Crucial role of prostaglandin D In urethane‐anesthetized rats, CGS21680 inhibited histamine release in both the frontal cortex and medial pre‐optic area in a dose‐dependent manner, and increased GABA release specifically in the histaminergic tuberomammillary nucleus but not in the frontal cortex.
Affiliation:Department of Molecular Behavioral Biology, Osaka Bioscience Institute, 6-2-4 Furuedai, Suita, Osaka 565-0874, Japan. 5, without CGS21680 infusion, the picrotoxin perfusion of the TMN increased the histamine release in the FrCx in a dose‐dependent manner. Because the GABA antagonist blocked the CGS21680‐induced inhibition of histamine release in a dose‐dependent manner (Fig. The fluorescence detector (Hitachi, Tokyo, Japan) was set at 340 and 445 nm wavelengths for excitation and emission, respectively. Because the GABA antagonist blocked the CGS21680‐induced inhibition of histamine release in a dose‐dependent manner (Fig. 2001, 2003). 1. 2002; Dere et al. Influence of age, body temperature, GABAA receptor inhibition and caffeine on the Hering–Breuer inflation reflex in unanesthetized rat pups.
All other chemicals were of analytical grade. Glutamate Activates the Histaminergic Tuberomammillary Nucleus and Increases Wakefulness in Rats. (1999) found that infusion of CGS21680 into the subarachnoid space induced the largest increases in non‐REM and REM sleep, which were accompanied by intense c‐Fos expression in the VLPO (Scammell et al. receptors regulate the activity of sleep regulatory GABAergic neurons in the preoptic hypothalamus The A2AR plays a predominant role in the somnogenic effects of PGD2. Highlights on the Development of A2A Adenosine Receptor Agonists and Antagonists. Handbook of Contemporary Neuropharmacology. 1999). The inhibition of histamine release was observed in several brain regions, whereas a concomitant increase in GABA release was found only specifically in the TMN, where histaminergic neurons are located, but not in the FrCx (Fig. Here we used electroencephalogram and electromyogram recordings coupled with in vivo microdialysis to investigate the effects of an A2AR agonist, CGS21680, on sleep and on the release of histamine and GABA in the brain. In all cases, p < 0.05 was taken as the level of significance. The short and long solid bars indicate the duration of CGS21680 infusion and picrotoxin perfusion, respectively. Post‐operatively, each rat was allowed 10 days of recovery and was then transferred to a sound‐proof recording chamber where it was connected to an EEG/EMG recording cable for a 3‐day period of habituation to the experimental conditions.
These findings indicate that the VLPO is an important GABAergic source to inhibit the histaminergic neurons in the TMN.
These results suggest that CGS21680 increased GABA release in a TMN‐specific manner. To clarify the role of GABA release in the TMN in the CGS21680‐induced inhibition of histamine release, we perfused the TMN with the GABA receptor antagonist picrotoxin at doses of 100 and 200 pmol/min and monitored the histamine release in the FrCx with and without CGS21680 infusion into the SS‐rBF. However, the infusion of CGS21680 significantly increased GABA release in the TMN in a dose‐dependent manner. These findings suggest that a decrease in histaminergic transmission contributed to the sleep promoted by the A2AR agonist. Sleep regulation through adenosine neurotransmitter system. A functional genetic variation of adenosine deaminase affects the duration and intensity of deep sleep in humans, https://doi.org/10.1111/j.1471-4159.2004.02991.x, subarachnoid space underlying the rostral basal forebrain. On the other hand, inhibition of wake-promoting neurons via the A1R also mediates the sleep-inducing effects of adenosine, whereas activation of A1R in the lateral preoptic area induces wakefulness, suggesting that A1R regulates the sleep-wake cycle in a site-dependent manner. 1989) and rats (Nelson et al. TRPV1 channels in the nucleus of the solitary tract mediate thermal prolongation of the LCR in decerebrate piglets. By use of genemanipulated mice, the arousal effect of caffeine was shown to be dependent on the A2AR. 2(a), when the vehicle was infused, the extracellular histamine level was high; and the time spent in non‐REM and REM sleep was low, similar to those we found in freely moving rats without any treatments (Chu et al. Complement C5a exhibits anxiolytic-like activity via the prostaglandin D2−DP1 receptor system coupled to adenosine A2A and GABAA receptors. 1999). Different patterns of neural activity in the brain control the sleep-wake cycle. . 1991), and hyperpolarization of the TMN with GABAergic agonists in cats (Lin et al. monitored adenosine concentration in the mouse basal forebrain.
