Neuroscience最新文献

Angiogenesis is involved in the underlying musculoskeletal pain mechanism; therefore, embolization of blood vessels is expected to have an analgesic effect. We investigated the analgesic effect of intraarterial administration of imipenem cilastatin sodium (IPM/CS) in knee osteoarthritis (OA) model rats using behavioral measures and in vivo patch-clamp recording. To develop the knee OA model, monosodium iodoacetate (MIA) was administered to the right knee joint. First, we infused IPM/CS in the right femoral artery and investigated the knee joint mechanical pressure threshold using a digital device. Next, the nociceptive signals originating from the knee were analyzed via the spontaneous excitatory postsynaptic current (sEPSC) record within the neural cells in the dorsal spinal horn using the in vivo patch-clamp approach. In knee OA rats, the mechanical thresholds at the damaged knee were decreased compared with those of the contralateral knee, whereas these thresholds remained stable in the sham group. The pressure threshold of knee OA rats was significantly increased following intraarterial infusion of IPM/CS but not saline. However, the pain thresholds of knee OA rats were unaltered. A notable rise in the average sEPSC frequency was detected in knee OA rats compared with the sham group. The sEPSC decreased in knee OA rats following intraarterial infusion of IPM/CS but not saline. These results indicated that intraarterial infusion of IPM/CS attenuated pain caused by knee OA. Hence, this method could serve as a strategy for pain alleviation in patients with knee osteoarthritis.

Over the past fifty years, research has enhanced our understanding of meditation and its effects on cognition. Meditation is particularly promising due to its long-term (trait) effects, which persist outside meditation sessions. Advances in neuroimaging have enabled the study of these effects using neural markers such as mismatch negativity (MMN), which reflects the involuntary shift of attention to unexpected acoustic changes. This shift is modulated by attentional control, a key area where focused attention (FA) meditation training offers improvements. However, studies investigating the trait effects of FA meditation on MMN have produced mixed results, with previous research introducing confounds from short-term (state) effects that may influence trait-specific assessments. Furthermore, most research has focused on breath-based FA meditation, overlooking other prominent forms of FA meditation that might differentially modulate MMN, as per recent studies. The current study, therefore, examines mantra meditation, a widely practiced form of FA meditation, with an adequately powered sample to address the mixed findings in the literature. The study employs an intensity oddball paradigm instead of commonly used frequency oddball paradigms to assess whether MMN arises from higher-order cognitive processes or sensory adaptation. The findings reveal similar MMN amplitude in experts and novices, suggesting that MMN may be insensitive to meditation expertise or influenced by the enhanced attentional skills of novices. Additionally, a unidirectional polarity shift in event-related potential to deviant stimuli suggests that meditation effects on MMN should be interpreted in the context of higher-order deviance detection mechanism.

Alzheimer's disease (AD) is predominantly the most recurring and devastating neurological condition among the elderly population, characterized by the accumulation of amyloid-β (Aβ) and phosphorylated tau proteins, and is accompanied by progressive decline of learning and memory. Due to its complex and multifactorial etiology, a wide variety of therapeutic interventions have been developed. Despite constant advancements in the field, effective treatments that ameliorate the severity of Alzheimer's symptoms or cease their progression are still insufficient. Mounting evidence suggests that synaptic dysfunction could be an essential component of AD pathogenesis as synapse signaling is impaired in the aging brain, which contributes to synaptic decline. Therefore, improving neuroplasticity such as synaptic plasticity or neurogenesis could be a promising therapeutic approach for alleviating the effects of AD. This article reviews the cellular and molecular threads of neuroplasticity as well as targets that restore neuronal survival and plasticity to provide functional recoveries, including receptors, downstream signaling pathways, ion channels, transporters, enzymes, and neurotrophic factors.