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home:diseases:anxiety [08.13.2019] – [Evidence of infectious cause] sallieq | home:diseases:anxiety [01.26.2020] – [Research into various drug effects] sallieq | ||
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Interviews of patients with other diseases are [[home: | Interviews of patients with other diseases are [[home: | ||
+ | ===== Evidence of infectious cause ===== | ||
+ | Mark Lyte of the Texas Tech University School of Pharmacy noticed that lab mice dosed with // | ||
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+ | //**L.E. Goehler** et al.// | ||
+ | Further, Neufeld //et al.// showed that germ-free mice exhibited reduced anxiety-like behavior as well as significant neurochemical changes in the brain compared to specific-pathogen-free mice. (({{pubmed> | ||
+ | The frequency with which patients of certain Th1 diseases also experience anxiety(({{pubmed> | ||
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+ | It is my opinion that early and prominent symptoms of Th1 disease are psychological which have been interpreted as anxiety, depression, insomnia, learning disabilities etc. These symptoms like physical ones are exacerbated during effective treatment of Th1 [diseases]. | ||
+ | By understanding this, one can lessen some of the impact of those symptoms, just as one can with the physical symptoms. Not knowing why one is ' | ||
+ | //**Greg Blaney, MD**// </ | ||
+ | ===== Research into various drug effects ===== | ||
{{tag> | {{tag> | ||
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+ | Findings suggest that a low dose of THC produces subjective stress-relieving effects in line with those commonly reported among cannabis users, but that higher doses may non-specifically increase negative mood. (({{pubmed> | ||
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+ | Baseline symptoms of depression (but not anxiety or stress) appeared to be exacerbated across time/ | ||
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+ | Perhaps most well-studied is the role the CeA plays in unconditioned and conditioned fear generation (Ciocchi et al., 2010, Li et al., 2013, Tye et al., 2011), fear extinction, and conditioned inhibition (Amano et al., 2010), as well as conditioned orienting responses to emotionally salient stimuli (El-Amamy and Holland, 2007, Groshek et al., 2005). | ||
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+ | the mechanisms by which stress increases amygdala-dmPFC synaptic strength and generates anxiety-like behaviors are not well understood. Here, we show that the mouse basolateral amygdala (BLA)-prelimbic prefrontal cortex (plPFC) circuit is engaged by stress and activation of this pathway in anxiogenic. [[https:// | ||
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===== Notes and comments ===== | ===== Notes and comments ===== | ||