Instrumental learning within the spinal cord: IV. Induction and retention of the behavioral deficit observed after noncontingent shock.

Crown, Eric D.; Ferguson, Adam R.; Joynes, Robin L.; Grau, James W.

doi:10.1037/0735-7044.116.6.1032

Cited by 64 publications

(171 citation statements)

References 52 publications

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“…Separate groups received nothing (0 s) or 30 min of uncontrollable, intermittent tailshock. The shocks were 1.5 mA, 0.08 s in duration, and occurred on a variable time schedule (range 0.2 to 3.8 s) with a mean interstimulus interval of 2.0 s. (Shock at an intensity of 1.5 mA [AC, constant current] is known to engage antinociceptive mechanisms within the spinal cord [18,19], vigorous defensive behavior in intact rats, and pain in humans [see 8,9].) An experimenter blind to the subject's drug treatment recorded whether the shocked rats vocalized during the first minute of stimulation.…”

Section: Shock Treatmentsmentioning

confidence: 99%

The impact of morphine after a spinal cord injury

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Liu

Washburn

et al. 2007

Behavioural Brain Research

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Nociceptive stimulation, at an intensity that elicits pain-related behavior, attenuates recovery of locomotor and bladder functions, and increases tissue loss after a contusion injury. These data imply that nociceptive input (e.g., from tissue damage) can enhance the loss of function after injury, and that potential clinical treatments, such pretreatment with an analgesic, may protect the damaged system from further secondary injury. The current study examined this hypothesis and showed that a potential treatment (morphine) did not have a protective effect. In fact, morphine appeared to exacerbate the effects of nociceptive stimulation. Experiment 1 showed that after spinal cord injury 20 mg/kg of systemic morphine was necessary to induce strong antinociception and block behavioral reactivity to shock treatment, a dose that was much higher than that needed for sham controls. In Experiment 2, contused rats were given one of three doses of morphine (Vehicle, 10, 20 mg/kg) prior to exposure to uncontrollable electrical stimulation or restraint alone. Despite decreasing nociceptive reactivity, morphine did not attenuate the long-term consequences of shock. Rats treated with morphine and shock had higher mortality rates, and displayed allodynic responses to innocuous sensory stimuli three weeks later. Independent of shock, morphine per se undermined recovery of sensory function. Rats treated with morphine alone also had significantly larger lesions than those treated with saline. These results suggest that nociceptive stimulation affects recovery despite a blockade of pain-elicited behavior. The results are clinically important because they suggest that opiate treatment may adversely affect the recovery of function after injury.

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Section: Shock Treatmentsmentioning

confidence: 99%

The impact of morphine after a spinal cord injury

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Liu

Washburn

et al. 2007

Behavioural Brain Research

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“…The question addressed in the present study, therefore, was whether bipedal step-training (StepTr) or unipedal hindlimb stand-training (Stand-Tr) in neonatal spinally transected rats changed the potential to perform a novel, acute instrumental spinal learning task relative to non-trained (Non-Tr) rats [3,4,6,7,25,27]. During the 30 min instrumental learning task, spinally transected rats receive shock to the tibialis anterior (TA) muscle whenever the leg is extended, and learn to maintain the leg in a flexed position, thereby minimizing net shock exposure [25].…”

Section: Introductionmentioning

confidence: 99%

Two chronic motor training paradigms differentially influence acute instrumental learning in spinally transected rats

