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Alzheimer’s disease (AD) is increasingly associated with early circuit dysfunction preceding cognitive decline, including neuronal hyperactivity and neuropsychiatric symptoms linked to mesolimbic pathways. The nucleus accumbens (nAc), a central regulator of reward and motivational processing, exhibits early alterations in excitation/inhibition balance in patients and experimental models; however, the synaptic mechanisms underlying this vulnerability remain unclear. Here, we identify a cell-type-specific synaptic mechanism in the nAc linking early intraneuronal Aβ accumulation to circuit dysfunction. Using a double transgenic APP/PS1 mouse model expressing tdTomato in dopamine D1 receptor-positive medium spiny neurons (D1R+ MSNs), we show that long-term depression (LTD) is selectively impaired in D1R+ MSNs despite comparable Aβ levels across neuronal subtypes, revealing differential functional vulnerability. This deficit is associated with an increased contribution of calcium-permeable AMPA receptors (CP-AMPARs) and a disruption of mGluR1/5-dependent LTD, a key mechanism regulating AMPAR trafficking. Pharmacological blockade of CP-AMPARs restores synaptic depression, indicating altered receptor composition as a central feature of this phenotype. These synaptic alterations co-occur with reduced dopaminergic signaling and selective behavioral changes characterized by increased consumption of palatable reward and altered baseline context preference, while associative learning remains preserved. Together, these findings reveal a postsynaptic mechanism in which impaired mGluR-dependent plasticity permits persistent CP-AMPAR signaling, shifting synaptic balance toward increased excitatory drive and mesolimbic hyperactivity in AD.