Dopamine is critical to promote normal reward-learning. What happens when this system is hijacked in the presence of powerful drugs like nicotine, cocaine, or methamphetamines? Are there physiological properties of the cells in the brain that allow these drugs to have such a strong influence on individuals?
Previous work has demonstrated that axonal modulation is capable of influencing dopaminergic neuron activity. In the Kramer Lab, we are currently interested in the role of cholinergic interneuron (CIN) input onto dopaminergic axons. Interestingly, in regions of the brain controlling both reward and motor systems (the nucleus accumbens and striatum, respectively), CINs make synaptic-like connections with distal dopaminergic axons that can lead to increased excitability In the axon. This may have important consequences for the release of dopamine In normal reward-learning, and can help us better understand how drugs of abuse like nicotine affect dopamine release.