BACKGROUND:γ-Aminobutyric acid-mediated (GABAergic) neurons in the preoptic area (POA) play a crucial role in sleep regulation, with distinct subpopulations promoting wakefulness and sleep. Dexmedetomidine has the unique property of inducing arousable sedation, but the underlying mechanisms remain incompletely understood. In this study, the authors propose that POA-derived GABAergic neurons regulate natural sleep and wakefulness states through different projections and act similarly for dexmedetomidine-induced sedation and arousability. METHODS:In this study, 99 male and 56 female Gad2-IRES-Cre mice and 10 male C57BL/6J mice (n = 165) were used. The power density in the electroencephalography/electromyography bands was used to assess the depth of dexmedetomidine-induced sedation and to determine the sleep-wakefulness states. A fiber photometry/patch clamp was used to detect changes in the excitability of GABAergic neurons projecting from the POA to the ventral tegmental area (VTA; GABA POA-VTA neurons) and to the lateral hypothalamus (LH; GABA POA-LH neurons). Chemogenetics was used to modulate the excitability of the GABA POA-VTA and GABA POA-LH neurons. Viral tracing was used to map the functional connectivity between POA-derived GABAergic neurons and their targets in the VTA and LH. RESULTS:According to the electroencephalography, electromyography, and fiber photometry recordings, GABA POA-VTA neurons showed elevated activity during natural wakefulness or 40 μg/kg dexmedetomidine-induced sedation. Chemogenetic activation of GABA POA-VTA neurons increased natural wakefulness and reduced dexmedetomidine-induced sedation. The GABA POA-VTA and GABA POA-LH neurons played opposing roles in natural sleep and dexmedetomidine-induced sedation. Retrograde tracing revealed a minimal overlap between these two neuronal subpopulations. Orthodromic tracing demonstrated that GABA POA-VTA neurons preferentially innervated VTA-derived GABAergic neurons, whereas GABA POA-LH neurons mainly projected to LH orexin neurons. CONCLUSIONS:In addition to mediating the sedative versus arousal effects of dexmedetomidine, two distinct subpopulations of GABAergic neurons in the POA are also responsible for promoting natural sleep and wakefulness, respectively.

PURPOSE:Air pollution is an emerging risk factor for adverse surgical outcomes, but its impact on postoperative kidney health is unclear. This study aimed to examine the association between exposure to multiple air pollutants and the risk of acute kidney injury (AKI) after surgery. METHODS:We conducted a retrospective cohort study among inpatients who underwent surgery under anesthesia at three academic medical centers from 2015 to 2023. The Air Quality Health Index (AQHI) was used to comprehensively quantify and score multiple ambient air pollutants. In this study, short-term exposure was defined as the 30-day average prior to surgery, with long-term exposure defined as the 2-year average. The main endpoint was the occurrence of AKI within 7 days after surgery, stage 2 or 3 acute kidney injury (AKI 2+), and acute kidney disease (AKD). RESULTS:This study included 112, 643 surgical patients (with an average age of 54 years, 48.4% of whom were male), among whom 95.3% underwent non-cardiac surgeries and 80.8% had non-emergency surgeries. In the quartile-based analysis of long-term AQHI exposure, higher AQHI levels were associated with increased odds of renal injury AKI (aOR(adjusted Odds Ratio) 1.24; 95% CI, 1.14-1.34), AKI 2+ (aOR 1.29; 95% CI, 1.19-1.53), and AKD (aOR 1.18; 95% CI, 0.97-1.43). However, in the short-term exposure analysis, associations were attenuated but remained significant. AKI (aOR 1.24; 95% CI, 1.14-1.34), AKI 2+ (aOR 1.28; 95% CI, 1.12-1.45), and AKD (aOR 1.18; 95% CI, 1.12-1.45). CONCLUSION:This study found that air pollution significantly impacts postoperative adverse renal outcomes.

Current treatments for Parkinson's disease (PD) fail to halt dopaminergic neurodegeneration and remain largely ineffective against cognitive impairment. Here, we developed IP@ALipo, a nanoplatform that co-delivers the clinical drug pramipexole (PPX) and PEGylated iron oxide nanozyme particles (PEG-IO) via Angiopep-2-modified liposomes capable of crossing the blood-brain barrier (BBB). In the PD mouse model, in vivo photometry showed that a single dose of IP@ALipo significantly enhanced dopaminergic signaling from the substantia nigra pars compacta (SNc) to the striatum (STr) via its PPX component. Facilitated by PEG-IO in IP@ALipo, repeated administration further suppressed cerebral ROS and promoted sustained dopaminergic recovery, resulting in improved motor function. Importantly, the PEG-IO component also preserved hippocampal neurons and restored synaptic architecture, yielding pronounced cognitive benefits. This study demonstrates a nanozyme-augmented strategy for clinical drugs that not only sustains nigrostriatal dopaminergic recovery but also provides cognitive improvements beyond conventional Parkinson's treatments, offering a comprehensive therapeutic approach.

