Objective To investigate the change in GABA receptor-activated current in dorsal root ganglion (DRG) neurons in rats with neuropathic pain. Methods Twenty adult SD rats of both sexes weighing 100-150 g were randomly divided into 2 gorups: sham operation group (group S, n = 5) and neuropathic pain group (group NP, n= 15). Neuropathic pain was induced by ligation of right L5 spinal nerve. The animals were sacrificed at 5 days after operation. The L5 DRG( neurons in group NP and L3-5 DRG neurons in group S were immediately isolated. Whole-cellpatch- clamp technique was used. The extracellular solution contained GABA 100μmol/L.The frequency and amplitude of the GABA-activated current in DRG neurons and the changes in action potential (threshold potential, rheobase and overshoot) and resting potential before and after GABA administration were recorded. Results GABA 100μmol/L induced rapid inactivation of inward current in most neurons. Compared with the baseline before application of GABA, in group S GABA induced depolarization,increased resting potential and decreased amplitude and rheobase of action potential in large and medium DRG neurons, while in group NP GABA increased resting potential but induced no significant change in threshold potential and rheobase and overshoot of action potential. The frequency and amplitude of GABA-activated current and the degree of change in resting potential and rheobase and overshoot of action potential were significantly lower in group NP than in group S.Spontaneous discharge occurred in small DRG neurons in both groups. No GABA-activated current was observed in all DRG neurons with spontaneous discharge. Conclusions Neuropathic pain is induced by decreasing GABA-mediated inhibition signals in large and medium DRG neurons leading to increased excitability of neurons.

Objective:To develop and validate a risk prediction model for cognitive frailty in elderly patients with type 2 diabetes.Methods:A total of 483 elderly patients with type 2 diabetes who visited Tianjin First Central Hospital from June to December 2022 were selected using convenience sampling. They were randomly divided into a modeling group ( n=338) and a validation group ( n=145). Data were collected using a self-designed general information questionnaire, the Short-Form Mini Nutritional Assessment (MNA-SF), the Geriatric Depression Scale-15 (GDS-15), the Frailty Phenotype (FP), the Montreal Cognitive Assessment (MoCA), and the Clinical Dementia Rating (CDR). Logistic regression analysis was performed to identify the influencing factors. A cognitive frailty risk prediction nomogram model was constructed based on the results. The model was validated in the validation group, and its predictive performance and clinical applicability were evaluated using the area under the receiver operating characteristic curve ( AUC), calibration curve, and clinical decision curve analysis. A total of 483 questionnaires were distributed and all were returned as valid, resulting in a 100.0% response rate. Results:The prevalence of cognitive frailty in the 483 elderly patients with type 2 diabetes was 20.3% (98/483). Age, regular exercise, duration of diabetes, HbA1c levels, depression and nutritional status were identified as predictive factors in the model. The AUC of the model was 0.886, and the Hosmer-Lemeshow test showed a χ 2 value of 8.004 ( P=0.433). The optimal cutoff value was 0.335, and the accuracy was 89.0%. Conclusions:The prediction model demonstrates good fit and strong predictive performance, and can intuitively and easily identify elderly patients with type 2 diabetes who are at high risk of cognitive frailty, providing a reference for early screening and intervention.