The effect of L-tryptophan on the food intake, rectal temperature, and blood metabolic parameters of 7-day-old chicks during feeding, fasting, and acute heat stress.

BACKGROUND: Exposure to a high ambient temperature (HT) can cause heat stress, which has a negative impact on physiological functions. L-tryptophan (L-Trp) as a precursor of serotonergic and kynurenine (Kyn) pathways, has a calmative effect during different stress statuses. AIMS: This study was carried out to determine the influence of intraperitoneal injection of Trp on feeding behavior, rectal temperature, and some blood parameters in the heat stress condition. METHODS: L-tryptophan (25 and 50 mg/kg body weight, BW) was administered intraperitoneally during either HT (39°C) or control temperature (CT; 31°C) for 5 h whilst fed or fasted in 7-day-old chicks. RESULTS: L-tryptophan caused elevation in decreased food intake and significantly decreased rectal temperature during acute heat stress at the dose of 50 mg/kg BW. Rectal temperature reduced in the fasted state at the dose of 50 mg/kg BW, and at the dose of 25 mg/kg BW Trp in the fed state in comparison with the other experimental groups. Reduction of serum glucose, triglyceride, and corticosterone levels was seen during the fed state. L-tryptophan had a significant reducing effect on the serum corticosterone level in the fasted state in comparison with the fed state, and also revealed a significant decline at the dose of 25 mg/kg BW on the elevated serum corticosterone under heat stress. CONCLUSION: Administration of L-tryptophan leads to increase cumulative food intake and decrease rectal temperature during heat stress. Also, L-Trp causes to decline increased serum corticosterone level under heat stress and fasted state. These findings indicated the potential regulator role of Trp to modulate stress response in heat-exposed chicks.

The effect of central administration of alpha-pinene on capsaicin-induced dental pulp nociception.

AIM: To assess the effects of central administration of α-pinene alone and in combination with either bicuculline or naloxone, as GABAA and µ-opioid receptor antagonists, respectively, on capsaicin-induced dental pulp stimulation in rats. METHODOLOGY: Forty-eight adult male Wistar rats aged 2 months (230-270 g) were cannulated via their lateral ventricles for the central administration of the drugs. α-Pinene was injected at 0.1, 0.2 and 0.4 µmol L-1 . Then, dental pulp stimulation was induced by intradental application of capsaicin solution (100 µg), and nociceptive scores were recorded for up to 40 min. For investigation of the anti-inflammatory effects of α-pinene, expression of COX-2 in the subnucleolus caudalis (Vc) of rats was determined using immunofluorescence staining. Nonparametric repeated measure Friedman and Kruskal-Wallis tests as well as parametric one-way analysis of variance were used for the statistical analysis. RESULTS: α-Pinene at 0.2 and 0.4 µmol L-1 was able to decrease capsaicin-induced nociception. Moreover, there was a significant increase in the expression of COX-2-positive cells in the Vc of capsaicin-treated rats (P < 0.01). This effect was prohibited by α-pinene (0.4 µmol L-1 ). Co-administration of bicuculline (1 µg per rat) or naloxone (6 µg per rat) with α-pinene (0.4 µmol L-1 ), however, prevented the inhibitory effects of α-pinene on both capsaicin-induced pulp nociception and COX-2 over-expression. CONCLUSIONS: Pinene exhibited significant curable effects on capsaicin-induced pulpal nociception and inflammation mainly via pharmacological interfacing with GABAA and µ-opioid receptors.

Activation of orexin-1 receptors in the ventrolateral periaqueductal grey matter (vlPAG) modulates pulpal nociception and the induction of substance P in vlPAG and trigeminal nucleus caudalis.