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Crown

Ferguson

et al. 2007

Behavioural Brain Research

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The effect of two chronic motor training paradigms on the ability of the lumbar spinal cord to perform an acute instrumental learning task was examined in neonatally (postnatal day 5; P5) spinal cord transected (i.e., spinal) rats. At ∼P30, rats began either unipedal hindlimb stand training (Stand-Tr; 20-25 min/day, 5 days/wk), or bipedal hindlimb step training (Step-Tr; 20 min/day; 5 days/wk) for 7 wks. Non-trained spinal rats (Non-Tr) served as controls. After 7 wks all groups were tested on the flexor-biased instrumental learning paradigm. We hypothesized that 1) Step-Tr rats would exhibit an increased capacity to learn the flexor-biased task relative to Non-Tr subjects, as locomotion involves repetitive training of the tibialis anterior (TA), the ankle flexor whose activation is important for successful instrumental learning, and 2) Stand-Tr rats would exhibit a deficit in acute motor learning, as unipedal training activates the ipsilateral ankle extensors, but not flexors. Results showed no differences in acute learning potential between Non-Tr and Step-Tr rats, while the Stand-Tr group showed a reduced capacity to learn the acute task. Further investigation of the Stand-Tr group showed that, while both the ipsilateral and contralateral hindlimbs were significantly impaired in their acute learning potential, the contralateral, untrained hindlimbs exhibited significantly greater learning deficits. These results suggest that different types of chronic peripheral input may have a significant impact on the ability to learn a novel motor task, and demonstrate the potential for experiencedependent plasticity in the spinal cord in the absence of supraspinal connectivity.

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“…Prior research suggests that the learning deficit lasts 24-48 h (Crown et al 2002). Because the design of experiment 2 required a surgical procedure (spinal transection) between treatment and testing, shock treatment and instrumental testing were separated by 48 h. The fact that a robust deficit was observed in rats that received an anesthetic dose of pentobarbital and uncontrollable intermittent stimulation under these conditions suggests that shock treatment also has a lasting effect in intact rats.…”

Section: Discussionmentioning

confidence: 99%

“…Uncontrollable intermittent stimulation-Shock treatment occurred while subjects were loosely restrained in Plexiglas tubes as previously described in Crown et al (2002). Intermittent constant current AC (60 Hz) shock was applied through electrodes taped to the tail.…”

Section: Behavioral Proceduresmentioning

confidence: 99%

“…Rats that receive uncontrollable intermittent stimulation independent of leg position do not exhibit an increase in flexion duration and later fail to learn when tested with controllable shock (Grau et al 1998). This loss of learning capacity (behavioral deficit) lasts up to 24 h and appears to be NMDAR-mediated (Crown et al 2002;Ferguson et al 2006).…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2007

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Rationale-Spinal cord plasticity can be assessed in spinal rats using an instrumental learning paradigm in which subjects learn an instrumental response, hindlimb flexion, to minimize shock exposure. Prior exposure to uncontrollable intermittent stimulation blocks learning in spinal rats but has no effect if given before spinal transection, suggesting that supraspinal systems modulate nociceptive input to the spinal cord, rendering it less susceptible to the detrimental consequences of uncontrollable stimulation.Objective-The present study examines whether disrupting brain function with pentobarbital blocks descending inhibitory systems that normally modulate nociceptive input, making the spinal cord more sensitive to the adverse effect of uncontrollable intermittent stimulation. Materials and methods-MaleSprague-Dawley rats received uncontrollable intermittent stimulation during pentobarbital anesthesia after (experiment 1) or before (experiment 2) spinal cord transection. They were then tested for instrumental learning at a later time point. Experiment 3 examined whether these manipulations affected nociceptive (thermal) thresholds.Results-Experiment 1 showed that pentobarbital had no effect on the induction of the learning deficit after spinal cord transection. Experiment 2 showed that intact rats anesthetized during uncontrollable intermittent stimulation failed to learn when later transected and tested for instrumental learning. Experiment 3 found that uncontrollable intermittent stimulation induced an antinociception in intact subjects that was blocked by pentobarbital. Conclusions-The results suggest a surgical dose of pentobarbital (50 mg/kg) suppresses supraspinal (experiment 2) but not spinal (experiment 1) systems that modulate nociceptive input to the spinal cord by blocking the antinociception that is induced by this input (experiment 3).

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Instrumental learning within the spinal cord: IV. Induction and retention of the behavioral deficit observed after noncontingent shock.

Cited by 64 publications

References 52 publications

The impact of morphine after a spinal cord injury

The impact of morphine after a spinal cord injury

Two chronic motor training paradigms differentially influence acute instrumental learning in spinally transected rats

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

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