EE, EE rats were moved to Is, for 2 weeks.

Peripheral corticotropin-releasing hormone may protect the gastric musosa against indometacin-induced injury through involvement of glucocorticoids.

The hypothalamic-pituitary-adrenocortical (HPA) system is a key hormonal branch of the brain-gut axis in stress and corticotropin-releasing hormone (CRH) is a principal stimulator of the HPA system. According to our finding activation of the HPA system has gastroprotective role in stress and CRH may protect the gastric mucosa against stress-induced injury through involvement of glucocorticoids. To extend this idea to indomethacin-induced gastric injury in the present work we studied whether CRH may protect the gastric mucosa against ulcerogenic action of indomethacin (IM) through involvement of glucocorticoids.

Non-Invasive Remote Ischemic Preconditioning May Protect the Gastric Mucosa Against Ischemia-Reperfusion-Induced Injury Through Involvement of Glucocorticoids.

Remote ischemic preconditioning (RIPC) is one of the most effective approaches to attenuate tissue injury caused by severe ischemia-reperfusion (I/R). Experimental studies have demonstrated that RIPC is capable of producing a protective effect not only on heart, but also on brain, lungs, kidneys, liver, intestine, and stomach. We previously demonstrated that glucocorticoids participate in protective effect of local gastric ischemic preconditioning against I/R-induced gastric injury.

Influence of forced treadmill and voluntary wheel running on the sensitivity of gastric mucosa to ulcerogenic stimuli in male rats.

Physical activity is crucial for maintaining health. Here we investigated the preconditioning effects of exercise on the vulnerability of gastric mucosa to ulcerogenic action of indomethacin (IM, 35 mg/kg, s.c.

Physiological and Pharmacological Effects of Glucocorticoids on the Gastrointestinal Tract.

The review considers the data on the physiological and pharmacological effects of glucocorticoids on the gastric mucosa and focuses on the gastroprotective role of stress-produced glucocorticoids as well as on the transformation of physiological gastroprotective effects of glucocorticoids to pathological proulcerogenic consequences. The results of experimental studies on the re-evaluation of the traditional notion that stress-produced glucocorticoids are ulcerogenic led us to the opposite conclusion suggested that these hormones play an important role in the maintenance of the gastric mucosal integrity. Exogenous glucocorticoids may exert both gastroprotective and proulcerogenic effects.

Effects of stress preconditioning on vulnerability of gastric and small intestinal mucosa to ulcerogenic action of indomethacin in rats.

The preconditioning effect of a mild stressor can reduce the ulcerogenic effect of a severe stressor on the gastric mucosa. The aim of the study was to investigate the effect of preconditioning stress on the gastric and the small intestinal injury caused by a single injection of indomethacin (IM) in conscious rats. Preliminary fasting (24 hours) rats were subjected IM administration (35 mg/kg, subcutaneously) with preconditioning stress (30 min cold-restraint at 10°C and further 1 hour keeping in cages at room temperature) or without stress.

Vulnerability of gastric and small intestinal mucosa to ulcerogenic action of indomethacin in C57/BL6/J mice and transient receptor potential channel vanilloid type 1 knockout mice.

Capsaicin-sensitive sensory nerves are densely distributed in the gastrointestinal system and involved in maintenance of gastrointestinal mucosal integrity. capsaicin selectively stimulates nociceptive neurons and its action is mediated through the transient receptor potential channel vanilloid type 1 (TRPV1) receptor. Activation TRPV1 receptors that play a fundamental role in pain signaling, may also exert protective effects against gastrointestinal injury.

The peripheral corticotropin-releasing factor (CRF)-induced analgesic effect on somatic pain sensitivity in conscious rats: involving CRF, opioid and glucocorticoid receptors.

The corticotropin-releasing factor (CRF) is involved in somatic pain regulation and may produce an analgesic effect in humans and animals, although the mechanisms of the CRF-induced analgesia remain unclear. CRF action is mediated by the CRF receptors of subtypes 1 and 2 (CRF-R1 and CRF-R2, respectively). Activation of the hypothalamic -pituitary -adrenocortical axis (HPA) is provided by CRF-R1; but CRF-R2 are also involved in the regulation of the HPA axis, and, respectively, glucocorticoids, the end hormones of the HPA axis, also participate in somatic pain regulation.

Involvement of corticotropin-releasing factor receptors type 2, located in periaquaductal gray matter, in central and peripheral CRF-induced analgesic effect on somatic pain sensitivity in rats.

Corticotropin-releasing factor (CRF) is involved in the regulation of pain sensitivity and can induce an analgesic effect in animals and humans. The periaqueductal gray matter (PAGM) of the midbrain is one of the key structures of the antinociceptive system. The aim of the study was to investigate the involvement of CRF receptor type 2 (CRF-R2 receptors), localized in the PAGM, in the analgesic effect caused by central or systemic CRF on somatic pain sensitivity in conscious rats.

[Role of the Periaqueductal Gray Matter of the Midbrain in Regulation of Somatic Pain Sensitivity During Stress: Participation of Corticotropin-Releasing Factor and Glucocorticoid Hormones].

Periaqueductal gray matter of the midbrain (PAGM) plays a crucial role in the regulation of pain sensitivity under stress, involving in the stress-induced analgesia. A key hormonal system of adaptation under stress is the hypothalamic-pituitary-adrenocortical (HPA) axis. HPA axis's hormones, corticotropin-releasing factor (CRF) and glucocorticoids, are involved in stress-induced analgesia.

Effect of glucocorticoid receptor blockade on analgesic effect of corticotropin-releasing factor.