Although nonsteroidal anti-inflammatory drugs (NSAIDs) have been widely used in multimodal pain management under the concept of enhanced recovery after surgery (ERAS), adverse reactions and safety events caused by their unreasonable use have become increasingly prominent. Drawing on the latest literature and evidence-based medicine domestically and abroad, and based on the research and practice frontiers of domestic perioperative analgesia, this working group has reached a consensus on several key domain—including the application regimens of NSAIDs for perioperative analgesia, drug interactions, and precautions as well as prevention strategies in special populations—yielding 12 definitive recommendations. This consensus aims to provide guidance for the standardized selection and application of NSAIDs for perioperative analgesia, and to further promote the rational, safe, and effective use of NSAIDs.

Postoperative depression adversely influences breast cancer patients' clinical outcomes. Our prior study demonstrated that intraoperative esketamine ameliorated postoperative depression in breast cancer patients, yet the underlying neural mechanism remains incompletely understood. We performed a double-blind randomized controlled trial in 35 breast cancer patients with preoperative depressive symptoms, who were randomly given intraoperative esketamine 0.25 mg·kg⁻¹ (n = 18) or saline placebo (n = 17) over the initial 40 min of anesthesia. Resting-state functional magnetic resonance imaging data were collected at preoperative baseline and postoperative day 1 follow-up to calculate brain functional network measures. In contrast to no significant change in the placebo group, the esketamine group showed increased degree centrality of the left inferior frontal gyrus, opercular part from baseline to follow-up, which was related to improvement in depressive symptoms. Additionally, we found significant associations of baseline network measures at the global, nodal, and edge levels with short-term and long-term improvements in depressive symptoms following esketamine administration. These findings may not only provide novel insights into the neural mechanism by which esketamine exerts its antidepressant efficacy during the perioperative period, but also highlight the prospect of functional network measures as useful predictors of antidepressant response to esketamine in patients with breast cancer.

Cognitive impairment is the primary manifestation of neuroinflammation-related central nervous system diseases. Intranasal administration is an effective method, bypassing the blood-brain barrier and delivering drugs to the brain. Herein, we designed a biomimetic self-propelled nanomotor with an inflammation-targeting capacity. This nanomotor comprised a hollow mesoporous manganese dioxide (HMnO2) core and a polydopamine (PDA) shell. HMnO2 effectively catalyzed the conversion of endogenous H2O2 into H2O and O2, enabling the movement of the nanomotor into a wider area to reduce neuroinflammation. The nanomotor was loaded with the natural compound urolithin A (UA), which significantly improved the bioavailability of the compound and enhanced mitophagy. Furthermore, PDA modification imparted the nanomotor with strong adhesive properties, enabling them to anchor effectively to the olfactory nerve and enhancing delivery to the brain. In vitro, PDA@HMnO2@UA alleviated mitochondrial dysfunction, oxidative stress, and inflammation levels by enhancing mitophagy in lipopolysaccharide (LPS)-induced BV2 cells. Following intranasal administration, PDA@HMnO2@UA exerted neuroprotective effects by alleviating microglial activation, neuroinflammation, and neuronal loss, ultimately rescuing the neurocognitive function in the LPS-induced neuroinflammation model. In summary, this study presents an ideal nanomotor platform based on the 3-N strategy, which means “Nanomotor loaded with a Natural product to traverse a Natural anatomical pathway,” that can alleviate cognitive impairments caused by neuroinflammation, offering a promising delivery approach for treating neuroinflammatory diseases.