TRPV1 channels in the nucleus of the solitary tract mediate thermal prolongation of the LCR in decerebrate piglets.
Role of histamine H 1 receptor in caffeine induced locomotor sensitization.
Gating and the Need for Sleep: Dissociable Effects of Adenosine A1 and A2A Receptors. The horizontal solid bar indicates the duration of vehicle or CGS21680 infusion. 1999). 1992), the GABA‐synthesizing enzyme glutamic acid decarboxylase (Senba et al.
Adenosine is a neurochemical which you know best from your morning cup of coffee. 4(d), CGS21680 at 2.5 and 5 pmol/min increased the release with the maximal magnitude being about 185% and 243% of the control, respectively; and then the GABA level gradually returned to the basal level. When an experiment was over, rats were killed with an overdose of pentobarbital sodium and injected through the implanted cannula, or perfused through the microdialysis probes with a microquantity of pontamine sky‐blue dye solution (0.5% wt/vol) to verify the site of cannula placement for CGS21680 administration, and the sites of microdialysis probes implanted in the FrCx, MPO, and TMN. Use the link below to share a full-text version of this article with your friends and colleagues. Chapter 2.5 Microdialysis as a platform for multidisciplinary strategies. The GABA released in the TMN may originate from the VLPO.
1985; Huang et al. Adenosine role in brain functions: Pathophysiological influence on Parkinson's disease and other brain disorders. receptors regulate the activity of sleep regulatory GABAergic neurons in the preoptic hypothalamus Two stainless steel wire electrodes were placed into the neck muscles for EMG recordings. Adenosinergic Control of Sleep/Wake Behavior. Morphine Inhibits Sleep-Promoting Neurons in the Ventrolateral Preoptic Area Via Mu Receptors and Induces Wakefulness in Rats. Correlation of extracellular level of histamine in the FrCx with time spent in wakefulness (a), non‐REM (b), and REM (c) sleep during the 6‐h CGS21680 infusion and 3 h after the infusion in rats.
The dialysates were kept at − 20°C until they could be assayed by HPLC‐fluorometry for histamine or GABA.
1995). The vigilance states were automatically classified off‐line by 10‐s epochs, into wakefulness, non‐REM sleep, and REM sleep by SLEEPSING software, according to the standard criteria (Huang et al. Each value represents the mean ± SEM of five or six rats. Abstract. Adenosine A2A receptors in ventral striatum, hypothalamus and nociceptive circuitry. Handbook of Contemporary Neuropharmacology. Statistical analyses were performed by use of Student's t‐test. Proceedings of the National Academy of Sciences. Caffeine promotes glutamate and histamine release in the posterior hypothalamus. Glutamate Activates the Histaminergic Tuberomammillary Nucleus and Increases Wakefulness in Rats. The endogenous somnogen prostaglandin (PG) D2 increases the extracellular level of adenosine under the subarachnoid space of the basal forebrain and promotes physiological sleep.
1996, 1998, 1999; Gerashchenko et al. Effects of CGS21680 on the histamine release in the FrCx (a) and MPO (b) as well as on the GABA release in the FrCx (c) and TMN (d) in anesthetized rats.
The extracellular concentration of adenosine increases in the cortex and basal forebrain during prolonged wakefulness and decreases during the sleep recovery period. Neuroanatomically, the shell and rostral pole of the nucleus accumbens project efferents to putative state‐regulatory regions including the VLPO (Chou et al. 2A
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