Potentiation of AMPAR function is not limited to cocaine, as non-contingent injections of nicotine, alcohol, amphetamine, or morphine can also elicit a LTP-like potentiation of glutamate transmission onto VTA DA neurons (Saal et al., 2003). Thus, glutamatergic synapses onto VTA DA neurons are equally enhanced following reward-related learning and after exposure to drugs of abuse; however, the potentiation of glutamatergic input onto VTA DA neurons is transient. Following non-drug reward-related learning, synaptic potentiation persists for 2 to 7 days depending on the behavioral task (Chen et al., 2008; Stuber et al., 2008), but is absent by 14 days after the last reward-learning training session (Chen et al., 2008). Similarly, a short-lasting potentiation is also observed following a single intraperitoneal (i.p.) cocaine injection, with enhanced AMPAR function evident after 1 and 5 but not 10 days of abstinence (Ungless et al., 2001). Because relapse to cocaine-seeking behavior can occur even after a prolonged period of abstinence, one wonders whether repeated cocaine exposures would induce a longer-lasting potentiation of VTA DA neurons. Surprisingly, even when rats were administered non-contingent cocaine injections across
