Glial Cell Plasticity in the Ventral Pallidum Following Opioid Dependence
Faculty Mentor Information
Dr. Lauren Faget, Boise State University
Presentation Date
7-16-2026
Abstract
Opioid use disorder (OUD) produces persistent neurobiological adaptations within brain circuits that regulate motivation, reward, and relapse. While neuronal plasticity has been extensively studied, far less is known about how glial cells contribute to these maladaptive changes. The ventral pallidum (VP), a critical hub of the brain's reward network, contains diverse neuronal populations together with abundant astrocytes and microglia, making it an ideal region to investigate neuron-glia interactions during opioid dependence. We established a mouse model of opioid dependence using escalating doses of morphine (20–50 mg/kg, once daily for 5 days) and confirmed dependence by assessing naloxone-precipitated withdrawal behaviors. Brains were collected 24 hours after the final morphine injection for molecular analysis. Using RNAscope in situ hybridization, we observed a preliminary trend toward increased expression of the mu opioid receptor gene (Oprm1) within the VP following opioid dependence (n = 2). In parallel, immunohistochemistry for astrocytes (GFAP) and microglia (Iba1) is being used to determine whether opioid dependence alters glial cell density within the VP. Together, these studies will provide new insight into glial and neuronal adaptations associated with opioid dependence and may identify novel cellular targets for future therapeutic intervention.
Glial Cell Plasticity in the Ventral Pallidum Following Opioid Dependence
Opioid use disorder (OUD) produces persistent neurobiological adaptations within brain circuits that regulate motivation, reward, and relapse. While neuronal plasticity has been extensively studied, far less is known about how glial cells contribute to these maladaptive changes. The ventral pallidum (VP), a critical hub of the brain's reward network, contains diverse neuronal populations together with abundant astrocytes and microglia, making it an ideal region to investigate neuron-glia interactions during opioid dependence. We established a mouse model of opioid dependence using escalating doses of morphine (20–50 mg/kg, once daily for 5 days) and confirmed dependence by assessing naloxone-precipitated withdrawal behaviors. Brains were collected 24 hours after the final morphine injection for molecular analysis. Using RNAscope in situ hybridization, we observed a preliminary trend toward increased expression of the mu opioid receptor gene (Oprm1) within the VP following opioid dependence (n = 2). In parallel, immunohistochemistry for astrocytes (GFAP) and microglia (Iba1) is being used to determine whether opioid dependence alters glial cell density within the VP. Together, these studies will provide new insight into glial and neuronal adaptations associated with opioid dependence and may identify novel cellular targets for future therapeutic intervention.