Different studies have shown some interesting things about the sense of olfaction. It would be interesting to understand better how long-term toxic exposures alter the general patterns of operation of receptors in neurons and what circumstances make one more vulnerable. Zhang expressed that gap junctons modulate activity and sensitivity of olfactory neurons that have been shown to have receptors for one odorant whereas, cortical neurons get imputs from a number of different ones. (Buck) Kay writes that when the nose is first exposed to odor the molecules are absorbed into the olfactory receptor cells that line the mucous membranes at the back of the nostrils. There are some 350 varieties of these receptor cells, each specialized to detect certain odor molecules which convert this information into nerve impulses and then transmit them to the brain’s two olfactory bulbs (one for each nostril), which sit just behind the nose. The olfactory bulbs then translates the impulses into information the brain can understand and are sent on to the olfactory cortex where the "odor information" is processed.
Several recent studies show disruptions in the sense of smell are indicative of the early signs of diseases including Alzheimer's disease, autism, Parkinson's disease and schizophrenia. Dr. Wilson, an expert in the neurobiology of olfaction explains that olfaction is a unique "sense" because it has direct links to the amygdala that is important for regulating emotion and physiology and to the prefrontal cortex that is involved with cognition and planning. He also points out that this connection is also the short path that links olfaction with memory. (Kay) As noted, olfactory disfunction is a "early-warning" sign of schizophrenia and Turetsky's data indicates structural and functional abnormalities run from the cortex to the olfactory system. "These reflect, in part, a genetically mediated neurodevelopmental etiology. Gross structural and functional anomalies are mirrored by cellular and molecular abnormalities that suggest decreased or faulty innervation and/or dysregulation of intracellular signaling. A unifying mechanistic hypothesis may be the epigenetic regulation of gene expression." This is also in line with some of the most current hypotheses of neuroinflammation and epigenetic influences in autism.
"gap junctional communication in the olfactory epithelium modulates olfactory activity at the peripheral level and alters glomerular activation patterns (odor maps) in the olfactory bulb. Topological changes in odor maps due to gap junctional modulation could affect perception of odor quality or quantity." (Zhang)To what extent do disruptions of Tregs contribute to disease development?
Many patients that have chemical sensitivity describe that the worst of the symptoms began occurring after a bout of infection. Multiple chemical sensitivity is a condition where symptoms such as nausea, respiratory problems, mood changes, cognitive problems and numerous other repored symptoms occur at a very low exposure of an "odor" stimulus. In the past, we have suggestedTreg impairment may be important for the development of many responses in MCS which may be long lasting or transient depending on factors including other secondary exposures that influence or prevent their activity. In addition, Treg disfunction has been implicated in a number of co-morbid health conditions such as inflammatory bowel disease and the sensitivities in autism. Interestingly, many common current treatments for MCS were used for treatments for autism before they were used for MCS. Recent reports have also suggested that suppression of regulatory T cells from air pollution may be an important factor in the development and augmentation of respiratory disease like asthma. (Berkley) Air pollutants and particulate matter contain a variety of contaminants including LPS endotoxin from bacteria, hydrocarbons and metals. A recent study demonstrates that LPS a common contaminant of most environments can alter the expression of Cx43 and caveolin-3. The former Cx43 is a connexin protein that has been found to be important for the integrity of gap junctions shown to dictate olfactory sensitivity. Interestingly, regulatory T cells also play a role in the communication activities of gap junctions. Taking these recent studies into consideration the newest research on regulatory T cells in promotion of the adaptive response and maintaining tolerance support, one could propose that altered communication may play a role in chemical sensitivity and odor and olfactory function and prvode parallel support to the recent research of how Tregs disfunction may influence respiratory problems from air pollution. In addition, because their is a relationship gap functions to activity of NO/cGMP and its downstream targets and related biological roles in relation to memory -- this could explain some of the cognitive problems associated with MCS. Generally, suppression of Tregs and their role in gap function has implications for both animals and humans. In animals impairment of the olfactory system may negatively influence instinctual patterns of navigation and other behaviors.
Related: Dysfunction of Methylation and Nrf2 in Environmental Illness - Is This A Better Explanation than NO/ONOO- ?
****Read more research blogs: Kimberly Kramer
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