Modulation of cholinergic neurotransmission via nicotinic acetylcholine receptors is known to alter alcohol-drinking behavior. It is not known if muscarinic acetylcholine receptor subtypes have similar effects. The muscarinic M4 receptor is highly expressed in the brain reinforcement system and involved in regulation of cholinergic and dopaminergic transmission. Here we investigate, for the first time, the role of the M₄ receptor in alcohol consumption using M₄ knockout (M₄^-/-) and wild-type (M₄^+/+) mice. Experimentally naïve M₄^-/- and M₄^+/+ mice were trained to orally self-administer 5%, 8% and 10% alcohol in 60min sessions, 6 days/week, after having undergone a standard sucrose fading training procedure on a fixed ratio schedule. The mice were further subjected to an extinction period followed by a 1 day reinstatement trial. M₄^-/- mice consumed more alcohol at 5% and 8% compared to their M₄^+/+ littermates. The highest alcohol concentration used (10%) did not immediately result in divergent drinking patterns, but after 4 weeks of 10% alcohol self-administration, baseline levels as well as a pattern of M₄^-/- mice consuming more alcohol than their M₄^+/+ controls were re-established. Moreover, the M₄^-/- mice displayed a reduced capacity to extinguish their alcohol-seeking behavior. Taken together, alcohol consumption is elevated in M₄^-/- mice, indicating that the M4 receptor is involved in mediating the reinforcing effects of alcohol. The M₄ receptor should be further explored as a potential target for pharmacological (positive allosteric modulators or future agonists) treatment of alcohol use disorders.