Perioperative neurocognitive disorders (PND) contribute substantially to morbidity and mortality; however, no therapeutic target has yet been identified. We hypothesized that the neural circuit underlying this surgical complication involves corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus of the hypothalamus (PVN). Using optogenetics, chemogenetics, electrophysiology, and behavioral tests, we demonstrate that surgery activates PVN CRH neurons. These neurons, via CRH receptor 1 (CRHR1), innervate glutamatergic (Glu) neurons in the hippocampal subiculum (Sub), ultimately leading to memory impairments. The PVN CRH receive projections from Glu neurons in the parabrachial nucleus (PBN), a brain region involved in processing peripheral sensory stimuli. Postoperative memory deficit is associated with activation of the PBN Glu-PVN CRH-Sub Glu circuit; chemogenetic inhibition of this circuitry rescues the memory deficit. Additionally, surgery-induced upregulation of circulating interleukin-1β (IL-1β) mediates activation of the PBN Glu-PVN CRH-Sub Glu circuit. This provides direct evidence linking peripheral inflammation to central cognitive dysfunction via a defined neural pathway. These findings advance our understanding of brain-body interactions in neurocognitive disorders and identify an anatomical target for potential intervention in PND.

BACKGROUND:Regional anesthesia (RA) are extensively utilized in lung-resection surgery for pain relief. However, the associations between RA and postoperative pulmonary complications (PPCs) remain inconclusive. Therefore, we aimed to investigate the associations between RA and the incidence of PPCs in adults undergoing lung-resection surgery. METHODS:This retrospective cohort study included adult patients who underwent lung-resection surgery under general anesthesia (GA) at a large comprehensive teaching hospital in China. The primary outcome was PPCs within 7 days. RESULTS:A total of 9,208 patients were enrolled and assigned into group GA, which received GA alone, or group GA+RA, which received GA combined with RA. Within the GA+RA group, patients were further categorized into the GA + PRA group (GA combined with peripheral regional anesthesia) and the GA + EA group (GA combined with epidural anesthesia). Following matching, the GA+RA group showed a non-significant trend toward lower incidence of PPCs (HR 0.93; 95% CI, 0.86-1.01; p = 0.078). However, a significant decreasing trend was observed in specific subgroups, including patients with a surgical duration ≤ 2 h (HR, 0.74 [0.64-0.86]) and those undergoing thoracoscopic surgery (HR, 0.90 [0.83-0.98]). GA combined with PRA also reduced the risk of postoperative congestive heart failure (HR, 0.37 [0.20-0.68]) and pain (HR, 0.89 [0.84-0.95]). CONCLUSIONS:In this retrospective cohort study, the addition of RA to GA was not associated with a significantreduction in PPCs within 7 days after lung resection compared to GA alone. Exploratory analyses identified potential subgroup-specific benefits that warrant prospective validation. TRIAL REGISTRATION:Chinese Clinical Trial Registry (ChiCTR2400090895).

This study aimed to evaluate the predictive value of preoperative point-of-care ultrasound measurements of the quadriceps and vastus intermedius muscles for postoperative delirium (POD). We found that preoperative ultrasound-measured quadriceps muscle thickness, combined with age, is a strong predictor of POD in older adult patients, offering a practical tool for early risk assessment. The non-invasive measurement can be routinely performed preoperatively, enabling early risk stratification and targeted interventions, thereby supporting optimized perioperative management pathways for geriatric patients. Postoperative delirium (POD) is a common neurological complication in older patients. Frailty is an independent risk factor for POD, and sarcopenia has been increasingly linked to cognitive decline through the emerging concept of the brain–muscle axis. This study aimed to evaluate the predictive value of preoperative point-of-care ultrasound (POCUS) measurements of the quadriceps and vastus intermedius muscles for POD. In this prospective observational study, 236 patients aged ≥ 65 years [median (IQR): 72 (69–76)] scheduled for major non-cardiac surgery were enrolled. The POCUS was used to quantitate preoperative quadriceps femoris muscle thickness (QF-MT). POD was assessed daily until postoperative day 7 using the 3-Minute Diagnostic Interview for CAM-defined Delirium (3D-CAM) or the CAM-ICU. Univariate and multivariate logistic regression analyses were performed to identify key factors associated with POD. Receiver operating characteristic (ROC) curve analysis was used to evaluate the predictive efficacy of ultrasonic parameters. POD occurred in 33 patients (14.0

