Human and animal studies have elucidated the apparent neurodevelopmental effects resulting from neonatal anesthesia. Observations of learning and behavioral deficits in children, who were exposed to anesthesia early in development, have instigated a flurry of studies that have predominantly utilized animal models to further interrogate the mechanisms of neonatal anesthesia-induced neurotoxicity. Specifically, while neonatal anesthesia has demonstrated its propensity to affect multiple cell types in the brain, it has shown to have a particularly detrimental effect on the gamma aminobutyric acid (GABA)ergic system, which contributes to the observed learning and behavioral deficits. The damage to GABAergic neurons, resulting from neonatal anesthesia, seems to involve structure-specific changes in excitatory-inhibitory balance and neurovascular coupling, which manifest following a significant interval after neonatal anesthesia exposure. Thus, to better understand how neonatal anesthesia affects the GABAergic system, we first review the early development of the GABAergic system in various structures that have been the focus of neonatal anesthesia research. This is followed by an explanation that, due to the prolonged developmental curve of the GABAergic system, the entirety of the negative effects of neonatal anesthesia on learning and behavior in children are not immediately evident, but instead take a substantial amount of time (years) to fully develop. In order to address these concerns going forward, we subsequently offer a variety of in vivo methods which can be used to record these delayed effects.

Cancers of the central nervous system are particularly difficult to treat due to a variety of factors. Surgical approaches are impeded by the skull—an issue which is compounded by the severity of possible harm that can result from damage to the parenchymal tissue. As a result, chemotherapeutic agents have been the standard of care for brain tumors. While some drugs can be effective on a case-by-case basis, there remains a critical need to improve the efficacy of chemotherapeutic agents for neurological cancers. Recently, advances in iron oxide nanoparticle research have highlighted how their unique properties could be leveraged to address the shortcomings of conventional therapeutics. Iron oxide nanoparticles combine the advantages of good biocompatibility, magnetic susceptibility, and functionalization via a range of coating techniques. Thus, iron oxide nanoparticles could be used in both the imaging of brain cancers with magnetic resonance imaging, as well as acting as trafficking vehicles across the blood–brain barrier for targeted drug delivery. Moreover, their ability to support minimally invasive therapies such as magnetic hyperthermia makes them particularly appealing for neuro-oncological applications, where precision and safety are paramount. In this review, we will outline the application of iron oxide nanoparticles in various clinical settings including imaging and drug delivery paradigms. Importantly, this review presents a novel approach of combining surface engineering and internal magnetic targeting for deep-seated brain tumors, proposing the surgical implantation of internal magnets as a next-generation strategy to overcome the limitations of external magnetic fields.

Neonatal anesthesia, while often essential for surgeries or imaging procedures, is accompanied by significant risks to redox balance in the brain due to the relatively weak antioxidant system in children. Oxidative stress is characterized by concentrations of reactive oxygen species (ROS) that are elevated beyond what can be accommodated by the antioxidant defense system. In neonatal anesthesia, this has been proposed to be a contributing factor to some of the negative consequences (e.g., learning deficits and behavioral abnormalities) that are associated with early anesthetic exposure. In order to assess the relationship between neonatal anesthesia and oxidative stress, we first review the mechanisms of action of common anesthetic agents, the key pathways that produce the majority of ROS, and the main antioxidants. We then explore the possible immediate, short-term, and long-term pathways of neonatal-anesthesia-induced oxidative stress. We review a large body of literature describing oxidative stress to be evident during and immediately following neonatal anesthesia. Moreover, our review suggests that the short-term pathway has a temporally limited effect on oxidative stress, while the long-term pathway can manifest years later due to the altered development of neurons and neurovascular interactions.