New collaborative research involving UTCSP members suggests that it is possible to abolish side effects of morphine without interfering with its analgesic effects.
Opiates, such as morphine, are widely used to treat pain. Unfortunately a problematic side effect of opiates is hyperalgesia, which paradoxically involves an amplified sense of pain. New research suggests that it is possible to abolish morphine-induced hyperalgesia without interfering with analgesic effects in mice.
The work, published in the February 2013 edition of Nature Neuroscience, involved a series studies conducted to delineate the molecular mechanisms involved in morphine-induced hyperalgesia. Intriguingly, microglial cells (non-neuronal “support” cells in the central nervous system) were shown to be key players in the mechanistic pathway. Specifically, the researchers demonstrated that when microglia release a protein known as brain-derived neurotrophic factor (BDNF), this sends a signal to neurons in the spinal cord, which leads to the disruption of chlorine homeostasis and hyperalgesia.
The data could lead to new therapies that would reduce or abolish problematic side effects of opiates.
Co-authors on the study included U of T researchers Tuan Trang, Wenbo Zhang, Daniela Mohr, Simon Beggs & Michael W Salter.
Reference:
Ferrini, Francesco, et al. "Morphine hyperalgesia gated through microglia-mediated disruption of neuronal Cl-homeostasis." Nature neuroscience (2013).