Objective To observe the effect of propofol"bridging"30 minutes before the end of surgery to prevent postoperative nausea and vomiting(PONV)in patients undergoing gynecological laparoscopic surgery under sevoflurane anesthesia.Methods A total of 70 patients undergoing general anesthesia for elective gynecological laparoscopic surgery at the First Affiliated Hospital of Anhui Medical University from June 2022 to September 2023 were enrolled prospectively,who were randomly assigned to either sevoflurane anesthesia group(group S,n=35)or propofol"bridging"group(group P,n=35).Standardized induction protocols were applied in both groups.After induction,anesthesia was maintained with sevoflurane and remifentanil throughout surgery in group S,while the same anesthesia was maintained in group P,but sevoflurane was withdrawn 30 minutes before the end of surgery,followed by intravenous pump infusion of propofol as a bridge until surgery concluded.The patients in both groups were monitored by bispectral index(BIS)to maintain the appropriate anesthesia depth and keep the anesthesia depth stable during the bridging period.The incidence of PONV within 24 h after surgery,the incidence of moderate-to-severe PONV and the use of rescue antiemetics during 0-8 h,＞8-16 h,and＞16-24 h postoperatively were recorded in the two groups.Results Compared with the group S,in the group P,the incidence of PONV was significantly reduced within 24 h after surgery(17.1％vs 42.9％,x2=5.51,P=0.019),the incidence of moderate-to-severe PONV and the use of rescue antiemetics were significantly decreased 0-8 h postoperatively(P＜0.05),and the inhalation time and dosage of sevoflurane were significantly reduced(P＜0.05).Conclusion Propofol"bridging"can effectively reduce the incidence of PONV within 24 h after gynecologic laparoscopic surgery under sevoflurane anesthesia,and decrease the incidence of moderate-to-severe PONV and the use of rescue antiemetics in the early postoperative period.

BACKGROUND:Perioperative neurocognitive disorders (PNDs) are common complications in elderly surgical patients. Possible pathogenic mechanisms for the development of PNDs include loss of synaptic connections mediated by microglial activation, although the precise mechanisms are not fully understood. METHODS:Male and female C57BL/6J or male Cx3cr1-CreERT2 mice, aged 8-12 weeks, were subjected to aseptic tibial fracture surgery, and cognitive tests were carried out 3 days after surgery. Through a combination of bulk RNA sequencing, Western immunoblotting, immunofluorescence, and Golgi staining of the hippocampus, we investigated the role of complement C1q in activating microglia and phagocytosing synaptic connections in the pathogenesis of postoperative neurocognitive disorder. RESULTS:Postoperative mice displayed memory deficits in both the Y-maze (P<0.001) and the trace fear conditioning (TFC) paradigms (P=0.002); these memory deficits were associated with increased microglial activation, complement C1q upregulation, classical complement pathway transcriptomic upregulation, and synapse loss (all P<0.05). After surgery, there was a ∼2-fold increase in colocalisation of C1qa with Homer1 (excitatory) or gephyrin (inhibitory) synaptic proteins in microglia (P<0.001). Postoperative memory decline and synapse loss did not occur after treatment with microglial activity inhibitor minocycline, after exposure to C1q neutralising antibody JL-1, or after C1q depletion from CA1 microglia. Activation of NF-κB was correlated with elevated levels of complement C1q in models, and selective inhibition of NF-κB activation with pyrrolidinedithiocarbamate ammonium (PDTC) attenuated the surgery-induced elevation of C1q and improved cognitive function. CONCLUSIONS:The results demonstrate that hippocampal microglia prune both excitatory and inhibitory synapses in a C1q-dependent manner, contributing to postoperative synapse loss and cognitive dysfunction. Targeting C1q and NF-κB activation could be a promising therapeutic intervention to ameliorate perioperative neurocognitive disorders.

Purpose:This trial aims to compare the effects of intraoperative low-dose dexmedetomidine combined with esketamine versus esketamine alone on postpartum depressive and esketamine-related neuropsychiatric adverse events in cesarean delivery. Patients and Methods:In this randomized controlled trial, 134 parturients scheduled for cesarean delivery under combined spinal-epidural anesthesia were enrolled. Following umbilical cord clamping, patients were randomly allocated to receive either 0.25 mg/kg esketamine combined with 0.5 μg/kg dexmedetomidine (Group DE, n=67) or 0.25 mg/kg esketamine alone (Group E, n=67). The study assessed Edinburgh Postnatal Depression Scale (EPDS) scores on postpartum days 7 and 42, the incidence of esketamine-related neuropsychiatric adverse events, maternal satisfaction, postoperative pain scores, and other adverse events. Results:On postpartum day 7, the Group DE exhibited significantly lower EPDS scores than the Group E (median [IQR]: 3.00 [2.00-4.00] vs 4.00 [3.00-5.00]; P < 0.001). This between-group difference was no longer significant at the 42-day follow-up. The overall incidence of neuropsychiatric adverse events was significantly reduced in the Group DE [22 (32.84%) vs 39 (58.21%), P =0.003], with notably fewer cases of dizziness (19.40% vs 35.82%, P =0.034) and headache (8.96% vs 23.88%, P =0.020). Additionally, the Group DE had lower rates of nausea (8.96% vs 23.88%, P =0.020) and tachycardia (20.90% vs 47.76%, P =0.001), and higher maternal satisfaction scores [10.00 (9.00-10.00) vs 9.00 (9.00-10.00), P =0.005]. Conclusion:Combined low-dose dexmedetomidine and esketamine during cesarean section provides a short-term improvement in early postpartum depressive symptoms, reduces intraoperative neuropsychiatric adverse events, and enhances maternal satisfaction, with a favorable maternal and neonatal safety profile.