The role of glucocorticoid receptors in the analgesic effect of corticotropin-releasing factor in rats was studied after glucocorticoid receptor blockade with antagonist RU 38486. Glucocorticoid hormones can potentiate the analgesic effect of corticotropin-releasing factor or modulate the mechanisms of this effect, which depends on the type of painful stimulus.

Central corticotropin-releasing factor (CRF) may attenuate somatic pain sensitivity through involvement of glucocorticoids.

Corticotropin-releasing factor (CRF) is an important regulator of physiological functions and behavior in stress. Analgesia is one of the characteristics of stress reaction and CRF is involved in providing stress-induced analgesia, however, the underlying mechanisms remain to be determined. Exogenous CRF mimics stress effects on pain sensitivity and causes analgesic effect.

Analgesic actions of corticotropin-releasing factor (CRF) on somatic pain sensitivity: involvement of glucocorticoid and CRF-2 receptors.

The aim of the present work was to study the involvement of glucocorticoid receptors and corticotropin-releasing factor type 2 receptors (CRF-2 receptors) in mediating the analgesic effects of CRF on somatic pain sensitivity. The involvement of glucocorticoid and CRF-2 receptors in the development of analgesia evoked by systemic administration of CRF was studied by blockade of these receptors by their specific antagonists RU 38486 and astressin 2-B, respectively, in anesthetized rats. Pain sensitivity was tested before and 30 min after administration of CRF in terms of the threshold of the pain reaction induced by stimulation of the rat's tail with an electric current.

The role of hypothalamo-hypophyseal-adrenocortical system hormones in controlling pain sensitivity.

The present review addresses analysis of data demonstrating the role of the hypothalamo-hypophyseal-adrenocortical axis (HHACA) in controlling pain sensitivity. Experiments on rats have demonstrated the analgesic effects of exogenous hormones of all components of the HHACA - corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and glucocorticoids - in the same models, and have also shown that the opioid and non-opioid mechanisms contribute to the development of the analgesia induced by these hormones. Endogenous glucocorticoids are involved in the development of analgesia mediated by non-opioid mechanisms.

The role of the hormones of the hypothalamo-hypophyseal-adrenocortical system in the analgesic effect of corticotropin-releasing hormone.

Experiments on anesthetized male rats were performed to study the role of the hormones of the hypothalamo-hypophyseal-adrenocortical system (HHACS) in analgesia induced by central or systemic administration of corticoliberin-releasing hormone (CRF). Studies of the contribution of HHACS hormones were performed by blocking HHACS function by administration of hydrocortisone at a pharmacological dose one week before experiments started. Blockade of HHACS function, resulting in the inability of the system to increase hormone levels, resulted in a decrease in the analgesic effect resulting from systemic administration of CRF and completely abolished the analgesic effect after central administration of CRF.

Analgesic effect of corticotropin-releasing hormone: involvement of the hypothalamic-pituitary-adrenocortical axis into its realization.

Involvement of hypothalamic-pituitary-adrenocortical axis into the analgesic effect of corticotropin-releasing hormone after its systemic administration was studied in experiments on rats. Pharmacological blockade of the hypothalamic-pituitary-adrenocortical axis decreased the duration and degree of the analgesic effect of corticotropin-releasing hormone. This analgesic effect can be mediated via two pathways: related to hormones of the hypothalamic-pituitary-adrenocortical axis and independent of these hormones.

Somatic pain sensitivity during formation and healing of acetic acid-induced gastric ulcers in conscious rats.

A classical feature of visceral pain is its referring to somatic locations. Gastric ulcer is a source of visceral pain. In the present study we investigated whether gastric ulcers may trigger the changes in somatic nociception.

The role of adrenocorticotropic hormone in the inhibition of pain reactions in conscious rats.

Experiments on conscious male Sprague-Dawley rats were performed to study the effects of adrenocorticotropic hormone (ACTH) on pain reactions. Pain sensitivity was assessed in terms of the latent period of tail withdrawal in response to heat. Systemic administration of ACTH and glucocorticoids to animals with normal levels of hormone production led to increases in the latent period of the tailflick reaction.

Mechanisms of the effects of adrenocorticotropic hormone on pain sensitivity in rats.

Experiments on anaesthetized male Sprague-Dawley rats were performed to study the effects of adrenocorticotropic hormone (ACTH) on pain sensitivity. Systemic administration of ACTH to animals with normal hormone production induced rapidly developing (starting at 3 min) and prolonged (30 min) increases in pain response thresholds. Blockade of opiate receptors led to suppression of the initial stage of the analgesic effect of ACTH: the response was seen only from 15 to 30 min.

Effect of ACTH on pain sensitivity in rats.

Systemic administration of ACTH to rats with normal hormone production induced a rapid (started 3 min postinjection) and long-term (persisted 30 min) elevation of pain threshold. Complete inhibition of glucocorticoid production shortened the duration of ACTH-induced analgesia to 15 min. The biphasic effect of ACTH on pain sensitivity is probably mediated by short-term glucocorticoid-independent and long-term glucocorticoid-dependent mechanisms.

Stress-induced analgesia. The role of hormones produced by the hypophyseal-adrenocortical system.

Experimental studies on the effects of stress on blood corticosteroid levels and the appearance of analgesia were carried out on rats anesthetized with Nembutai (4 mg/100 g). Stress, consisting of stimulation of the hind footpad with a current at 0.7 mA, produced parallel changes in plasma corticosteroid concentrations and the threshold of a pain response.

Corticosteroid feedback: II. Role of hypothalamus and hypophysis.

The role of the paraventricular nucleus (PVN) of the hypothalamus and the hypophysis in ensuring the corticosteroid feedback of the pituitary-adrenocortical system (PACS) in rats was characterized by administration of increasing doses of hydrocortisone. The doses 100, 300 and 1200 micrograms/100 g b.w.