Neonatal hind-paw injury disrupts acquisition of an instrumental response in adult spinal rats.

The present study was designed to evaluate the impact of neonatal injury on adult spinal plasticity in rats. Subjects were randomly assigned to 1 of 4 experimental conditions: (a) hind-paw injury at Postnatal Day (PD) 2, (b) hind-paw injury at PD 5, (c) anesthesia exposure only on PD 2, or (d) anesthesia exposure only on PD 5. Subjects receiving a unilateral neonatal hind-paw injury showed decreased mechanical threshold (hyperalgesia) on the previously injured hind paw throughout development. This decrease in threshold survived spinal transection (at T2) at 12 weeks of age. Injured subjects also showed significant impairment in a spinal instrumental learning task performed by the previously injured hind paw. This disruption of learning indicates a disruption of spinal plasticity that may be due to induction of long-term changes in nociceptive processing within the spinal cord. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Local anesthetic treatment significantly attenuates acute pain responding but does not prevent the neonatal injury-induced reduction in adult spinal behavioral plasticity.

Recent findings indicate that neonatal injury results in decreased spinal plasticity in adult subjects (E. E. Young, K. M. Baumbauer, A. E. Elliot, & R. L. Joynes, 2007). Previous research has shown that acute manipulations of pain processing (i.e., administration of formalin, carrageenan, capsaicin) result in a loss of spinal behavioral plasticity (A. R. Ferguson, E. D. Crown, & J. W. Grau, 2006). Moreover, neonatal injury results in a lasting reduction in adult spinally mediated plasticity resembling the deficit seen following acute manipulations in adults (E. E. Young et al., 2007). The present study was designed to determine whether the effects of neonatal injury could be prevented by lidocaine administration during the initial healing period. Subjects (injured or uninjured) received lidocaine or saline on 1 of 4 administration schedules (preinjury only, postinjury only, for 24 hr postsurgery, or for 72 hr postsurgery). Results demonstrated that lidocaine administration did not prevent the hypersensitivity and reduced spinal plasticity associated with neonatal injury. This suggests that (a) the mechanisms underlying neonatal injury are independent of peripheral input in the initial healing period and (b) lidocaine is ineffective at preventing long-term spinal plasticity changes following neonatal injury. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Administration of a Ca2+/calmodulin-dependent protein kinase II (CaMKII) inhibitor prevents the learning deficit observed in spinal rats after noncontingent shock administration.

Research has shown that spinal rats given shock to the hind leg when it is in an extended position (contingent shock) will learn to maintain a flexion response. However, subjects that experience shock irrespective of leg position (noncontingent shock) do not exhibit this learning. The current studies examined the role of Ca2+/calmodulin-dependent protein kinase II (CaMKII) in this learning deficit. Subjects were given intrathecal injections of CaMKII inhibitor solution or artificial cerebrospinal fluid (aCSF) 15 min prior to and immediately or 4 hr following noncontingent shock training. Results demonstrate that the CaMKII inhibitor successfully reversed the learning deficit when injected prior to and immediately following training. These results indicate the importance of CaMKII in the learning deficit present in spinal animals trained with noncontingent shock. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Impact of shock on pain reactivity: III. The magnitude of hypoalgesia observed depends on test location.

Pain reactivity is often assessed in rodents by measuring the latency of tail withdrawal from radiant heat (the tail-flick test). Using this test, the authors show that the magnitude of antinociception observed in spinal rats depends on test location; antinociception is observed at, and distal to, where shock is applied, but not at more proximal sites (Experiments 1 & 2). Experiment 3 evaluates the generality of this observation by testing 3 other shock schedules that are known to elicit distinct forms of antinociception. In all but 1 case, the magnitude of antinociception varied as a function of test location. Experiment 4 shows that morphine also has a greater impact at distal test locations. Experiment 5 assessed the impact of tailshock on reactivity to radiant heat applied to the foot. Of the 5 distinct forms of shock-induced antinociception studied, only 2 produce a robust antinociception at this test location. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The neonatal injury-induced spinal learning deficit in adult rats: Central mechanisms.

