Envision this scenario. It’s the end of a grueling hike and you’re racing back to civilization along a trail in the mountains as darkness falls. You’ve become separated from your fellow hikers when all of a sudden the last beams of sunlight fade and the moonless night descends. You reach into your backpack for your flashlight only to realize that the batteries are dead. Accustomed to relying on your visual system, you panic upon being plunged into temporary blindness. But wait! All of a sudden the previously inaudible footsteps of your companions become heightened as you discriminate where they are and race off in the direction of their voices.
Neuroscience research has demonstrated that disruption of sensory input from one sense can improve the function of the remaining senses, such as auditory localization or tactile feedback. When sensory deprivation occurs early during development, there is a disruption in synaptic connections in the corresponding area of cortex. For example, using our theme of blindness in the absence of visual sensory experience, functional neural circuits are impaired in the visual cortex but the sensory cortex is more responsive to input from other senses. This adaptation, or cross-modal plasticity, is complex because individuals who undergo sensory deprivation early during development have enhanced compensation from other senses than individuals who lose the function of one of their senses later in life.
In exciting research published in the journal Nature Neuroscience, a research team led by Dr. Yu Xiang found that the negative effects of sensory deprivation early in development could be reduced with oxytocin injections combined with a regiment of enhanced sensory experience. Oxytocin is a neuropeptide that is synthesized and secreted in response to sensory experience as a regulator of social and emotional behaviors. The hypothesis in question was whether sensory deprivation in mice (whisker removal at birth) would influence the somatosensory cortex alone (expected) or whether a cross-modal effect would be seen in the primary visual cortex (V1) and the auditory cortex (Au1). In an interesting turn of events, by recording from neurons in the primary auditory and visual cortex, it was determined that whisker deprivation reduced excitatory synaptic transmission both in the somatosensory cortex and cross-modally in areas of cortex unrelated to tactile feedback (whisker-mediated input).
In a clever experiment, the researchers set out to determine if raising the mice in the dark (visual sensory deprivation) would influence firing rates in the somatosensory cortex. Indeed, deprivation of visual input cross-modally negatively affected the somatosensory circuitry. Any form of sensory deprivation – be it whisker removal or dark rearing – caused a reduction in oxytocin. By injecting oxytocin, the team was able to elevate excitatory synaptic transmission and restore the impairments caused by sensory deprivation.
This research is particularly compelling when viewed in the context of autism, a developmental disorder associated with impairments in sensitivity to sensory input and social behavior. Oxytocin signaling has previously been described as important for regulating social and emotional behavior later in life. This work suggests that oxytocin may play a role early in development to regulate function in sensory cortices. This work raises the question of whether oxytocin could be a viable treatment option for restoring impairments in the development of the sensory cortex.
Merabet L.B., Rizzo J.F., Amedi A., Somers D.C. & Pascual-Leone A. (2005). Opinion: What blindness can tell us about seeing again: merging neuroplasticity and neuroprostheses, Nature Reviews Neuroscience, 6 (1) 71-77. DOI: 10.1038/nrn1586
Zheng J.J., Li S.J., Zhang X.D., Miao W.Y., Zhang D., Yao H. & Yu X. (2014). Oxytocin mediates early experience–dependent cross-modal plasticity in the sensory cortices, Nature Neuroscience, 17 (3) 391-399. DOI: 10.1038/nn.3634
Images adapted from Ocean/Corbis by Kate Jones.