Butterfly effects and Neurons ByDr. Farzad Massoudi

Both animals and humans have shown that damaged innervations in the peripheral nervous system (PNS) can be rebuilt.The damaged neurite swells and goes through retrograde degeneration after an injury.After the debris is removed, it begins to sprout and repair the connections that are broken.As long as the perikarya remain intact and have made contact with the Schwann cells in the endoneurial channel, damaged axons can regenerate.Regenerating axons have the potential to reinnervate the initial target and reestablish connections and function under the right conditions.However, only a small portion of what transpires after the PNS injury is depicted in this scenario.The data presented in this issue of NRR demonstrate the effects of PNS damage on the central nervous system (CNS) in addition to the injured neuron.They also talk about the possibility that after injury, factors that control neural proliferation and differentiation in the developing nervous system may be brought back to life and contribute to both adult neurogenesis and neural proliferation.

images Lorenz system r28 s10 b2–6666.png by Wikimol and Lorenz attractor.svg by Dschwen, Author Wikimol, Dschwen

The majority of researchers maintain that neurogenesis in mature mammals is restricted to the CNS’s subventricular zone and the subgranular zone of the dentate gyrus.With the exception of the olfactory neuroepithelium, neurogenesis in the PNS is thought to be active only during prenatal development.Accordingly, understanding circumstances under which grown-up neurogenesis can be actuated in physiologically non-neurogenic locales is one of the significant moves for creating remedial techniques to fix neurological harm.With the exception of the sensory ganglia, little is known about the PNS’s induced neurogenesis.The review by Czaja examines the more than one hundred years of research on adult neurogenesis in the PNS and reveals evidence regarding the underestimated potential for the generation of new neurons in the adult PNS.

Hodges and Forster also go over the data that show that carotid body denervation triggers both central and peripheral plasticity.The carotid body is a small group of cells that come from the neural crest and are found at the beginning of the internal carotid artery.Carotid bodies are the primary site of peripheral oxygene chemoreception and provide a tonic facilitory input to the respiratory network.The altered excitatory and/or inhibitory neuromodulator mechanisms that contribute to the initial respiratory depression and subsequent respiratory plasticity following carotid body denervation are the subject of a discussion by Hodges and Forster.The respiratory network’s capacity for plasticity following neurologic injury in humans may be better understood if the central effects of carotid body denervation are studied.

It has been reported that stimulating the vagus nerve in the brain increases neurogenesis and neural plasticity.However, the underlying mechanism of this action remains a mystery.Ronchi et al. looked into whether cells in the hippocampus’s dentate gyrus respond to vagus nerve damage.Adult neurogenesis in the dentate gyrus of the hippocampus was altered by both the vagotomy and capsaicin-induced damage to unmyelinated vagal afferents, according to their findings.In addition, they demonstrated that in adult rats, damage to the subdiaphragmatic vagus is followed by activation of microglia and lasting changes in the neural environment in the dentate gyrus.

The investigation of transcriptional changes resulting from experimental manipulations of the nervous system is frequently carried out using quantitative RT-PCR (qPCR). Due to the dynamic nature of endogenous transcription, the lack of a suitable reference gene makes it difficult to interpret qPCR results, despite its widespread use. Johnston et al. looked into using luciferase, an exogenous spike-in mRNA, as an internal reference gene for the 2-Ct normalization method to address this deficiency. The dynamic expression of the endogenous reference was demonstrated by the exogenous luciferase mRNA reference. They demonstrated that misinterpreting other genes of interest would result from the variability of the endogenous reference. An alternative for the analysis of qPCR data in the injury model that is both consistent and simple to implement is the utilization of the exogenous spike-in reference.

This issue’s research demonstrates that peripheral nerve damage is not limited to the PNS’s plasticity. In both the PNS and the CNS, the need to create new neurons and make new connections dramatically rises after injury. The chain of events induced by the peripheral nerves causes the CNS circuits to be reorganized. The injured nervous system’s developmental mechanisms are replicated by this demand for new connections. As a result, we shouldn’t ignore the fact that even a small change in the PNS can have a big impact on the CNS in the future, causing the neural butterfly effect and an unexpected brain storm.