Ethanol-induced modulation of synaptic output from the dorsolateral striatum in rat is regulated by cholinergic interneurons

• Published in: Neurochemistry international Vol. 58; no. 6; pp. 693 - 699
• Main Authors: Adermark, Louise, Clarke, Rhona B.C., Söderpalm, Bo, Ericson, Mia
• Format: Journal Article
• Language: English
• Published: Kidlington Elsevier Ltd 01-05-2011; Elsevier
• Subjects: Alcohol; Animals; Basal ganglia; Biological and medical sciences; Cholinergic; Corpus Striatum; Corpus Striatum - drug effects; Corpus Striatum - physiology; drug effects; Ethanol; Ethanol - pharmacology; Female; Field potential; Fundamental and applied biological sciences. Psychology; GABA; Glycine receptors; In Vitro Techniques; Interneurons; Interneurons - physiology; Male; metabolism; pharmacology; physiology; Psychiatry; Psykiatri; Rats; Rats, Wistar; Receptors; Receptors, Cholinergic - metabolism; Synapses; Synapses - drug effects; Synapses - metabolism; Vertebrates: nervous system and sense organs; Wistar; Basal ganglia; MLA; Glycine receptors; GABA; EtOH; NMDAR; AP-5; PMBA; Alcohol; Field potential; Ethanol; Rat; Rodentia; Central nervous system; Electrophysiology; Corpus striatum; Basal ganglion; Encephalon; Interneuron; Vertebrata; Mammalia; Animal; Glycine receptor; Neurotransmitter
• ISSN: 0197-0186; 1872-9754; 1872-9754
• DOI: 10.1016/j.neuint.2011.02.009

► Ethanol exerts dual actions on striatal output that are initiated simultaneously. ► Acute ethanol-treatment induces a GABAAR-sensitive short-term depression. ► Ethanol washout induces a long-term facilitation of striatal output. ► Ethanol-induced facilitation is regulated by cholinergic interneurons. ► This study provide important clues for understanding acute ethanol intoxication.
The striatum is the largest input nucleus to the basal ganglia and associated with reward-based behavior. We assessed whether acute ethanol (EtOH) exposure could modulate synaptic efficacy in the dorsolateral striatum of juvenile Wistar rats. Since acute EtOH administration can both increase and decrease the probability of release of different neurotransmitters from synaptic terminals, we used field potential recordings to evaluate the net effect of EtOH on striatal output. We showed that 50
mM EtOH but not 20, 80 or 100
mM, depresses population spike (PS) amplitude in the dorsolateral striatum. This depression of synaptic output is insensitive to the N-methyl-
d-aspartic acid (NMDA) receptor inhibitor DL-2-amino-5-phosphonopentanoic acid (AP-5, 50
μM), but is blocked in slices treated with glycine receptor antagonists (strychnine, 1
μM; PMBA, 50
μM), nicotinic acetylcholine receptor antagonists (mecamylamine, 10
μM; methyllycaconitine citrate (MLA), 40
nM), or GABA
A receptor inhibitors (picrotoxin, 100
μM; bicuculline, 2
μM, 20
μM). A long-term facilitation of synaptic output, which is more pronounced in slices from adult Wistar rats, is detected following EtOH washout (50, 80, 100
mM). This long-term enhancement of PS amplitude is regulated by cholinergic interneurons and completely blocked by mecamylamine, MLA or the non-selective muscarinic antagonist scopolamine (10
μM). Administration of 100
mM EtOH significantly depresses PS amplitude in scopolamine-treated slices, suggesting that EtOH exerts dual actions on striatal output that are initiated instantly upon drug wash-on. In conclusion, EtOH modulates striatal microcircuitry and neurotransmission in a way that could be of importance for understanding the intoxicating properties as well as the acute reward sensation of EtOH.