Lumbar spinal stenosis (LSS) is a common disease in the elderly, mostly due to degenerative changes in the lumbar spinal complex. Decompression surgery is the standard surgical treatment for LSS. ...Classically, total laminectomy-which involves resection of the spinous process, entire laminae and medial facet-has been the standard decompression technique; however, it can cause post-surgical instability. To overcome this disadvantage, various minimally invasive techniques that preserve the stabilization structures of the spine have been developed, and surgeons have begun to re-evaluate decompression surgery from the standpoint of reduced invasiveness and cost. More than two decades have passed since the introduction of microendoscopic spine surgery, and studies continue to shed light on its advantages and limitations as new knowledge becomes available. This article is a narrative review of the available literature, along with authors' experience, regarding the indications, surgical techniques, clinical outcomes, and limitations/complications of microendoscopic decompression for LSS.
We report that, in the rat hippocampus, learning leads to a significant increase in extracellular lactate levels that derive from glycogen, an energy reserve selectively localized in astrocytes. ...Astrocytic glycogen breakdown and lactate release are essential for long-term but not short-term memory formation, and for the maintenance of long-term potentiation (LTP) of synaptic strength elicited in vivo. Disrupting the expression of the astrocytic lactate transporters monocarboxylate transporter 4 (MCT4) or MCT1 causes amnesia, which, like LTP impairment, is rescued by L-lactate but not equicaloric glucose. Disrupting the expression of the neuronal lactate transporter MCT2 also leads to amnesia that is unaffected by either L-lactate or glucose, suggesting that lactate import into neurons is necessary for long-term memory. Glycogenolysis and astrocytic lactate transporters are also critical for the induction of molecular changes required for memory formation, including the induction of phospho-CREB, Arc, and phospho-cofilin. We conclude that astrocyte-neuron lactate transport is required for long-term memory formation.
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► Learning results in glycogenolysis-dependent lactate increase in the hippocampus ► Inhibiting glycogenolysis in the hippocampus blocks long-term memory and LTP ► Knockdown of astrocytic lactate transporters abolishes long-term memory ► Knockdown of neuronal lactate transporter abolishes long-term memory
Emotionally relevant experiences form strong and long-lasting memories by critically engaging the stress hormone/neurotransmitter noradrenaline, which mediates and modulates the consolidation of ...these memories. Noradrenaline acts through adrenergic receptors (ARs), of which β₂-adrenergic receptors (βARs) are of particular importance. The differential anatomical and cellular distribution of βAR subtypes in the brain suggests that they play distinct roles in memory processing, although much about their specific contributions and mechanisms of action remains to be understood. Here we show that astrocytic rather than neuronal β₂ARs in the hippocampus play a key role in the consolidation of a fear-based contextual memory. These hippocampal β₂ARs, but not β₁ARs, are coupled to the training-dependent release of lactate from astrocytes, which is necessary for long-term memory formation and for underlying molecular changes. This key metabolic role of astrocytic β₂ARs may represent a novel target mechanism for stress-related psychopathologies and neurodegeneration.
Purpose
An osteoporotic vertebral fracture (OVF) is a common disease that causes disabilities in elderly patients. In particular, patients with nonunion following an OVF often experience severe back ...pain and require surgical intervention. However, nonunion diagnosis generally takes more than six months. Although several studies have advocated the use of magnetic resonance imaging (MRI) observations as predictive factors, they exhibit insufficient accuracy. The purpose of this study was to create a predictive model for OVF nonunion using machine learning (ML).
Methods
We used datasets from two prospective cohort studies for OVF nonunion prediction based on conservative treatment. Among 573 patients with acute OVFs exceeding 65 years in age enrolled in this study, 505 were analyzed. The demographic data, fracture type, and MRI observations of both studies were analyzed using ML. The ML architecture utilized in this study included a logistic regression model, decision tree, extreme gradient boosting (XGBoost), and random forest (RF). The datasets were processed using Python.
Results
The two ML algorithms, XGBoost and RF, exhibited higher area under the receiver operating characteristic curves (AUCs) than the logistic regression and decision tree models (AUC = 0.860 and 0.845 for RF and XGBoost, respectively). The present study found that MRI findings, anterior height ratio, kyphotic angle, BMI, VAS, age, posterior wall injury, fracture level, and smoking habit ranked as important features in the ML algorithms.
