Numerous neuropathologies originate from dysregulation in the excitatory or inhibitory activities of specific neuronal populations within the brain, including opioid addiction . Opioids represent the apex of analgesics currently employed in clinical settings. Their mechanism of action involves binding to opioid receptors distributed throughout the Central Nervous System (CNS), leading to a diminution in the propagation of nociceptive signals . The paramount efficacy of opioids as analgesics, however, is attributed not just to their role in pain modulation but also to their capacity to induce dopamine release. Dopamine, a neurotransmitter predominantly secreted by neurons in the Nucleus Accumbensa brain region integral to the reward system and the reinforcement of rewarding behaviorselicits sensations of euphoria and well-being . Kainate receptors (KARs), belonging to the ionotropic glutamate receptors (iGluRs) subfamily, are essential for both postsynaptic neurotransmission and presynaptic regulation of transmitter release in the vertebrate brain . These receptors differ from AMPA and NMDA receptors by producing small-amplitude excitatory postsynaptic currents with slow kinetics in the hippocampus regions of the central nervous system . KARs also play a crucial role in the development of neuronal circuits, interacting with G proteins, and are implicated in various disorders, including autism, epilepsy, schizophrenia, and neuropathic pain. Subunits from the low and high kainate affinity gene families make up KARs . While the highaffinity family (GluK4-GluK5) must partner with low-affinity subunits to function, the low-affinity family (GluK1-GluK3) can form both homomeric and heteromeric receptors . This assembly produces various receptor configurations, contributing to their diverse functional properties .