Advances in neuroimaging technology have been instrumental in uncovering the dramatic neurological changes that result from blindness, as well as revealing the inner workings of the human brain. Specifically, modern imaging techniques enable us to examine how the brain adapts and "re-wires" itself as a result of changes in behavior, the environment, injury, or disease; a process referred to as neuroplasticity. Following an overview of commonly employed neuroimaging techniques, we discuss structural and functional neuroplastic brain changes associated with profound visual deprivation. In particular, we highlight how associated structural changes often occur within areas that process intact senses (such as hearing, touch, and smell) while functional changes tend to implicate areas of the brain normally ascribed to the processing of visual information. Evidence will primarily focus on profound blindness due to ocular cause, but related work in cerebral/cortical visual impairment (CVI) will also be discussed. The potential importance of these findings within the context of education and rehabilitation is proposed.
Previous research from our laboratory has determined that in the absence of a gustatory response or taste hedonics, intraperitoneal (i.p.) glucose administration enhanced morphine-mediated analgesia in rats and had antinociceptive actions on its own. Two experiments examined the potential of a central mechanism for glucose's actions on morphine-mediated antinociception. Morphine (2.5 µg) was infused into the periaqueductal gray (PAG) while glucose (300 mg/kg) was injected into the peritoneal cavity, or glucose (32 nmol) was infused into the PAG while morphine (3.2 mg/kg) was injected i.p. Doses of morphine and glucose were selected based on our own prior research for being below the threshold for analgesic efficacy. Antinociception was assessed using the hot-water tail-withdrawal procedure. Tail-withdrawal latency was tested at baseline (before), and 12, 24 and 36 minutes after the i.p. injection. The results indicated that 300 mg/kg glucose, administered i.p. effectively increased the antinociceptive potency of a low dose of centrally administered morphine, while central infusion of glucose enhanced peripheral morphine-mediated antinociception. These outcomes support previous evidence of glucose's influence on the antinociception actions of opioid drugs. Furthermore, they suggest that glucose produces its enhancing actions on morphine-mediated antinociception in the brain. These results support the hypothesis that glucose does not need to go through a gustatory mechanism or taste hedonics to alter morphine's antinociceptive actions.
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