Conclusion
ML-based algorithms might be more effective than conventional methods for nonunion prediction following OVFs.
Glycogenolysis and lactate transport from astrocytes to neurons is required for long-term memory formation, but the role of this lactate is poorly understood. Here we show that the Krebs cycle ...substrates pyruvate and ketone body B3HB can functionally replace lactate in rescuing memory impairment caused by inhibition of glycogenolysis or expression knockdown of glia monocarboxylate transporters (MCTs) 1 and 4 in the dorsal hippocampus of rats. In contrast, either metabolite is unable to rescue memory impairment produced by expression knockdown of MCT2, which is selectively expressed by neurons, indicating that a critical role of astrocytic lactate is to provide energy for neuronal responses required for long-term memory. These responses include learning-induced mRNA translation in both excitatory and inhibitory neurons, as well as expression of Arc/Arg3.1. Thus, astrocytic lactate acts as an energy substrate to fuel learning-induced de novo neuronal translation critical for long-term memory.
During fear conditioning, animals learn an association between a previously neutral or conditioned stimulus (CS) and an aversive or unconditioned stimulus (US). Subsequent reexposure to the CS alone ...triggers two competing processes. Brief reexposure to the CS initiates reconsolidation processes that serve to stabilize or maintain the original CS-US memory. In contrast, more prolonged reexposure to the CS leads to the formation of an inhibitory extinction (CS-no US) memory. Previous studies have established that both reconsolidation and extinction require gene expression. Consistent with this, here we first show that genetic disruption of cAMP-responsive element-binding protein (CREB)-mediated transcription blocks both reconsolidation and long-term extinction of contextual fear memory. We next asked whether reconsolidation and extinction engage CREB-mediated transcription in distinct brain regions. Accordingly, we used immunohistochemical approaches to characterize the activation of the transcription factor CREB as well as the expression of the CREB-dependent gene Arc (activity-regulated cytoskeleton-associated protein) after brief versus prolonged reexposure to a previously conditioned context. After brief reexposure, we observed significant activation of CREB-mediated gene expression in the hippocampus and amygdala. In contrast, after the prolonged reexposure, we observed significant activation of CREB-mediated gene expression in the amygdala and prefrontal cortex. Finally, we showed that blocking protein synthesis in either the hippocampus or the amygdala blocked reconsolidation of contextual fear memory, whereas similar blockade in the amygdala and prefrontal cortex prevented the formation of extinction memory. These experiments establish that reactivated contextual fear memories undergo CREB-dependent reconsolidation or extinction in distinct brain regions.
When processing current sensory inputs, animals refer to related past experiences. Current information is then incorporated into the related neural network to update previously stored memories. ...However, the neuronal mechanism underlying the impact of memories of prior experiences on current learning is not well understood. Here, we found that a cellular ensemble in the posterior parietal cortex (PPC) that is activated during past experience mediates an interaction between past and current information to update memory through a PPC-anterior cingulate cortex circuit in mice. Moreover, optogenetic silencing of the PPC ensemble immediately after retrieval dissociated the interaction without affecting individual memories stored in the hippocampus and amygdala. Thus, a specific subpopulation of PPC cells represents past information and instructs downstream brain regions to update previous memories.
Behavioural tagging is the transformation of a short-term memory, induced by a weak experience, into a long-term memory (LTM) due to the temporal association with a novel experience. The mechanism by ...which neuronal ensembles, each carrying a memory engram of one of the experiences, interact to achieve behavioural tagging is unknown. Here we show that retrieval of a LTM formed by behavioural tagging of a weak experience depends on the degree of overlap with the neuronal ensemble corresponding to a novel experience. The numbers of neurons activated by weak training in a novel object recognition (NOR) task and by a novel context exploration (NCE) task, denoted as overlapping neurons, increases in the hippocampal CA1 when behavioural tagging is successfully achieved. Optical silencing of an NCE-related ensemble suppresses NOR-LTM retrieval. Thus, a population of cells recruited by NOR is tagged and then preferentially incorporated into the memory trace for NCE to achieve behavioural tagging.
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