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Increased density of μ-opioid receptors in the postmortem brain of suicide victims
TLDR
The results suggest an increase of mu-opioid receptors in suicide associated to some brain areas showing the mu2-opIOid receptor subtype. Expand
Up‐Regulation of Immunolabeled α2A‐Adrenoceptors, Gi Coupling Proteins, and Regulatory Receptor Kinases in the Prefrontal Cortex of Depressed Suicides
TLDR
The increased levels in concert of α2A‐adrenoceptors, Gα1/2 proteins, and GRK 2/3 in brains of depressed suicide victims support the existence of supersensitive α2Drenoceptor in subjects with major depression. Expand
Attenuation of tolerance to opioid‐induced antinociception and protection against morphine‐induced decrease of neurofilament proteins by idazoxan and other I2‐imidazoline ligands
TLDR
The main aim of this study was to assess if idazoxan, an α2‐adrenoceptor antagonist that also interacts with imidazoline receptors, could also modulate opioid tolerance in rats and to establish which type of imidzoline receptors (or other receptors) are involved. Expand
Protection by imidazol(ine) drugs and agmatine of glutamate‐induced neurotoxicity in cultured cerebellar granule cells through blockade of NMDA receptor
TLDR
It is concluded that imidazol(ine) drugs and agmatine are neuroprotective against glutamate‐induced necrotic neuronal cell death in vitro and that this effect is mediated through NMDA receptor blockade by interacting with a site located within the NMDA channel pore. Expand
Chronic morphine induces up‐regulation of the pro‐apoptotic Fas receptor and down‐regulation of the anti‐apoptotic Bcl‐2 oncoprotein in rat brain
TLDR
It is indicated that morphine, through the sustained activation of opioid receptors, can promote abnormal programmed cell death by enhancing the expression of pro‐apoptotic Fas receptor protein and damping theexpression of anti‐ap optotic Bcl‐2 oncoprotein. Expand
Activation of I2‐imidazoline receptors enhances supraspinal morphine analgesia in mice: a model to detect agonist and antagonist activities at these receptors
TLDR
Functional interaction between I2‐imidazoline and opioid receptors is demonstrated and the involvement of Gi‐Go transducer proteins in this modulatory effect is suggested. Expand
Autoradiographic Demonstration of Increased α2‐Adrenoceptor Agonist Binding Sites in the Hippocampus and Frontal Cortex of Depressed Suicide Victims
TLDR
The results indicate that suicide is associated with increases in the high‐affinity state of brain α2‐adrenoceptors and that there is a pronounced localized increase of this inhibitory receptor in the hippocampus of depressed suicide victims. Expand
Role of lipid polymorphism in G protein-membrane interactions: nonlamellar-prone phospholipids and peripheral protein binding to membranes.
TLDR
Although G protein alpha-subunits were able to bind to lipid bilayers, the presence of nonlamellar-prone phospholipids (phosphatidylethanolamines) enhanced their binding to model membranes, indicating that it could constitute a general mode of protein-lipid interactions, relevant in the activity and translocation of some peripheral (amphitropic) proteins from soluble to particulate compartments. Expand
Immunodensity and mRNA expression of A2A adenosine, D2 dopamine, and CB1 cannabinoid receptors in postmortem frontal cortex of subjects with schizophrenia: effect of antipsychotic treatment
TLDR
The findings suggest that antipsychotics induce down-regulation of CB1 receptors in brain, which could represent an adaptative mechanism that reduces the endocannabinoid-mediated suppression of GABA release, contributing to the normalization of cognitive functions in the disorder. Expand
Inhibition of monoamine oxidase A and B activities by imidazol(ine)/guanidine drugs, nature of the interaction and distinction from I2‐imidazoline receptors in rat liver
TLDR
The main aim of this study was to assess the inhibitory effects and nature of the inhibition of imidazol(ine)/guanidine drugs on rat liver MAO‐A andMAO‐B isoforms and to compare their inhibitory potencies with their affinities for the sites labelled by [3H]‐clonidine in the same tissue. Expand
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