Adverse Effect of Air Pollution on Odor Perception

status: publishe

Administration of URB597, Oleoylethanolamide or Palmitoylethanolamide Increases Waking and Dopamine in Rats

-acylethanolamines or acylethanolamides. The hydrolysis of OEA and PEA is catalyzed by the fatty acid amide hydrolase (FAAH). A number of FAAH inhibitors that increase the levels of OEA and PEA in the brain have been developed, including URB597. In the present report, we examined whether URB597, OEA or PEA injected into wake-related brain areas, such as lateral hypothalamus (LH) or dorsal raphe nuclei (DRN) would promote wakefulness (W) in rats.Male Wistar rats (250–300 g) were implanted for sleep studies with electrodes to record the electroencephalogram and electromyogram as well as a cannulae aimed either into LH or into DRN. Sleep stages were scored to determine W, slow wave sleep (SWS) and rapid eye movement sleep (REMS). Power spectra bands underly neurophysiological mechanisms of the sleep-wake cycle and provide information about quality rather than quantity of sleep, thus fast Fourier transformation analysis was collected after the pharmacological trials for alpha (for W; α = 8–12 Hz), delta (for SWS; δ = 0.5–4.0 Hz) and theta (for REMS; θ = 6.0–12.0 Hz). Finally, microdialysis samples were collected from a cannula placed into the nucleus accumbens (AcbC) and the levels of dopamine (DA) were determined by HPLC means after the injection of URB597, OEA or PEA. We found that microinjection of compounds (10, 20, 30 µg/1 µL; each) into LH or DRN during the lights-on period increased W and decreased SWS as well as REMS and enhanced DA extracellular levels.URB597, OEA or PEA promoted waking and enhanced DA if injected into LH or DRN. The wake-promoting effects of these compounds could be linked with the enhancement in levels of DA and indirectly mediated by anandamide

Adrenal Medullary Grafts Restore Olfactory Deficits and Catecholamine Levels of 6-OHDA Amygdala Lesioned Animals

Aside from motor and cognitive deficits, Parkinson patients also manifest a little-studied olfactory deficit. Since in Parkinson's disease there is a dopamine depletion of the amygdala due to mesocorticolimbic system degeneration, we decided to test olfactory and taste performance of 6-OHDA amygdala lesioned rats, as well as the possible restoration of either function with adrenal medullary transplants

La radioquímica de la [18-F]-FDG: la primera experiencia en México

El presente trabajo describe el método para la síntesis de la 2-[18F]-flúor-2-desoxi-D-glucosa, el radiofármaco de mayor uso en medicina nuclear para el diagnóstico del cáncer. El proceso consiste en dos reacciones químicas: i) [18F-]-radiofluoración nucleofílica y ii) una hidrólisis catalizada por ácido. La primera reacción incorpora al [18F]-flúor marcado dentro del precursor orgánico 1,3,4,6-tetra-O-acetil-2-O-trifluorometanosulfonilo-β-D-manopiranosa (triflato de manosa). El mecanismo de esta reacción es una sustitución nucleofílica bimolecular ( SN2) con el ion [18F-]-fluoruro; en la segunda reacción, la hidrólisis ácida de los grupos acetilos genera los grupos hidroxilos libres en la [18F]-FDG. El proceso incluye una destilación azeotrópica y varios pasos de purificación

Vol. 10, Núm. 2 (2012)

La narcolepsia es una enfermedad crónica neurodegenerativa,caracterizada por una regulación anormaldel ciclo vigilia-sueño (CVS), la cual cursa conexcesiva somnolencia diurna (ESD) y manifestacionesanormales del sueño REM (cataplejia, parálisisdel sueño y alucinaciones hipnagógicas y/o hipnopómpicas).Los mecanismos centrales de controldel CVS están alterados en la narcolepsia, teniendouna función crucial en su fisiopatología el hipotálamo,y concretamente el sistema orexinérgico

Cannabidiol, a constituent of Cannabis sativa, modulates sleep in rats

AbstractΔ9-tetrahydrocannabinol (Δ9-THC) and cannabidiol (CBD) are two major constituents of Cannabis sativa. Δ9-THC modulates sleep, but no clear evidence on the role of CBD is available. In order to determine the effects of CBD on sleep, it was administered intracerebroventricular (icv) in a dose of 10μg/5μl at the beginning of either the lights-on or the lights-off period. We found that CBD administered during the lights-on period increased wakefulness (W) and decreased rapid eye movement sleep (REMS). No changes on sleep were observed during the dark phase. Icv injections of CBD (10μg/5μl) induced an enhancement of c-Fos expression in waking-related brain areas such as hypothalamus and dorsal raphe nucleus (DRD). Microdialysis in unanesthetized rats was carried out to characterize the effects of icv administration of CBD (10μg/5μl) on extracellular levels of dopamine (DA) within the nucleus accumbens. CBD induced an increase in DA release. Finally, in order to test if the waking properties of CBD could be blocked by the sleep-inducing endocannabinoid anandamide (ANA), animals received ANA (10μg/2.5μl, icv) followed 15min later by CBD (10μg/2.5μl). Results showed that the waking properties of CBD were not blocked by ANA. In conclusion, we found that CBD modulates waking via activation of neurons in the hypothalamus and DRD. Both regions are apparently involved in the generation of alertness. Also, CBD increases DA levels as measured by microdialysis and HPLC procedures. Since CBD induces alertness, it might be of therapeutic value in sleep disorders such as excessive somnolence

Odor memory stability after reinnervation of the olfactory bulb.

The olfactory system, particularly the olfactory epithelium, presents a unique opportunity to study the regenerative capabilities of the brain, because of its ability to recover after damage. In this study, we ablated olfactory sensory neurons with methimazole and followed the anatomical and functional recovery of circuits expressing genetic markers for I7 and M72 receptors (M72-IRES-tau-LacZ and I7-IRES-tau-GFP). Our results show that 45 days after methimazole-induced lesion, axonal projections to the bulb of M72 and I7 populations are largely reestablished. Furthermore, regenerated glomeruli are re-formed within the same areas as those of control, unexposed mice. This anatomical regeneration correlates with functional recovery of a previously learned odorant-discrimination task, dependent on the cognate ligands for M72 and I7. Following regeneration, mice also recover innate responsiveness to TMT and urine. Our findings show that regeneration of neuronal circuits in the olfactory system can be achieved with remarkable precision and underscore the importance of glomerular organization to evoke memory traces stored in the brain