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Quantitative autoradiographic mapping of serotonin receptors in the rat brain. I. Serotonin-1 receptors
Quantitative autoradiographic mapping of serotonin receptors in the rat brain. II. Serotonin-2 receptors
Serotonin receptors in the human brain—IV. Autoradiographic mapping of serotonin-2 receptors
A single in-vivo exposure to delta 9THC blocks endocannabinoid-mediated synaptic plasticity.
- S. Mato, V. Chevaleyre, David Robbe, Á. Pazos, P. Castillo, O. Manzoni
- BiologyNature Neuroscience
In mice, a single in-vivo exposure to Delta 9-tetrahydrocannabinol (THC) abolishes the retrograde signaling that underlies eCB-mediated synaptic plasticity in both nucleus accumbens and hippocampus in vitro.
Ontogenetic development of cannabinoid receptor expression and signal transduction functionality in the human brain
Early pattern of expression of functionally active cannabinoid receptors, along with the transient and atypical localization of these proteins in white matter areas during the prenatal stages, suggest an specific role of the endocannabinoid system in the events related to human neural development.
Serotonin receptors in the human brain—III. Autoradiographic mapping of serotonin-1 receptors
Are Wistar-Kyoto rats a genetic animal model of depression resistant to antidepressants?
Cannabidiol induces rapid-acting antidepressant-like effects and enhances cortical 5-HT/glutamate neurotransmission: role of 5-HT1A receptors
Reducing GABAA α5 Receptor-Mediated Inhibition Rescues Functional and Neuromorphological Deficits in a Mouse Model of Down Syndrome
- C. Martínez-Cué, P. Martínez, Maria-Clemencia Hernández
- Biology, PsychologyJournal of Neuroscience
- 27 February 2013
Reducing GABAergic inhibition with RO4938581 can reverse functional and neuromorphological deficits of TS mice by facilitating brain plasticity and support the potential therapeutic use of selective GABAA α5 NAMs to treat cognitive dysfunction in DS.
BDNF impairment in the hippocampus is related to enhanced despair behavior in CB1 knockout mice
The results suggest that the lack of CB1 receptor originates an enhanced response to stress and deficiency in neuronal plasticity by decreasing BDNF levels in the hippocampus that lead to impairment in the responses to emotional disturbances.