Force perceptual bias caused by muscle activity in unimanual steering.

This study sought to investigate whether force perceptual bias was affected by differences in posture while steering an automobile using a psychophysical experiment to examine the relationship with muscle activity. The human perceptual characteristics of weight and force are known to be nonlinear, and a perceptual bias can occur, that is, bias that causes a perception of something that is larger or smaller than the actual scale. This is considered to be caused by physical and/or psychological conditions. Sense of effort is believed to be one influential factor. It is known to correlate with muscle activity intensity, and bias may be caused by muscle activity changes. In the current study, we hypothesized that force perceptual bias would depend on posture due to the intensity of muscle activity changes caused by changing postures during steering operation. By investigating this hypothesis, we can clarify the relationship between sense of effort and muscle activity. To investigate this issue, we conducted a psychophysical experiment to confirm postural dependence, and estimated muscle activity using a three-dimensional musculoskeletal model simulation with postural and arm force data during the experiment. In addition, prediction of bias was conducted based on a simulation in the psychophysical experiment using these data. The results revealed that bias existed, as measured by differences in postures. Additionally, a significant moderate correlation was found between the predicted bias and the actual bias, indicating the existence of a relationship between muscle activity and bias.

Prediction of Perceived Steering Wheel Operation Force by Muscle Activity.

Humans feel forces or weights while grasping and manipulating an object. There is a difference between the physical and perceived forces because the physical characteristics of an object and/or human psychophysical characteristics affect perceived force. Sense of effort plays an important role in deciding the movement made by humans. In this study, we propose a computational method to predict the perceived force by evaluating the muscle activity as a function of effort in the operation of a steering wheel based on a 3D-musculoskeletal model simulation. We found that the perceived-force characteristics depend on the driving posture, though the applied force is the same. We evaluated the results, and showed that the mean of the absolute error is 1.78 N for the experiments conducted on four different vehicles in commercially available.

Activation of different signals identified with glia cells contribute to the progression of hyperalgesia.

Hyperalgesia results from a decreased pain threshold, often subsequent to peripheral tissue damage. Recent reports revealed several promising mechanisms of hyperalgesia, but many issues remain unclear. The glial activation accompanying inflammation of neurotransmission in the spinal cord might be related to the initiation and maintenance of hyperalgesia. The present study investigated the pharmacological pain-modifying effects of mitogen-associated protein kinase (MAPK)-related inhibitors identified with glia cells over time during inflammatory pain. A model of inflammatory pain was produced by injecting mustard oil (MO) into the hind paws of rats. Following MO injection, the changes in paws flinching as the early onset of pain and paw withdrawal latency (PWL) in response to thermal stimulation were measured as delayed-onset hyperalgesia. Before and after the MO injection, one of the inhibitors, a p38-MAPK (SB), nuclear factor (NF)-κB (PDTC), BDNF-trk-B (K252a), or JNK-1 (SP), was administered and flinching and PWL were measured. In the SB, PDTC, and k252a groups, early flinching following MO injection was moderately suppressed. Hyperalgesia was significantly suppressed in the left-right difference of PWL in animals receiving SB, k252a, or PDTC pre-treatment. In animals receiving post-treatment, the suppressive effects were most potent in the SP group. The present results revealed that microglial activation resulting from the release of the phosphatase p38-MAPK, the transcription factor NF-κB, and BDNF contributes to the early stage of inflammatory pain. Astrocyte activation accompanying JNK activation contributes to subsequent hyperalgesia. Activation of different signals identified with glia cells is thought to contribute to the progression of hyperalgesia, which represents an applicable finding for the treatment of hyperalgesia.

Intracerebroventricular 4-methylcatechol (4-MC) ameliorates chronic pain associated with depression-like behavior via induction of brain-derived neurotrophic factor (BDNF).

Neuropathic pain concurrent with mood disorder from peripheral nerve injury is a serious clinical problem that significantly affects quality of life. Recent studies have suggested that a lack of brain-derived neurotrophic factor (BDNF) in the limbic system may cause this pain-emotion. BDNF is induced in cultured neurons by 4-methylcatechol (4-MC), but the role of 4-MC-induced BDNF in pain-emotion is poorly understood. Thus, we assessed the possible involvement of BDNF in brain in depression-like behavior during chronic pain following peripheral nerve injury. In addition, we examined whether intracerebroventricular (i.c.v.) 4-MC prevents chronic pain in rats and produces an antidepressant effect. Sprague-Dawley rats implanted intracerebroventricularly with a PE-10 tube were subjected to chronic constriction injury (CCI). Pain was assessed by a reduction in paw withdrawal latency (PWL) to heat stimuli after CCI. We also used a forced swimming testing (FST; time of immobility, in seconds) from day 14 to day 21 after CCI. Modulation of pain and emotional behavior was performed by injection of PD0325901 (a MEK1/2 inhibitor). 4-MC (100 nM) was continuously administered i.c.v. for 3 days during the period from day 14 to day 21 after CCI. To block analgesic and antidepressant effects, anti-BDNF antibody or K252a (a TrkB receptor inhibitor) was injected in combination with 4-MC. Naloxone was also coadministered to confirm the analgesic effect of 4-MC. During the chronic stage after CCI, the rats showed a sustained decrease in PWL (thermal hyperalgesia) associated with extension of the time of immobility (depression-like behavior). PD0325901 significantly reduced the decrease in PWL and the increased time of immobility after CCI. The decreased PWL and increased time of immobility were also reduced by 4-MC and by treatment with an ERK1/2 inhibitor. These effects of 4-MC i.c.v. were reversed by anti-BDNF and K252a. The analgesic effect of 4-MC i.c.v. was also antagonized by naloxone. Based on these results, we suggest that a lack of BDNF and activation of ERK1/2 in the pain-emotion network in the CNS may be involved in depression-like behavior during chronic pain. 4-MC i.c.v. ameliorates chronic pain and depression-like behavior by producing of BDNF and normalization of ERK1/2 activation. Therefore, enhancement of BDNF may be a new treatment strategy for chronic pain associated with depression.