Pathology-Specific Modulation of Corticostriatal Circuitry by Chronic Alcohol Consumption in Alzheimer's Disease Mouse Models.

Unlabelled: Chronic alcohol use is a major modifiable risk factor for Alzheimer's disease (AD), yet the mechanisms by which it modulates AD pathophysiology remain unclear. Here, we examined circuit-level and pathological changes in two distinct AD mouse models, humanized Aβ knock-in (hAPP-KI) (Aβ-driven) and PS19 (tau-driven), subjected to a chronic intermittent alcohol exposure paradigm. In hAPP-KI mice, alcohol increased Aβ accumulation and excitatory transmission in the medial prefrontal cortex (mPFC) while reducing corticostriatal transmission and striatal cholinergic output.

Abstinence and extinction drive opposing changes in striatal activity and dopamine signaling during alcohol relapse.

Relapse remains a major challenge in the treatment of alcohol use disorder, driven in part by persistent neuroadaptations. However, how different post-alcohol experiences, such as passive withdrawal (abstinence) versus active extinction training, differentially shape the neural circuits and synaptic mechanisms that influence relapse vulnerability remains unclear. Here, we show that these experiences have opposing effects on dorsomedial striatal (DMS) direct-pathway medium spiny neurons (dMSNs) and dopamine dynamics during cue-induced reinstatement of alcohol seeking.

Perinatal and prenatal alcohol exposure impairs striatal cholinergic function and cognitive flexibility in adult offspring.

Fetal Alcohol Spectrum Disorder (FASD), caused by perinatal alcohol exposure (PeAE) and prenatal alcohol exposure (PAE), is characterized by significant cognitive impairments, including reduced cognitive flexibility. Despite the critical role of cholinergic interneurons (CINs) in the dorsomedial striatum (DMS) for cognitive and behavioral flexibility, their contribution to neurobehavioral deficits in FASD remains unclear. To address this gap, this research explored the impact of PeAE and PAE on CIN populations and activity, cognitive flexibility, and compulsive drinking behaviors in adult offspring.

Prenatal Alcohol Exposure Impairs Striatal Cholinergic Function and Cognitive Flexibility in Adult Offspring.

Fetal Alcohol Spectrum Disorder (FASD), caused by prenatal alcohol exposure (PAE), is characterized by significant cognitive impairments, including reduced cognitive flexibility. Despite the critical role of cholinergic interneurons (CINs) in the dorsomedial striatum (DMS) for cognitive and behavioral flexibility, their contribution to neurobehavioral deficits in FASD remains unclear. To address this gap, this research explored the impact of PAE on CIN populations and activity, cognitive flexibility, and compulsive drinking behaviors in adult offspring.

Abstinence and Extinction Drive Opposing Changes in Striatal Activity and Dopamine Signaling During Alcohol Relapse.

Unlabelled: Relapse remains a major obstacle in the treatment of alcohol use disorder, often driven in part by enduring neuroadaptations. However, how different treatment strategies-such as abstinence versus extinction training-modulate the underlying neural circuits and synaptic mechanisms that shape relapse vulnerability remains poorly understood. In this study, we demonstrate that abstinence and extinction distinctly influence dorsomedial striatal (DMS) direct-pathway medium spiny neuron (dMSN) activity and dopamine signaling during cue-induced reinstatement of alcohol seeking.

Transcriptome sequence reveal the roles of MaGME777 and MabHLH770 in drought tolerance in Musa acuminata.

Banana, a globally cultivated fruit, faces significant constraints in distribution and sustainable production due to drought stress. This study investigated drought tolerance in Cavendish bananas using RNA-seq time-course analysis and molecular biology experiments. Plants were subjected to dehydration treatments, and physiological indicators such as electrolyte leakage, proline content, malonaldehyde, peroxidase activity, and hydrogen peroxide content were assessed.

Dynamic responses of striatal cholinergic interneurons control behavioral flexibility.

Striatal cholinergic interneurons (CINs) are key to regulating behavioral flexibility, involving both extinguishing learned actions and adopting new ones. However, the mechanisms driving these processes remain elusive. In this study, we initially demonstrate that chronic alcohol consumption disrupts the burst-pause dynamics of CINs and impairs behavioral flexibility.

Traumatic Brain Injury Exacerbates Alcohol Consumption and Neuroinflammation with Decline in Cognition and Cholinergic Activity.

Traumatic brain injury (TBI) is a global health challenge, responsible for 30% of injury-related deaths and significantly contributing to disability. Annually, over 50 million TBIs occur worldwide, with most adult patients at emergency departments showing alcohol in their system. TBI is also a known risk factor for alcohol abuse, yet its interaction with alcohol consumption remains poorly understood.

Experimental Models of Alcohol Use Disorder and Their Application for Pathophysiological Investigations.

Alcohol use disorder (AUD) is a complex disorder characterized by compulsive alcohol use and a lack of control over alcohol intake. Several experimental methods using mouse models have been developed to improve research regarding this disorder. Mouse behavioral paradigms are advantageous in inducing alcohol dependence and evaluating alcohol intake, circumventing ethical issues, and increasing experimental control over human-based experiments.

