Browsing by Subject "Pain Threshold"

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    CaMKII Controls Whether Touch Is Painful
    (Society for Neuroscience, 2015-10-21) Yu, Hongwei; Pan, Bin; Weyer, Andy; Wu, Hsiang-En; Meng, Jingwei; Fischer, Gregory; Vilceanu, Daniel; Light, Alan R.; Stucky, Cheryl; Rice, Frank L.; Hudmon, Andy; Hogan, Quinn; Department of Biochemistry & Molecular Biology, IU School of Medicine
    The sensation of touch is initiated when fast conducting low-threshold mechanoreceptors (Aβ-LTMRs) generate impulses at their terminals in the skin. Plasticity in this system is evident in the process of adaption, in which a period of diminished sensitivity follows prior stimulation. CaMKII is an ideal candidate for mediating activity-dependent plasticity in touch because it shifts into an enhanced activation state after neuronal depolarizations and can thereby reflect past firing history. Here we show that sensory neuron CaMKII autophosphorylation encodes the level of Aβ-LTMR activity in rat models of sensory deprivation (whisker clipping, tail suspension, casting). Blockade of CaMKII signaling limits normal adaptation of action potential generation in Aβ-LTMRs in excised skin. CaMKII activity is also required for natural filtering of impulse trains as they travel through the sensory neuron T-junction in the DRG. Blockade of CaMKII selectively in presynaptic Aβ-LTMRs removes dorsal horn inhibition that otherwise prevents Aβ-LTMR input from activating nociceptive lamina I neurons. Together, these consequences of reduced CaMKII function in Aβ-LTMRs cause low-intensity mechanical stimulation to produce pain behavior. We conclude that, without normal sensory activity to maintain adequate levels of CaMKII function, the touch pathway shifts into a pain system. In the clinical setting, sensory disuse may be a critical factor that enhances and prolongs chronic pain initiated by other conditions. SIGNIFICANCE STATEMENT: The sensation of touch is served by specialized sensory neurons termed low-threshold mechanoreceptors (LTMRs). We examined the role of CaMKII in regulating the function of these neurons. Loss of CaMKII function, such as occurred in rats during sensory deprivation, elevated the generation and propagation of impulses by LTMRs, and altered the spinal cord circuitry in such a way that low-threshold mechanical stimuli produced pain behavior. Because limbs are protected from use during a painful condition, this sensitization of LTMRs may perpetuate pain and prevent functional rehabilitation.
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    Quantification of Pain Thresholds in Orthodontic Patients Using Strain Gage Techniques
    (1992) Cordero, José Waldemar; Roberts, W. Eugene; Simmons, Kirt E.; Arbuckle, Gordon R.; Hohlt, William F.; Shanks, James J.
    The purpose of this study was to assess the suitability of a pain model that utilizes the application of force between teeth as the noxious stimulus. Also, the time course of pain threshold alterations in patients subjected to orthodontic treatment was explored. A simple pressure algometer utilizing strain gages was produced to apply and measure the force required to reach the pain threshold of incisor teeth (central-lateral pairs) for three consecutive days. Fifteen orthodontic patients were used (nine females, six males) with incisors in good alignment and with interproximal contact. Each patient was used for both control and experimental measurements in each arch. Baseline pain threshold measurements were taken on the first day and individual orthodontic springs placed on the experimental side. The control side was the adjacent central-lateral incisor pair on the other side of the arch where no spring was placed. Additional measurements were taken the second and third day in each quadrant. A great variability in pain response between patients was evident. Significantly lower pain threshold levels were observed a day after the initial spring activation followed by an increase in the pain threshold the second day after spring activation. In the mandibular arch, the treatment by day interaction was significant, with the experimental side pain threshold substantially lower than control on the second and third day. Pain thresholds in males were significantly higher only in the maxilla, although there was a tendency for lower pain sensitivity in males for both arches. An apparent crossover of sensitivity between arch sides was observed in this study. The present model was shown to be suitable to study pain thresholds associated with orthodontic forces, and the pressure algometer was able to quantify pain threshold with objective measurements. The model could be used clinically to screen patients with low pretreatment pain thresholds so modifications of treatment mechanics or pharmacologic means could be used to allay patient pain.