Research into the neural basis of recognition memory has traditionally focused on the remembrance of visual stimuli. The present study examined the neural basis of object recognition memory in the dark, with a view to determining the extent to which it shares common pathways with visual-based object recognition. Experiment 1 assessed the expression of the immediate-early gene c-fos in rats that discriminated novel from familiar objects in the dark (Group Novel). Comparisons made with a control group that explored only familiar objects (Group Familiar) showed that Group Novel had higher c-fos activity in the rostral perirhinal cortex and the lateral entorhinal cortex. Outside the temporal region, Group Novel showed relatively increased c-fos activity in the anterior medial thalamic nucleus and the anterior cingulate cortex. Both the hippocampal CA fields and the granular retrosplenial cortex showed borderline increases in c-fos activity with object novelty. The hippocampal findings prompted Experiment 2. Here, rats with hippocampal lesions were tested in the dark for object recognition memory at different retention delays. Across two replications, no evidence was found that hippocampal lesions impair nonvisual object recognition. The results indicate that in the dark, as in the light, interrelated parahippocampal sites are activated when rats explore novel stimuli. These findings reveal a network of linked c-fos activations that share superficial features with those associated with visual recognition but differ in the fine details; for example, in the locus of the perirhinal cortex activation. While there may also be a relative increase in c-fos activation in the extended-hippocampal system to object recognition in the dark, there was no evidence that this recognition memory problem required an intact hippocampus.
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http://dx.doi.org/10.1037/a0031216 | DOI Listing |
Objective: The aim of this study was to investigate the role of ferroptosis in the occurrence of postoperative cognitive dysfunction (POCD) using a mouse model and to elucidate whether electroacupuncture (EA) can improve POCD by suppressing ferroptosis via the transferrin receptor 1 (TFR1)-divalent metal transporter 1 (DMT1)-ferroportin (FPN) pathway.
Methods: The experiment involved three groups: the control group, the POCD group and the POCD + EA group. The POCD animal model was established using sevoflurane anesthesia and tibial fracture.
J Neuroinflammation
January 2025
Department of Neurosurgery, Emory University School of Medicine, Atlanta, GA, 30322, USA.
Following recent advances in post-thrombectomy stroke care, the role of neuroinflammation and neuroprotective strategies in mitigating secondary injury has gained prominence. Yet, while neuroprotection and anti-inflammatory agents have re-emerged in clinical trials, their success has been limited. The neuroinflammatory response in cerebral ischemia is robust and multifactorial, complicating therapeutic approaches targeting single pathways.
View Article and Find Full Text PDFNat Commun
January 2025
Guangxi Key Laboratory of Clean Pulp & Papermaking and Pollution Control, School of Light Industry and Food Engineering, Guangxi University, Nanning, 530004, PR China.
Skin-like sensors capable of detecting multiple stimuli simultaneously have great potential in cutting-edge human-machine interaction. However, realizing multimodal tactile recognition beyond human tactile perception still faces significant challenges. Here, an extreme environments-adaptive multimodal triboelectric sensor was developed, capable of detecting pressure/temperatures beyond the range of human perception.
View Article and Find Full Text PDFJ Vis
January 2025
Department of Psychology, New York University, New York, NY, USA.
Active object recognition, fundamental to tasks like reading and driving, relies on the ability to make time-sensitive decisions. People exhibit a flexible tradeoff between speed and accuracy, a crucial human skill. However, current computational models struggle to incorporate time.
View Article and Find Full Text PDFMetab Brain Dis
January 2025
Department of Biological Sciences (Pharmacology and Toxicology), National Institute of Pharmaceutical Education and Research (NIPER) Hyderabad, Balanagar, Hyderabad, 500037, Telangana, India.
The negative impact of repeated-mild traumatic brain injury (rmTBI) is profoundly seen in circadian-disrupted individuals. The unrelenting inflammation, glial activation, and gut dysbiosis are key neuropathological aberrations in the aftermath of rmTBI. In this study, we examined the impact of chitosan lactate (CL) on circadian disturbance (CD) + rmTBI-generated neurological dysfunctions and its prebiotic response on the gut-brain axis.
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