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The pharmacological properties and anatomical distribution of alpha2-, beta1- and beta2-adrenoceptors in pigeon and chick brains were studied by both homogenate binding and tissue section autoradiography. [3H]Bromoxidine (alpha2-adrenoceptor-), [3H]CGP 12177 (beta-adrenoceptor) and [125I]cyanopindolol (beta-adrenoceptor) were used as radioligands. In both species, [3H]bromoxidine binding to avian brain tissue showed a pharmacological profile similar to that previously reported for alpha2-adrenoceptors in mammals. Regarding the anatomical distribution, the areas with the highest densities of alpha2-adrenoceptors in the pigeon brain included the hyperstriatum, nuclei septalis, tectum opticum and some brainstem nuclei. Most beta-adrenoceptors found in tissue membranes and sections from chick and pigeon brain were of the beta2 subtype, in contrast to what has been reported in the mammalian brain, where the beta1 subtype is predominant. A striking difference was found between the two species regarding the densities of these receptors: while pigeon brain was extremely rich in [125I]cyanopindolol binding throughout the brain (mainly cerebellum) in the pigeon, the levels of labelling in the chick brain were much lower; the exception was the cerebellum, which displayed a higher density than other parts of the brain in both species. Overall, our results support the proposed anatomical equivalences between a number of structures in the avian and mammalian encephalon.

This study describes the neuroprotective effect of treatment with salubrinal 1 and 24 h following 15 min of ischemia in a twovessel occlusion model of global cerebral ischemia. The purpose of this study was to determine if salubrinal, an enhancer of the unfolded protein response, reduces the neural damage modulating the inflammatory response. The study was performed in CA1 and CA3 hippocampal areas as well as in the cerebral cortex whose different vulnerability to ischemic damage is widely described. Characterization of proteins was made by western blot, immunofluorescence, and ELISA, whereas mRNA levels were measured by Quantitative PCR. The salubrinal treatment decreased the cell demise in CA1 at 7 days as well as the levels of matrix metalloprotease 9 (MMP-9) in CA1 and cerebral cortex at 48 h and ICAM-1 and VCAM-1 cell adhesion molecules. However, increases in tumor necrosis factor a and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-jB) inflammatory markers were observed at 24 h. Glial fibrillary acidic protein levels were not modified by salubrinal treatment in CA1 and cerebral cortex. We describe a neuroprotective effect of the post-ischemic treatment with salubrinal, measured as a decrease both in CA1 cell demise and in the blood-brain barrier impairment. We hypothesize that the ability of salubrinal to counteract the CA1 cell demise is because of a reduced ability of this structure to elicit unfolded protein response which would account for its greater ischemic vulnerability. Data of both treated and non-treated animals suggest that the neurovascular unit present a structuredependent response to ischemia and a different course time for CA1/cerebral cortex compared with CA3. Finally, our study reveals a high responsiveness of endothelial cells to salubrinal in contrast to the limited responsiveness of astrocytes.

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