PLGA from PolySciTech used in research on neural interplay between physical stress and pain

 

The neurological experience of pain can vary widely and is controlled by a variety of factors in the brain. A classic example is when a person is cooking in a kitchen only to look down and realize that they were bleeding from a scratch on their hand that they didn’t even notice had happened. In this case a combination of distraction and activity suppressed the sensation of pain. To further understand the relationship between stress and pain management, researchers at Indian Institute of Science utilized PLGA (cat# AP041) from PolySciTech division of Akina, Inc. (www.polyscitech.com) to create clozapine N-oxide loaded microparticles for exploratory application of this agonist into the neural system as a way to control downstream processing of pain and stress experiences. This research holds promise to improve pain management therapies as well as further understanding of the workings of sensory processing in the brain. Read more: Barik, Arnab, Devanshi Shah, Pallavi Raj Sharma, and Rachit Agarwal. "The lateral septum plays a transforming role in acute stress-induced analgesia." bioRxiv (2023): 2023-01. https://www.biorxiv.org/content/biorxiv/early/2023/02/02/2023.01.30.526171.full.pdf

“Stress is a powerful modulator of pain. Specifically, acute stress due to physical restraint facilitates stress-induced analgesia (SIA). However, where, and how acute stress and pain pathways interface in the brain must be better understood. Here, we describe how the lateral septum (LS), a forebrain limbic nucleus, facilitates SIA through its downstream targets in the lateral hypothalamus (LH). We show that the LS→LH circuitry is sufficient to drive analgesia and is required for SIA. Further, we reveal that the LS→LH pathway is opioid-dependent and modulates pain through the pro-nociceptive neurons in the rostral ventromedial medulla (RVM). Remarkably, we found that the LS neurons are inhibitory, are recruited specifically when the mice struggle to escape under restraint, and, in turn, inhibit excitatory LH neurons. As a result, the RVM neurons downstream of LH are disengaged when the mice try to escape, thus suppressing nociception. Next, our data indicate that the efforts to escape are communicated by the lateral periaqueductal gray (lPAG) to the LS and activation of the upstream lPAG→LS circuit phenocopies LS→LH activation and results in analgesia. Thus, we have revealed a polysynaptic pathway that can transform escape behavior in mice under restraint to acute stress and resultant analgesia.”

Video: https://youtu.be/gngERZtmYoI