| Popis: |
Pain is composed of both physiological and affective/emotional components which potentiate one another. In addition, exposure to stress modulates pain and affective behaviors including, anxiety-like behavior and/or depression-like behaviors. Indeed, chronic exposure to stress has been known to enhance stress-induced hyperalgesia (SIH). The anterior cingulate cortex (ACC) is critically involved in pain sensation and emotions. Animal models of chronic pain, but not acute nociception have been found to induce synaptic plasticity on glutamatergic and GABAergic transmission in the rodent ACC. However, it is unclear whether acute stress exposure could produce SIH and cause synaptic plasticity in the ACC. Accordingly, we studied how acute exposure of stress by the elevated open platform (EOP) could affect mechanical threshold, thermal and cold latency in the adult mice. Thirty minutes of the EOP produced mechanical hypersensitivity lasting for 60 min and thermal hypersensitivity immediately after the exposure. Next, we tested whether the stress could alter the excitatory and inhibitory synaptic transmission in the ACC. We performed whole-cell patch-clamp recordings from layer II/III pyramidal neurons in the ACC and analyzed both glutamatergic and GABAergic transmission in mice following the EOP. Thirty minutes of the EOP altered the rise and decay time of spontaneous glutamatergic AMPA/GluK receptors mediated currents, but did not change the frequency or amplitude of excitatory transmission. By contrast, the kinetics of inhibitory synaptic currents were not altered by the EOP. These results suggest that acute stress by the elevated platform produces SIH and causes synaptic plasticity on excitatory transmission, but not inhibitory transmission in the ACC. |
