Role of cholinergic systems in pain modulation: I. Impact of scopolamine on environmentally induced hypoalgesia and pain reactivity.

Abstract

Scopolamine was found to block both brief shock-induced (3 0.75-s, 1.0-mA shocks) and conditioned hypoalgesia on the tail-flick test in rats. The drug also produced a general increase in pain reactivity as measured by both the tail-flick test and shock-induced vocalization. It was shown that this hyperalgesia cannot account for the effect of the drug on brief-shock or conditioned hypoalgesia. Scopolamine did not block the nonopioid analgesia observed after long shock (3 25-s, 1.0-mA shocks). When the effect of the drug on baseline levels of pain reactivity was controlled, it potentiated long shock-induced hypoalgesia. Scopolamine also increased reactivity to tactile stimulation, which suggests the hyperalgesia reflects a general increase in arousal. None of these effects were observed with methylscopolamine, which suggests they are not peripherally mediated.

Scopolamine and Pavlovian Fear Conditioning in Rats Dose-Effect Analysis

“…Thus, depending on experimental conditions, scopolamine seems to produce no effect on pain sensitivity, as we observed (also Houser & Hart, 1973), or hyperalgesia as others have observed (Grau et al, 1991;Watkins et al, 1984). In either case, the amnesic effects of scopolamine on learning cannot be attributed to decreased sensitivity to shock.…”

Shock-induced hyperalgesia: IV. Generality.

“…It has been suggested that pain inhibitory mechanisms are relatively difficult to engage, for pain presumably has an adaptive function in motivating escape and avoidance responses (e.g., Walters, 1994). In contrast, systems that enhance pain may be easier to engage, perhaps because these systems are tied to arousal (e.g., Grau et al, 1991). If this is true, behavioral changes indicative of hyperalgesia (e.g., lower vocalization thresholds to shock) should emerge at a lower shock intensity than antinociception (inferred from an increase in tail-flick latency).…”

“…The implication is that less severe stimuli elicit an antinociception that depends on forebrain-mediated higher psychological processes (Meagher, 1989;Meagher et al, 1993Meagher et al, , 1990. Unlike brief-moderate shocks, the antinociception observed after longmoderate shocks (three 25 s, 1 mA) is unaffected by both opioid antagonists (e.g., naltrexone) and manipulations designed to disrupt forebrain function but is eliminated by spinal transection (Grau et al, 1991;Meagher et al, 1993Meagher et al, , 1990. These observations, coupled with other studies (Grau et al, 1996), suggest that long-moderate shocks engage a "nonopioid" brainstem antinociceptive system.…”

Extremely Low Frequency Magnetic Field Exposure Attenuates Pain By Inactivation Of Descending Facilitatory System In Complete Spinal Cord Injured Rats

“…This procedure was repeated 3 times at the interval of 5 minutes and the average value was considered for statistical analysis. [17,18] The occurrence of tail flick was confirmed by the corresponding EMG record on oscilloscope.…”