Release of β-endorphin immunoreactivity from brain by activation of a hypothalamicN-methyl-d-aspartate receptor
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Increased β-endorphin levels and generalized decreased pain thresholds in patients with limited jaw opening and movement-evoked pain from the temporomandibular joint
2012, Journal of Oral and Maxillofacial SurgeryCitation Excerpt :βE is blocked by the agonist opioid in the arcuate nucleus, by the agonist dopamine type 2 receptor, or by glucocorticoids.37-39 Second, in a noninflammatory animal model, the most pronounced βE release from the pituitary gland was produced by the activation of the hypothalamus-pituitary-adrenal axis caused by concomitant stress and pain.11,29 Therefore, in this study, the elevated βE levels in patients with limited jaw opening and movement-evoked pain from the TMJ most probably are caused by inflammatory pain.
Midazolam attenuates the antinociception induced by d-serine or morphine at the supraspinal level in rats
2008, European Journal of PharmacologyExpression of c-Fos in arcuate nucleus induced by electroacupuncture: Relations to neurons containing opioids and glutamate
2007, Brain ResearchCitation Excerpt :As such, our data imply that the glutamatergic neurons, responsive to somatic nerve stimulation during EA, are particularly important in the ARC. These results confirm other studies suggesting that glutamate functions as a major excitatory neurotransmitter in the ARC, including induction of release of β-endorphin and hormones (Bach and Yaksh, 1995; Kiss et al., 1997; MacDonald et al., 1993). The present study also supports our previous physiological findings that EA excites ARC neurons and that activation of the ARC by the excitatory amino acid dl-homocysteic acid leads to the inhibition of visceral sympathoexcitatory reflexes.
Fear and power-dominance motivation: Proposed contributions of peptide hormones present in cerebrospinal fluid and plasma
2003, Neuroscience and Biobehavioral Reviews