Activity-dependent labeling and manipulation of fentanyl-recruited striatal ensembles using ArcTRAP approach.

Understanding the memory substrates underlying substance abuse requires the permanent tagging and manipulation of drug-recruited neural ensembles. Here, we present a protocol for activity-dependent labeling and chemogenetic manipulation of fentanyl-activated striatal ensembles using the ArcTRAP approach. We outline the necessary steps to breed ArcTRAP mice, prepare drugs and reagents, conduct behavioral training, and perform tagging and manipulation.

Linking input- and cell-type-specific synaptic plasticity to the reinforcement of alcohol-seeking behavior.

The reinforcement of voluntary alcohol-seeking behavior requires dopamine-dependent long-term synaptic plasticity in the striatum. Specifically, the long-term potentiation (LTP) of direct-pathway medium spiny neurons (dMSNs) in the dorsomedial striatum (DMS) promotes alcohol drinking. However, it remains unclear whether alcohol induces input-specific plasticity onto dMSNs and whether this plasticity directly drives instrumental conditioning.

A web-based nomogram model for predicting the overall survival of hepatocellular carcinoma patients with external beam radiation therapy: A population study based on SEER database and a Chinese cohort.

Background: External beam radiation therapy (EBRT) for hepatocellular carcinoma (HCC) is rarely used in clinical practice. This study aims to develop and validate a prognostic nomogram model to predict overall survival (OS) in HCC patients treated with EBRT.

Method: We extracted eligible data of HCC patients between 2004 and 2015 from the Surveillance, Epidemiology, and End Results (SEER) database.

Retrospective study of hypofractionated stereotactic radiotherapy combined with whole brain radiotherapy for patients with brain metastases.

Background And Purpose: To evaluate the clinical outcomes of hypofractionated stereotactic radiotherapy (HFSRT) combined with whole brain radiotherapy (WBRT) in patients with brain metastases (BMs).

Materials And Methods: From May 2018 to July 2020, 50 patients (111 lesions) received HFSRT (18 Gy/3F) + WBRT (40 Gy/20F). The RECIST 1.

Optogenetic induction of orbitostriatal long-term potentiation in the dorsomedial striatum elicits a persistent reduction of alcohol-seeking behavior in rats.

Uncontrolled drug-seeking and -taking behaviors are generally driven by maladaptive corticostriatal synaptic plasticity. The orbital frontal cortex (OFC) and its projections to the dorsomedial striatum (DMS) have been extensively implicated in drug-seeking and relapse behaviors. The influence of the synaptic plasticity of OFC projections to the DMS (OFC→DMS) on drug-seeking and -taking behaviors has not been fully characterized.

Role of Muscle Mass and Nutritional Assessment Tools in Evaluating the Nutritional Status of Patients With Locally Advanced Nasopharyngeal Carcinoma.

This study was to explore the role and necessity of muscle mass [fat-free mass index (FFMI) and appendicular skeletal muscle index (ASMI) measured by bioelectrical impedance analysis (BIA)] in nutritional status evaluation of patients with locally advanced (III, IVa) nasopharyngeal carcinoma (NPC). One hundred and thirty locally advanced NPC patients were recruited. Their nutritional status was assessed by albumin (ALB), body mass index (BMI), Nutritional Risk Screening 2002 (NRS 2002), Patient generated-Subjective Global Assessment (PG-SGA), and muscle mass.

Whole-Brain Mapping of Direct Inputs to Dopamine D1 and D2 Receptor-Expressing Medium Spiny Neurons in the Posterior Dorsomedial Striatum.

The posterior dorsomedial striatum (pDMS) is mainly composed of medium spiny neurons (MSNs) expressing either dopamine D1 receptors (D1Rs) or D2Rs. Activation of these two MSN types produces opposing effects on addictive behaviors. However, it remains unclear whether pDMS D1-MSNs or D2-MSNs receive afferent inputs from different brain regions or whether the extrastriatal afferents express distinct dopamine receptors.

MEG3 Induces Cervical Carcinoma Cells' Apoptosis Through Endoplasmic Reticulum Stress by miR-7-5p/STC1 Axis.

Many patients with advanced cervical cancer (CC) have a poor prognosis and their mortality rank the first among women with malignant tumors. It's essential to explore the molecular mechanism of CC in clinical practice. Long noncoding RNA maternally expressed gene 3 (MEG3) has been reported to downregulate in CC tissues.

MORC2 promotes cell growth and metastasis in human cholangiocarcinoma and is negatively regulated by miR-186-5p.

Microrchidia family CW-type zinc finger 2 (MORC2) is a ubiquitously expressed protein that contributes to chromatin remodeling, DNA repair, and lipogenesis. However, its role in cholangiocarcinoma (CCA) remains largely unknown. The aim of this study was to investigate the expression profile of MORC2 and its potential functions in CCA progression.

Correction: The influences of the M2R-GIRK4-RGS6 dependent parasympathetic pathway on electrophysiological properties of the mouse heart.

[This corrects the article DOI: 10.1371/journal.pone.