The CCNP Young Investigator Award highlights a systematic review of pharmacological adjuncts used with transcranial magnetic stimulation (TMS) to enhance synaptic plasticity in humans. The review analyzed 36 studies (28 in healthy individuals and 8 in clinical populations) from 2013 to March 2023, focusing on TMS protocols like repetitive TMS (rTMS), theta-burst stimulation (TBS), paired associative stimulation (PAS), and quadripulse stimulation (QPS). Most pharmacological agents targeted the glutamatergic NMDA receptor (15 studies) or dopamine receptors (13 studies). The NMDA receptor is essential for TMS-induced plasticity, though its sufficiency varies across protocols. Dopaminergic modulation is dose-dependent. GABAergic, cholinergic, noradrenergic, and serotonergic systems have limited evidence for modulating TMS plasticity. Clinical studies suggest pharmacological adjuncts may restore motor cortex plasticity, with potential applications in depression. Limitations include small sample sizes and crossover designs. The review concludes that pharmacologically enhanced TMS aligns with ex vivo findings, and future research with adequately powered samples will clarify mechanisms in health and disease. Key findings include NMDA receptor necessity, dopamine's dose-dependent role, and the impact of various neurotransmitter systems on TMS plasticity. The review underscores the complexity of TMS parameter space and synaptic plasticity interactions, emphasizing the need for further investigation into pharmacological augmentation for therapeutic applications.The CCNP Young Investigator Award highlights a systematic review of pharmacological adjuncts used with transcranial magnetic stimulation (TMS) to enhance synaptic plasticity in humans. The review analyzed 36 studies (28 in healthy individuals and 8 in clinical populations) from 2013 to March 2023, focusing on TMS protocols like repetitive TMS (rTMS), theta-burst stimulation (TBS), paired associative stimulation (PAS), and quadripulse stimulation (QPS). Most pharmacological agents targeted the glutamatergic NMDA receptor (15 studies) or dopamine receptors (13 studies). The NMDA receptor is essential for TMS-induced plasticity, though its sufficiency varies across protocols. Dopaminergic modulation is dose-dependent. GABAergic, cholinergic, noradrenergic, and serotonergic systems have limited evidence for modulating TMS plasticity. Clinical studies suggest pharmacological adjuncts may restore motor cortex plasticity, with potential applications in depression. Limitations include small sample sizes and crossover designs. The review concludes that pharmacologically enhanced TMS aligns with ex vivo findings, and future research with adequately powered samples will clarify mechanisms in health and disease. Key findings include NMDA receptor necessity, dopamine's dose-dependent role, and the impact of various neurotransmitter systems on TMS plasticity. The review underscores the complexity of TMS parameter space and synaptic plasticity interactions, emphasizing the need for further investigation into pharmacological augmentation for therapeutic applications.