Cocaine Enhances Gamma-Aminobutyric Acid Release From Reticular Thalamic Nucleus: Role of T-Type Calcium Channels.
This chapter discusses cocaine-mediated actions on thalamic networks gamma-aminobutyric acid (GABA) transmission. Cocaine effects are associated with catecholamine reuptake inhibitions but local anesthetic mechanisms have been described. We focused our attention on the cocaine effects on thalamic re...
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| Autores principales: | , |
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| Formato: | CHAP |
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| Acceso en línea: | http://hdl.handle.net/20.500.12110/paper_97801280_v_n_p511_Urbano |
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| Sumario: | This chapter discusses cocaine-mediated actions on thalamic networks gamma-aminobutyric acid (GABA) transmission. Cocaine effects are associated with catecholamine reuptake inhibitions but local anesthetic mechanisms have been described. We focused our attention on the cocaine effects on thalamic reticular nucleus, the main GABAergic afferents to sensory thalamic nuclei in rodents. Although cocaine can inhibit GABA release throughout the upregulation of presyanptic inhibitory serotonin (5-HT) 5-HT1A-typereceptors, local anesthetic-like effects of cocaine on thalamic reticular neurons can also contribute to the long-term thalamocortical alteration by this psychostimulant. Cocaine-mediated disruption of GABA neurotransmission might underlie aberrant thalamocortical physiology described in humans after repetitive cocaine use. © 2017 Elsevier Inc. All rights reserved. |
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