Journal of neurophysiology
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Comparative Study
Kappa opioids inhibit physiologically identified medullary pain modulating neurons and reduce morphine antinociception.
Microinjection of kappa opioid receptor (KOR) agonists into the rostral ventromedial medulla (RVM) attenuates mu-opioid receptor mediated antinociception and stress-induced analgesia, yet is also reported to have an analgesic effect. To determine how KOR agonists produce both antinociceptive and antianalgesic actions within the RVM, the KOR agonist U69593 was microinjected directly into the RVM while concurrently monitoring tail flick latencies and RVM neuronal activity. Among RVM neurons recorded in vivo, two types show robust changes in activity just prior to the nocifensive tail flick reflex: ON cells burst just prior to a tail flick and their activity is pronociceptive, whereas OFF cells pause just prior to the tail flick and their activity is antinociceptive. ⋯ Furthermore, U69593 inhibited ongoing activity in subsets of OFF cells (4/11) and NEUTRAL cells (3/9). Microinjection of U69593 into the RVM also attenuated morphine antinociception and suppressed the excitation of off cells. Together with previous in vivo and in vitro studies, these results are consistent with the idea that KOR agonists can be either pronociceptive through direct inhibition of OFF cells, or antianalgesic through both postsynaptic inhibition and presynaptic inhibition of glutamate inputs to RVM OFF cells.
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Comparative Study
Estrogen and inflammation increase the excitability of rat temporomandibular joint afferent neurons.
Several painful conditions, including temporomandibular disorders (TMD), are more prevalent and more severe in women than in men. Although the physiological basis for this sex difference remains to be determined, it is likely that estrogen is an underlying factor. The present study was performed to test the hypotheses that estrogen increases the excitability of rat temporomandibular joint (TMJ) afferents and exacerbates the inflammation-induced sensitization of these sensory neurons. ⋯ The effects were additive with neurons from rats receiving both estrogen and inflammation being the most excitable. The increases in excitability were associated with changes in passive properties and action potential waveform, suggesting that estrogen and inflammation affect the expression and/or properties of ion channels in TMJ neurons. Importantly, the influence of estrogen on both baseline and inflammation-induced changes in TMJ neuronal excitability may help explain the profound sex difference observed in TMD as well as suggest a novel target for the treatment of this pain condition.