AIM: To characterize the role of orexin-1 receptors (OX1Rs) in ventrolateral periaqueductal grey matter (vlPAG) on modulation of capsaicin-induced pulpal nociception in rats. METHODOLOGY: Sixty-six adult male Wistar rats (2 months old) weighing between 230 and 260 g were used. The animals were cannulated for microinjection of drugs into the vlPAG matter. Pulpalgia was induced by intradental application of capsaicin solution (100 µg) into the incisor teeth of the rats. Ten min prior to capsaicin application, orexin-A (50, 100 and 150 pmol L-1 per rat) was administered. Orexin-A (150 pmol L-1 ) was also co-administrated with SB-334867 (40 nmol L-1 per rat), an OX1Rs antagonist; or bicuculline (1 µg per rat), a GABAA receptors antagonist. Moreover, treatment effects on the release of pro-nociceptive modulator substance P (SP) in vlPAG and trigeminal nucleus caudalis (Vc) of rats were explored using an immunofluorescence technique. One-way analysis of variance was used for the statistical analysis. RESULTS: Orexin-A dose-dependently decreased capsaicin-induced nociceptive behaviour. However, SB-334867 (40 nmol L-1 per rat) pretreatment (P < 0.05), but not bicuculline (1 µg per rat), attenuated the analgesic effect of orexin-A (150 pmol L-1 ). The level of SP was significantly increased in Vc and decreased in vlPAG of capsaicin-treated rats (P < 0.05). Capsaicin-induced changes in SP levels, however, were prohibited by orexin-A treatment (150 pmol L-1 ) (P < 0.05). CONCLUSIONS: Orexin-A administration into the vlPAG was associated with an inhibitory effect on capsaicin-induced pulpal nociception and bidirectional effects on the induction of SP in vlPAG and Vc of rats. Central activation of OX1Rs is a potential therapeutic tool for pulpalgia.

Orexin-1 receptors in the rostral ventromedial medulla are involved in the modulation of capsaicin evoked pulpal nociception and impairment of learning and memory.

AIM: To investigate the role of rostral ventromedial medulla orexin-1 receptors in the modulation of orofacial nociception as well as nociception-induced learning and memory impairment in adult male rats. METHODOLOGY: Pulpal nociception was induced by intradental application of capsaicin (100 µg) into the incisors of rats. Orexin-1 receptors agonist (orexin-A, 10, 25 and 50 pmol L-1  rat-1 ) and antagonist (SB-334867-A, 40 and 80 nmol L-1  rat-1 ) were microinjected into the rostral ventromedial medulla prior to capsaicin administration. Total time spent on nocifensive behaviour was recorded by direct visualization of freely moving rats whilst learning and memory were evaluated by the Morris water maze test. One-way analysis of variance and repeated-measures were used for the statistical analysis. RESULTS: Capsaicin-treated rats had a significant increase of nocifensive behaviours (P < 0.001), as well as learning and memory impairment (P < 0.001). However, intraventromedial medulla prior micro-injection of orexin-A (50 pmol L-1  rat-1 ) significantly reduced the nociceptive behaviour (P < 0.001). This effect was blocked by pre-treatment with SB334867-A (80 nmol L-1  rat-1 ). Orexin-A (50 pmol L-1  rat-1 ) also inhibited nociception-induced learning and memory deficits. Moreover, administration of SB-334867-A (80 nmol L-1  rat-1 ) plus orexin-A (50 pmol L-1  rat-1 ) had no effect on learning and memory deficits induced by capsaicin. CONCLUSIONS: The data suggest that rostral ventromedial medulla orexin-A receptors are involved in pulpal nociceptive modulation and improvement of learning and memory deficits induced by intradental application of capsaicin.

Tetracycline-regulated expression of OLIG2 gene in human dental pulp stem cells lead to mouse sciatic nerve regeneration upon transplantation.

Numerous studies have indicated dental pulp stem cells (DPSCs) potency to differentiate into several types of cell lineages. Oligodendrocyte lineage transcription factor 2 (OLIG2) plays an important role in the oligodendrogenic pathway. In this study, a tetracycline (Tet)-inducible system expressing OLIG2 gene was transfected into human DPSCs to direct their differentiation toward oligodendrocyte progenitor cells (OPCs). Following induction, the expression of stage-specific markers was studied by Reverse Transcription quantitative Polymerase Chain Reaction (RT-qPCR), immunocytochemistry and western blotting. In the following, the cells were transplanted into the mouse model of local sciatic demyelination damage by lysolecithin. Recovery of lysolecithin-induced lesions in sciatic nerve was studied by treadmill exercise, von Frey filament test and hind paw withdrawal in response to a thermal stimulus. Improvement of behavioral symptoms was efficiently observed from the second week to the sixth week post-transplantation. Our findings showed that exogenous expression of the OLIG2 gene by a Tet-regulated system could be used as an efficient way to induce the differentiation of DPSCs into functional oligodendrocytes. Meanwhile, the DPSC-derived OPCs have relevant therapeutic potential in the animal model of sciatic nerve injury and therefore might represent a valuable tool for stem cell-based therapy in inflammatory and degenerative diseases of the peripheral and central nervous systems (CNSs).