Abstract
Morphine, a potent opioid analgesic, plays a critical role in pain management but elicits complex effects on the central nervous system (CNS), demonstrating both beneficial and detrimental outcomes. This paper reviews preclinical studies to examine morphine's interactions with the CNS, notably via binding to opioid receptors, leading to analgesia as well as a series of adverse effects, including addiction, tolerance, and neurological impairments. Acute exposure to morphine alters neurotransmitter activity, gene expression, and neuronal firing rates. In contrast, chronic use results in significant neuronal damage, altered memory functions, increased pain sensitivity, and neuroinflammation, highlighting the drug's impact on neurogenesis and neural cell viability. Additionally, morphine's protective properties against neurotoxic insults are discussed, alongside its potential to disrupt cellular and molecular pathways, culminating in neurotoxicity and cognitive deficits. Given the dual nature of morphine's impact on the CNS - protective vs. harmful, depending on specific conditions such as dosage, disease type, and administration frequency - this paper underscores the necessity for further research to untangle this complex interplay to leverage morphine's pain management benefits while minimizing its risks. A thorough evaluation of morphine administration practices can help reconcile these conflicting results.
Published Version
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