Failure of ethanol and acetaldehyde to alter in vivo norepinephrine release in the striatum and hippocampus of rats

Abstract

The effect of ethanol (EtOH) and acetaldehyde (AcH) on norepinephrine (NE) release was examined in the striatum and hippocampus of freely moving rats by means of in vivo microdialysis coupled with high-performance liquid chromatography and an electrochemical detector. Rats were treated intraperitoneally with EtOH (1 g/kg) or cyanamide (CY, 50 mg/kg, a potent aldehyde dehydrogenase inhibitor) plus EtOH (1 g/kg). No significant difference in NE levels in the dialysates was observed in the striatum and hippocampus in either the EtOH or CY+EtOH groups. NE levels in the hippocampal dialysates were about fivefolds higher than those in the striatum. The concentration of EtOH and AcH in the striatal dialysate reached a peak at 30 min after EtOH dosing and then gradually decreased in the CY+EtOH group. In the EtOH group the striatal concentration of EtOH also reached a peak at 30 min after EtOH dosing, and then gradually decreased while AcH was not detected. The present study suggests that there is no in vivo effect of brain EtOH or AcH on NE release in the striatum and hippocampus of awake rats.

Effects of Systemic Nicotine, Alcohol or Their Combination on Cholinergic Markers in the Frontal Cortex and Hippocampus of Rat

“…Our previous results demonstrate that Alc reaches a peak level (20.1 ± 1.1 mM) at 30 min and then declines significantly (6.9 ± 1.6 mM) at 120 min in the striatal dialysate of rats treated with Alc 1 g/kg [28]. In neither of the brain regions studied did Alc concentrations differ significantly in rats [29]. Peripheral Nic reaches the brain tissues through the blood-brain barrier and can accumulate in the brain regions, e.g., the cortex and hippocampus, which contain high-affinity binding sites for the compound [30].…”

Acute Low Alcohol Disrupts Hippocampus-Striatum Neural Correlate of Learning Strategy by Inhibition of PKA/CREB Pathway in Rats

“…Thus, a higher dose (2.0 g/kg) was chosen to compare with the dose of 1.0 g/kg in multiple spatial learning tests, since previous studies in which dose-response curves were examined demonstrated the reductions in locomotor activity (Stevenson et al, 2008; Mitchell et al, 2011). The time point of behavioral or recording initiation was chosen as previous findings, which indicated the concentration of alcohol in the striatum and hippocampus of awake rats reached a peak simultaneously at 30 min after dosing (Jamal et al, 2004; Lam and Gianoulakis, 2011). Matched controls receiving equivalent volumes of saline i.p.…”