I.v. cocaine induces rapid, transient excitation of striatal neurons via its action on peripheral neural elements: Single-cell, iontophoretic study in awake and anesthetized rats

摘要: Abstract Cocaine’s (COC) direct interaction with the dopamine (DA) transporter is usually considered most important action underlying psychomotor stimulant and reinforcing effects of this drug. However, some physiological, behavioral psycho-emotional COC are very rapid brief they remain intact during DA receptor blockade, suggesting possible involvement peripheral non-DA neural mechanisms. To assess issue, single-unit recording microiontophoresis was used to examine changes in impulse activity dorsal ventral striatal neurons i.v. (0.25–0.5 mg/kg) same rats under two conditions: awake blockade anesthetized urethane. In preparation ∼70% showed transient (latency ∼6 s, duration ∼15 s) COC-induced excitations. These were stronger than striatum. During anesthesia, these phasic fully blocked slowly decreased neuronal discharge rate. Cocaine-methiodide (COC-M), a derivative that cannot cross blood–brain barrier, also caused excitations awake, but not condition. contrast regular COC, COC-M had no tonic effect on rate either preparation. Most phasically excited by both forms short-latency tail-touch tail-pinch preparation, an strongly attenuated anesthesia. Finally, conditions somato-sensory stimuli salts iontophoretic glutamate (GLU). Although sensitive GLU preparations, response magnitude at current higher conditions. data suggest animals like stimuli, transiently excites via its elements transmission. While nature needs be clarified using other analytical techniques, might involve voltage-gated K + Na channels, which have high affinity for located terminals visceral sensory nerves densely innervate vessels. Therefore, along specific brain substrates, central excitatory may occur indirect action, involving afferents By providing signal triggering activation, such peripherally triggered play crucial role thus contributing learning development drug-taking behavior.