Neuroscience
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Environmental enrichment has been shown to increase cognitive abilities and accelerate recovery from a number of disease states. Typically, enrichment protocols last from four to eight weeks, however, it has previously been shown that two weeks of environmental enrichment is sufficient to increase cognitive abilities and the proliferation of the astroglial stem cell pool in juvenile mice. The current study examines whether a short-term enrichment protocol can induce similar effects in adults as compared to juveniles. ⋯ We found that short-term environmental enrichment decreased anxiety behaviour and increased overall memory abilities similarly in juveniles and adults. However, the rate of acquisition on the Morris water maze, hippocampal Sox2 and Ki67 expression, and neurosphere potential increased in response to enrichment only in juveniles, suggesting that the effects of enrichment on these measures are age dependant. Together, these data suggest that the potential beneficial effects of environmental manipulations decrease with age.
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Exercise affects positively on self-reported pain in musculoskeletal pain conditions possibly via top-down pain inhibitory networks. However, the role of cortical activity in these networks is unclear. The aim of the current exploratory study was to investigate the effects of acute exercise on cortical nociceptive processing and specifically the excitability in the human sensorimotor cortex. ⋯ In conclusion, acute exercise may have an effect on nociceptive processing in the sensorimotor cortex on oscillatory level. Research on cortical oscillations analyzing interaction between nociception and exercise is limited. This study presents results indicating brain oscillatory activity as a feasible research target for examining mechanisms interacting between exercise and cortical nociceptive processing.
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C1q/TNF-related protein 4 (CTRP4) has been reported to decrease food intake and regulate energy homeostasis. However, its underlying mechanism and signaling pathway remain unknown. Using an adenovirus-mediated hypothalamic CTRP4 overexpression model, we investigated the impact of CTRP4 on food intake and signal transducer and activator of transcription 3 (STAT3) signaling pathway in normal chow-fed mice. ⋯ The changes of neuropeptides were accompanied by significant increased STAT3 phosphorylation and decreased SOCS3 levels. The same changes of neuropeptides and STAT3 signaling were also found in N2a cells after CTRP4 overexpression intervention. Collectively, our data reveals that CTRP4 induces the activation of STAT3 signaling and decreases food intake.
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Lysosomal network dysfunction is a prominent feature of Alzheimer's disease (AD). Although transgenic mouse models of AD are known to model some aspects of lysosomal network dysfunction, the lysosomal network has not yet been examined in the knock-in AppNL-G-F/NL-G-F mouse. We aimed to determine whether AppNL-G-F/NL-G-F mice exhibit disruptions to the lysosomal network in the brain. ⋯ AppNL-G-F/NL-G-F mice also exhibited elevated activity of β-hexosaminidase and cathepsins D/E and elevated levels of selected lysosomal network proteins, namely LAMP1, cathepsin D and microtubule-associated protein light chain 3 (LC3-II) in the cerebral cortex, as determined by western blot. Elevation of cathepsin D did not change the extent of co-localisation between cathepsin D and LAMP1 in the AppNL-G-F/NL-G-F mice. These findings demonstrate that perturbations of the lysosomal network occur in the AppNL-G-F/NL-G-F mouse model, further validating its use an animal model of pre-symptomatic AD.
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Non-invasive treatment methods for neuropathic pain are lacking. We assess how modulatory low intensity focused ultrasound (liFUS) at the L5 dorsal root ganglion (DRG) affects behavioral responses and sensory nerve action potentials (SNAPs) in a common peroneal nerve injury (CPNI) model. Rats were assessed for mechanical and thermal responses using Von Frey filaments (VFF) and the hot plate test (HPT) following CPNI surgery. ⋯ This is the first in vivo study of the impact of liFUS on peripheral nerve electrophysiology in a model of chronic pain. This study demonstrates the effects of liFUS on peripheral nerve electrophysiology in vivo. We found that external liFUS treatment results in transient decreased latency in common peroneal nerve (CPN) sensory nerve action potentials (SNAPs) with no change in signal amplitude.