Bacterial infections often result in significant pain, negatively impacting patient outcomes and quality of life. Conventional therapies primarily focus on pathogen eradication but frequently overlook the associated pain, thereby limiting their overall clinical effectiveness. Herein, we propose a 'drug-caged drug' strategy in which the secondary amine group of the local anesthetic tetracaine (TTC) is selectively caged by nitric oxide (NO), forming the TTC-NO prodrug. The TTC-NO prodrug is co-loaded with the photocatalyst fac-Ir(ppy)3 into poly(ethylene glycol)-b-poly(ε-caprolactone) (PEG-b-PCL) micellar nanoparticles (TTC-NO@M), enabling dual uncaging of TTC and NO under mild visible light irradiation through a photocatalytic mechanism. We demonstrate that TTC-NO@M exhibits combined antibacterial, anti-inflammatory, and analgesic activities by simultaneously releasing NO and TTC. This strategy effectively treats MRSA-infected mice in both cutaneous wound and septic arthritis models while alleviating infection-associated pain. This work offers a promising approach to address the dual challenges of bacterial infections and the associated pain.

INTRODUCTION:Sepsis-associated encephalopathy (SAE) is a frequent and devastating complication of sepsis, yet effective targeted therapies remain unavailable. The locus coeruleus-hippocampus noradrenergic (LC-HP-NA) system is critical for neurocognitive regulation; however, its role and mechanisms in SAE remain poorly understood. OBJECTIVES:This study aims to confirm that LC-HP-NA activation alleviates sepsis-induced long-term neurocognitive impairment, and clarify the underlying mechanism, focusing on hippocampal astrocytic α2A-adrenoceptor (α2A-AR) and aquaporin-4 (AQP4)-related autophagy. METHODS:Using chemogenetics to activate the LC-HP-NA, genetic manipulation (astrocytic α2A-AR knockdown and AQP4 overexpression), in vivo sepsis mouse models, and in vitro lipopolysaccharide (LPS)-stimulated primary astrocyte cultures. Techniques included microdialysis, western blotting, immunofluorescence, Transmission Electron Microscope and behavioral tests. RESULTS:Sepsis impaired the LC-HP-NA system and long-term neurocognition, with increased hippocampal astrocytic AQP4 expression and inhibited autophagy. LC-HP-NA activation elevated hippocampal noradrenaline release, promoted astrocytic autophagy, suppressed astrocyte reactivity, restored synaptic structures, and improved long-term cognitive function. Notably, knockdown of hippocampal astrocytic α2A-AR or overexpression of astrocytic AQP4 eliminated the neuroprotective effects of LC-HP-NA activation. Mechanistically, in LPS-stimulated astrocytes, α2A-AR activation reduced AQP4 expression, enhanced PPAR-γ/mTOR-dependent autophagy, and decreased astrocyte reactivity, mediated by the cyclic adenosine monophosphate (cAMP)/ protein kinase A (PKA) signaling pathway. CONCLUSION:LC-HP-NA activation alleviates SAE via astrocytic α2A-AR, promoting AQP4-dependent autophagy through the cAMP/PKA. This provides a therapeutic target for SAE.