Previous research has shown that small injuries early in development can alter adult pain reactivity and processing of stimuli presented to the side of injury. However, the mechanisms involved and extent of altered adult spinal function following neonatal injury remain unclear. The present experiments were designed to 1) determine whether the effects of neonatal injury affect processing contralateral to the injury and 2) evaluate the role of cells expressing the NK1 receptor, shown to be involved in central sensitization in adults, in the negative effects of neonatal injury. The present findings indicate that the effects of neonatal injury are primarily isolated to the injured hind limb and do not result in a bilateral alteration in adult spinal function. In addition, the effects of neonatal injury appear to be partially dependent on cells expressing the NK1 receptor as ablating these cells at the time of injury or in adulthood results in attenuation of the neonatal injury-induced spinal learning deficit. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Intrathecal administration of neurokinin 1 and neurokinin 2 receptor antagonists undermines the savings effect in spinal rats seen in an instrumental learning paradigm.

Research has demonstrated that the isolated spinal cord is capable of modifying its behavior in response to changes in environmental stimuli. Previous studies have shown that rats with complete thoracic spinal transections can learn to maintain a flexion response when shock delivery is paired with leg position. The current experiments examined whether neurokinin (NK) 1 and 2 receptors are involved in the acquisition and retention of this prolonged flexion response. Results demonstrated that L-703,606 (NK1 antagonist) facilitated response acquisition, whereas MEN-10,376 (NK2 antagonist) hindered acquisition. Furthermore, pretraining administration of either antagonist undermined subjects' ability to reacquire the prolonged flexion response during testing. These results demonstrate the importance of NK receptors in spinally mediated behavioral plasticity. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Temperature-independent low-voltage wide-bandwidth optical modulators

Temperature-independent electro-optic modulators have been constructed using lithium niobate. A frequency response extending to 2 GHz has been achieved with a relatively low drive power. The modulators have been used with a 0.63 ?m laser and are easily aligned on a standard optical bench.     

Mechanisms of Pavlovian conditioning: Role of protection from habituation in spinal conditioning.

Conditioned antinociception can be established in spinal rats by pairing stimulation to one hind leg (the conditioned stimulus [CS]) with an intense tailshock (the unconditioned stimulus [US]). After this training, the paired CS (CS+) elicits greater antinociception on the tail-flick test than a CS that was explicitly unpaired (CS–). Five experiments are reported that suggest that this effect reflects protection from habituation. Experiment 1 showed that the CS (legshock) induces antinociception before training. Presenting the CS alone weakened (habituated) its antinociceptive impact (Experiment 2). Less habituation was observed when the CS was paired with the US (Experiment 3). Decreasing habituation to the CS– (by increasing the interval between trials) and facilitating habituation to the CS+ (by increasing the number of trials) effectively eliminated the CS+/CS– difference (Experiments 4 and 5). (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Instrumental learning within the spinal cord: I. Behavioral properties

Four experiments are reported that explore whether spinal neurons can support instrumental learning. During training, one group of spinal rats (master) received legshock whenever one hindlimb was extended. Another group (yoked) received legshock independent of leg position. Master, but not yoked, rats learned to maintain their leg in a flexed position, exhibiting progressively longer flexions as a function of training (Experiment 1). All subjects were then tested by applying controllable shock to the same leg (Experiment 2). Master rats reacquired the instrumental response more rapidly (positive transfer), whereas yoked rats failed to learn (a learned helplessness-like effect). Disrupting response-outcome contiguity by delaying the onset and offset of shock by 100 ms eliminated learning (Experiment 3). Experiment 4 showed that shock onset contributes more to learning than does shock offset.     

Response-specific inhibition during general facilitation of defensive responses in Aplysia..

Siphon responses of Aplysia have been used to examine the neural basis of nociceptive behavioral inhibition. The authors tested the response specificity and functional significance of this inhibition. Video analysis showed that strong tail-nerve shock decreased the duration of siphon constriction evoked by weak siphon shock. Tail-nerve shock also caused the appearance of a novel flaring response to the test stimulus, which resembled the siphon response to tail-nerve shock. Novel flaring responses were expressed to both mechanical and electrical siphon stimuli. Tailshock facilitated another defensive response, inking, during the period of inhibited siphon constriction. Tailshock also facilitated tail contractions evoked by weak contralateral tail stimulation during this period. These results indicate that inhibition is not generalized across defensive responses and is specific to siphon responses that interfere with directed ink ejection toward an injured site. (PsycINFO Database Record (c) 2010 APA, all rights reserved)