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Subject Nicotine fights fear, anxiety, PTSD
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Original Message The ensemble of studies to date suggest that under certain conditions nicotine can act as an anxiolytic and an antidepressant, but that following chronic use, adaptations to nicotine can occur resulting in increased anxiety and depression following withdrawal.
[link to www.ncbi.nlm.nih.gov]

Psychiatric research has documented that enhanced noradrenergic postsynaptic responsiveness in the neuronal pathway (brain circuit) that originates in the locus coeruleus and end in the basolateral nucleus of the amygdala is a major factor in the pathophysiology of most stress-induced fear-circuitry disorders and especially in posttraumatic stress disorder (PTSD). The LC neurons are probably the origin of the first or second “leg” of the "PTSD circuit." An important 2005 study of deceased American army veterans from World War II, was shown combat-related PTSD to be associated with a postmortem diminished number of neurons in the locus coeruleus (LC) on the right side of the brain.
The locus coeruleus may figure in clinical depression, panic disorder, and anxiety.
The locus coeruleus is activated by stress, and will respond by increasing norepinephrine secretion, which in turn will alter cognitive function.
[link to en.wikipedia.org]

Systematically administered nicotine in low doses increases the firing rate of rat locus coeruleus (LC) neurons. In the present study, this action of nicotine was found to be prevented by pretreatment with kynurenic acid (1 μmol; i.c.v.).
[link to www.sciencedirect.com]

Contrary to a widely accepted theory, increased activity of locus coeruleus (LC) neurons does not appear to potentiate anxiety; instead, the influence of LC activity may be opposite to this.
[link to www.ncbi.nlm.nih.gov]

Previous electrophysiological experiments have shown that the marked but short-lasting excitation of locus coeruleus (LC) neurons seen after systemic administration of low doses of nicotine is of a peripheral origin. In addition, nicotine induces a weak but more long-lasting activation of LC neurons which is preferentially observed following administration of high doses of the drug.
[link to link.springer.com]
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