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Insulinomas represent <10% of pancreatic tumors. It is a functional neuroendocrine tumor that can cause recurrent and severe episodes of loss of consciousness due to hypoglycemia. Surgical removal is the only curative treatment. The selection of the optimal surgical technique must be individualized for each patient. Currently, there are emerging innovations in less invasive techniques that reduce morbidity. We present the case of a 23-year-old woman who underwent enucleation of an insulinoma localized at the tip of the pancreatic tail after laparoscopic surgery, with a focus on vascular and splenic preservation. The tumor was safely identified during surgery and enucleated without injury to the spleen and adjacent vascular structures or postoperative complications., Competing Interests: The authors declare that they have no conflict of interest., (Published by Oxford University Press and JSCR Publishing Ltd. © The Author(s) 2024.)

Perceptual learning improves our ability to interpret sensory stimuli present in our environment through experience. Despite its importance, the underlying mechanisms that enable perceptual learning in our sensory cortices are still not fully understood. In this study, we used in vivo two-photon imaging to investigate the functional and structural changes induced by visual stimulation in the mouse primary visual cortex (V1). Our results demonstrate that repeated stimulation leads to a refinement of V1 circuitry by decreasing the number of responsive neurons while potentiating their response. At the synaptic level, we observe a reduction in the number of dendritic spines and an overall increase in spine AMPA receptor levels in the same subset of neurons. In addition, visual stimulation induces synaptic potentiation in neighboring spines within individual dendrites. These findings provide insights into the mechanisms of synaptic plasticity underlying information processing in the neocortex., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)

Elucidating how synaptic molecules such as AMPA receptors mediate neuronal communication and tracking their dynamic expression during behavior is crucial to understand cognition and disease, but current technological barriers preclude large-scale exploration of molecular dynamics in vivo. We have developed a suite of innovative methodologies that break through these barriers: a new knockin mouse line with fluorescently tagged endogenous AMPA receptors, two-photon imaging of hundreds of thousands of labeled synapses in behaving mice, and computer vision-based automatic synapse detection. Using these tools, we can longitudinally track how the strength of populations of synapses changes during behavior. We used this approach to generate an unprecedentedly detailed spatiotemporal map of synapses undergoing changes in strength following sensory experience. More generally, these tools can be used as an optical probe capable of measuring functional synapse strength across entire brain areas during any behavioral paradigm, describing complex system-wide changes with molecular precision., Competing Interests: AG, RR, HT, QZ, AB, EL, IH, AS, RJ, JV, DT, RH No competing interests declared, MM Dr. Miller is a joint owner of AnatomyWorks. Dr. Miller's relationship with Anatomy-Works is being handled under full disclosure by the Johns Hopkins University, (© 2021, Graves et al.)

AMPA receptor (AMPAR) mobility within synapses has been extensively studied in vitro However, whether similar mobility properties apply to AMPARs in vivo has yet to be determined. Here, we use two-photon fluorescence recovery after photobleaching (FRAP) to study AMPAR mobility within individual dendritic spines in live animals using an overexpression vector. We demonstrate the existence of mobile and immobile fractions of AMPARs across multiple cortical regions and layers. Additionally, we find that AMPAR mobility can be altered in vivo in response to administration of corticosterone, a condition that mimics exposure to stress., (Copyright © 2021 Chen et al.)

Cysteine string protein α (CSPα) is a vesicle protein located in the presynaptic terminal of most synapses. CSPα is an essential molecular co-chaperone that facilitates the correct folding of proteins and the assembly of the exocytic machinery. The absence of this protein leads to altered neurotransmitter release and neurodegeneration in multiple model systems, from flies to mice. In humans, CSPα mutations are associated with the development of neuronal ceroid lipofuscinosis (NCL), a neurodegenerative disease characterized by intracellular accumulation of lysosomal material. Here, we review the physiological role of CSPα and the pathology resulting from the homozygous deletion of the gene or its mutations. In addition, we investigate whether long-term moderate reduction of the protein produces motor dysfunction. We found that 1-year-old CSPα heterozygous mice display a reduced ability to sustain motor unit recruitment during repetitive stimulation, which indicates that physiological levels of CSPα are required for normal neuromuscular responses in mice and, likely, in humans.