The central representation of an aversive event maintains the opioid and nonopioid forms of analgesia.

Abstract

Exposure to an aversive event, such as shock, can elicit either an opioid or nonopioid analgesia in rats. We suggest that the central representation of an aversive event in working memory activates both forms of analgesia. We formalize this basic hypothesis by coupling it with a current model of animal learning and memory, SOP (Wagner, 1981). SOP is designed to capture the standard operating procedures that govern memory systems. Our application of SOP suggests that manipulations which disrupt the maintenance of information in working memory should alter the magnitude and time course of analgesia. Three experiments are reported that support our proposal. Experiment 1 showed that analgesia decays more rapidly if the representation of the aversive event is displaced from working memory by presenting a postshock distractor. Experiment 2 demonstrated that the postshock distractor alters the magnitude and time course of both the opioid and nonopioid forms of analgesia. Experiment 3 demonstrated that pharmacologically disrupting working memory, by administering a high dose of pentobarbital, prevents mild shock from inducing a strong change in pain reactivity. Implications of the results are discussed.

Stress-induced analgesia

“…As Millan (2002) points out in his extensive review of the descending control of pain, the difference in the mechanisms of facilitation and inhibition of nociception are primarily in receptor subtypes coupled to differing intracellular mechanisms. Spinal pathways, through mechanisms elaborated from the gate-control theory, and supraspinal descending inhibitory pain pathways, both play a role in mediating SIA (Grau, 1987;Grau et al, 1990;Madden et al, 1977;Meagher et al, 1993;Meagher et al, 1990;Rhudy et al, 2004;. Nociceptive information is then relayed either directly to the cortex or indirectly to the cortex through the brainstem, midbrain, and thalamus via the ascending pain pathways (for review see Millan, 1999).…”

Exposure to intermittent nociceptive stimulation under pentobarbital anesthesia disrupts spinal cord function in rats

“…They, and others, have reported that descending inhibitory systems are suppressed by barbiturates (Frank and Ohta 1971;Collins et al 1990). Since these reports, others showed that pentobarbital blocks shock-induced analgesia (Terman et al 1984;Grau 1987) and other forms of anesthesia were shown to diminish the inhibition of dorsal horn neuron firing seen after noxious stimulation (Tomlinson et al 1983). The exact mechanism through which this occurs remains unknown, although the inhibitory neurotransmitter GABA appears to play a major role (Asana and Ogasawara 1981;Olsen and Snowman 1982;Sivam et al 1982).…”

Conditioned and unconditioned stress-induced analgesia: Stimulus preexposure and stimulus change

“…For example, it is possible that the analgesia at these time points is a nonassociatively derived reaction that is induced by the initial analgesic reaction as a consequence of that reaction. Alternatively, the shock itself may produce a biphasic reaction with one type followed by the other type (Grau, 1987b). Perhaps removing the subjects from the shock environment and placing them in a new environment led to the appearance of only the first analgesia not because the second reaction required shock cues, but because the removal and placement in the new environment disrupted the sequential processes.…”

“…Fanselow is explicit that his position is restricted to the outcome of procedures using small numbers of shocks (Fanselow, 1986). Grau (1987aGrau ( , 1987b has also emphasized the role of associative processes. Here, analgesia is placed within the context of Wagner's SOP model of associative processes (Wagner, 1981).…”

“…In considering the analgesia produced by shock, it is useful to separately consider reactions to small amounts of shock (1-20 shocks that are fairly brief in duration, say 5 sec or less) and large amounts of shock (80 or more shocks in this duration range). There is evidence for at least three different possibilities concerning the psychological nature of the analgesia observed after small amounts of shock: (1) It is an unconditioned reaction (UCR) to the shock itself or to some sensory consequence of the shock (Maier, 1986;Terman, Shavit, Lewis, Cannon, & Liebeskind, 1984); (2) it is a conditioned response (CR) and cannot be elicited directly by shock; fear is rapidly conditioned to contextual cues by shock, and the analgesia is a reaction to conditioned fear (Fanselow, 1984);and (3) it is a reaction to the memory representation of shock (Grau, 1987a(Grau, , 1987b. Maier (1986) has argued that exposure to inescapable shocks sufficient to produce "learned helplessness effects" elicits a new analgesic process that is neither a VCR to shock nor a reaction to conditioned fear or to representations of shock.…”