Projections from anteromedial thalamus nucleus to the midcingulate cortex mediate pain and anxiety-like behaviors in mice.

Prior research has demonstrated the involvement of the midcingulate cortex (MCC) and its downstream pathway in pain regulation. However, the mechanism via which pain information is conveyed to the MCC remains unclear. The present study utilized immunohistochemistry, chemogenetics, optogenetics, and behavior detection methods to explore the involvement of MCC, anteromedial thalamus nucleus (AM), and AM-MCC pathway in pain and emotional regulation. Chemogenetics or optogenetics methods were employed to activate/inhibit MCCCaMKIIα, AMCaMKIIα, AMCaMKIIα-MCC pathway. This manipulation evokes/relieves mechanical and partial heat hyperalgesia, as well as anxiety-like behaviors. In the complete Freund,s adjuvant (CFA) inflammatory pain model, chemogenetic inhibition of the AMCaMKIIα-MCCCaMKIIα pathway contributed to pain relief. Notably, this study presented the first evidence implicating the AM in the regulation of nociception and negative emotions. Additionally, it was observed that the MCC primarily receives projections from the AM, highlighting the crucial role of this pathway in the transmission of pain and emotional information.

The effects of phenylethanoid glycosides, derived from Herba cistanche, on cognitive deficits and antioxidant activities in male SAMP8 mice.

Cognitive deficits are closely associated with hippocampal synaptic changes. Phenylethanoid glycosides (PhG), derived from Herba cistanche, are known to exert protective effects on cognitive deficits in Alzheimer's disease (AD); however, the underlying mechanisms of this herbal extract on cognitive performance remain unclear. The aim of this study was thus to examine the protective mechanism attributed to PhG on cognitive deficits in an AD senescence accelerated mouse prone 8 (SAMP8) model. Cognitive deficit parameters examined included (1) Morris water maze (MWM) assessing cognitive performance and (2) quantification of dendritic spine density in hippocampal CA1 region by Golgi staining, a molecular biomarker of synaptic function. In addition, levels of malondialdehyde (MDA) and activities of superoxide dismutase (SOD) and gluthathione peroxidase (GSH-Px) were determined to examine the potential role of oxidant processes in cognitive dysfunction. Data showed that PhG significantly decreased escape latency and path length, associated with a rise in the percentage of time spent in the target quadrant and number of platform crossings. In addition, PhG significantly increased dendritic spine density in the hippocampal CA1 region accompanied by elevated expression levels of synaptophysin (SYN) and post synaptic density 95 (PSD-95), reduced MDA content, and elevated the activities of SOD and GSH-Px. Data suggest that the ability of PhG to ameliorate cognitive deficits in SAMP8 mice may be related to promotion in synaptic plasticity involving antioxidant processes.