STUDY OBJECTIVE:This study aims to evaluate the effects of preoperative low-dose dexmedetomidine administration for one night on the incidence of postoperative delirium in elderly patients with hip fracture. DESIGN:This was a randomized, double blind, placebo-controlled clinical trial. SETTING:Lu'an Hospital of Anhui Medical University, Anhui, China. PATIENTS:Patients aged ≥65 years with hip fracture (femoral neck, intertrochanteric, or subtrochanteric fracture) and scheduled for surgical repair(total hip arthroplasty, hemiarthroplasty, internal fixation with cannulated screw or intramedullary nail) under spinal anesthesia were eligible. INTERVENTION:Patients were randomized 1:1 to receive low-dose dexmedetomidine or placebo from 8:00 pm before surgery to 8:00 am the day of surgery. MEASUREMENTS:The primary outcome was the incidence of POD between postoperative days 1 and 7 or at hospital discharge. The secondary outcome measures included preoperative sleep quality, days of delirium, visual analog scale scores in quiet and active states on postoperative days 1-3, C-reactive protein level, number of analgesic pump presses, activities of daily living score at discharge and postoperative hospital stay. Perioperative adverse events were recorded. MAIN RESULTS:Of the 248 patients randomized to the placebo (n = 124) or dexmedetomidine (n = 124) group, 233 participants (117 in the placebo group and 116 in the dexmedetomidine group) were included in the modified intention-to-treat analysis. The incidence of POD was lower in the dexmedetomidine group (10.3 %) than placebo group (22.2 %, P = 0.014). Compared to the placebo group, the dexmedetomidine group had higher preoperative Leeds Sleep Evaluation Questionnaire (LSEQ) scores (P < 0.001), lower preoperative Insomnia Severity Index (ISI) scores (P < 0.001), and lower postoperative C-reactive protein (CRP) levels (P < 0.001). No differences in other secondary outcomes and perioperative adverse events were observed between the two groups. CONCLUSION:In patients aged ≥65 years undergoing elective hip fracture surgery under spinal anesthesia, continuous overnight administration of low-dose dexmedetomidine improved sleep quality on the night before surgery and reduced the incidence of POD.

Current therapies for Alzheimer's disease (AD) primarily target amyloid-β (Aβ) pathology using monoclonal antibodies, yet their limited efficacy partly results from unintended exacerbation of neural hyperexcitability. This highlights a critical but under-appreciated link between Aβ clearance and neuronal network dysfunction. Here, we designed R@AClipo, a nanotherapeutic platform that codelivers the TREM2 agonist peptide COG1410 and the glutamate modulator riluzole via Angiopep-2-modified liposomes capable of crossing the blood-brain barrier. In AD model mice, R@AClipo upregulated TREM2 expression and enhanced microglial-mediated Aβ clearance. Concurrently, it reduced glutamate accumulation and mitigated neuronal hyperexcitability, as measured by in vivo fiber photometry. Notably, TREM2-driven Aβ clearance alone modestly reduced hyperexcitability, independent of riluzole, contrasting with the excitatory effects frequently associated with antibody-based Aβ therapies. This combinatorial strategy improved cognitive performance and restored neural activity patterns without observable toxicity. Together, these findings support a physiologically compatible strategy that targets the pathological crosstalk between Aβ accumulation and neural hyperexcitability, offering a promising avenue for AD intervention.

AIMS:The mechanism underlying postoperative post-traumatic stress disorder (PTSD) remains unclear. However, studies have shown that acute postoperative pain is an independent risk factor for PTSD, which is also closely related to memory consolidation enhancement. Preoperative patients often experience unpleasant traumatic events, and postoperative pain usually occurs in the memory consolidation stage of these events. Therefore, inquiring whether acute postoperative pain affects memory consolidation and its possible mechanism may help to explain the causes of postoperative PTSD. METHODS AND RESULTS:In this study, we show that the surgical incision pain enhances the consolidation of emotional memory (in the passive avoidance test) and nonemotional memory (in the novel object recognition test) in mice. None of the behaviors evaluated were affected by anxiety or locomotor dysfunction (in the open-field test). Besides, we confirmed that surgical incision pain promotes memory enhancement by enhancing memory consolidation instead of memory retrieval. Furthermore, the consolidation of emotional memory and nonemotional memory was enhanced by the activation of the LC-HPC TH projection after surgical incision pain. Hippocampal CA1 dopamine receptors, rather than β adrenoceptors, mediate emotional and nonemotional memory consolidation enhancement after surgical incision pain. CONCLUSION:Thus, our results indicate that surgical incision pain enhances the memory consolidation of emotional memory and nonemotional memory in mice. Activation of the LC-HPC TH projection may contribute to memory consolidation enhancement induced by surgical incision pain, which involves the activity of dopamine receptors in CA1.