The dopamine neurons of the ventral midbrain form the core of the brain’s reward system and the plasticity of these neurons are essential in mediating the effects of positive reinforcement. To study the underlying neuronal mechanisms we used genetically modified mice (NR1DATCreERT2) that lacked NMDA glutamate receptors on dopamine neurons and thus had impaired plasticity on excitatory synapses. We found that mutant mice performed similarly as controls in food-self administration test under fixed, progressive or variable interval schedules. However, NR1DATCreERT2 mice failed to acquire instrumental responding for sensory stimuli in the operant sensation seeking test. Furthermore, when mice were tested for sweet taste preference under instrumental access (FR3) in an IntelliCage, mutants did not prefer the saccharine solution over pure water (52±11%) while control animals reached 98±13% preference. The anhedonia-like phenotype prompted us to test the animals in forced swimming test and we found that NR1DATCreERT2 animals spent more time immobile than controls. In summary, we believe that the loss of NMDA receptors on dopamine neurons caused decreased sensitivity to sensory stimuli, anhedonia and increased learned helplessness, without causing obvious impairments in instrumental learning. Supported by the grant OPUS 2011/03/B/NZ4/02211
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