The Journal of neuroscience : the official journal of the Society for Neuroscience
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Although it is well known that injury induces the generation of a substantial number of new olfactory sensory neurons (OSNs) in the adult olfactory epithelium (OE), it is not well understood whether olfactory sensory input influences the survival and maturation of these injury-induced OSNs in adults. Here, we investigated whether olfactory sensory deprivation affected the dynamic incorporation of newly generated OSNs 3, 7, 14, and 28 d after injury in adult mice. Mice were unilaterally deprived of olfactory sensory input by inserting a silicone tube into their nostrils. ⋯ Intrinsic functional imaging of the dorsal surface of the olfactory bulb at day 28 revealed that responses to odor stimulation were weaker in the deprived side compared with those in the nondeprived side. Furthermore, prevention of cell death in new neurons 7-14 d after injury promoted the recovery of the OE. These results indicate that, in the adult OE, sensory deprivation disrupts compensatory OSN regeneration after injury and that newly generated OSNs have a critical time window for sensory-input-dependent survival 7-14 d after injury.
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Accumulated evidence from experimental animal models suggests that neuronal loss within the dorsal horn is involved in the development and/or maintenance of peripheral neuropathic pain. However, to date, no study has specifically investigated whether such neuroanatomical changes also occur at this level in humans. Using brain imaging techniques, we sought to determine whether anatomical changes were present in the spinal trigeminal nucleus in subjects with chronic orofacial neuropathic pain. ⋯ In addition, tractography revealed no significant differences in diffusivity properties in the root entry zone of the trigeminal nerve, the spinal trigeminal tract, or the ventral trigeminothalamic tracts in painful trigeminal neuropathy subjects compared with controls. These data reveal that chronic neuropathic pain in humans is associated with discrete alterations in the anatomy of the primary synapse. These neuroanatomical changes may be critical for the generation and/or maintenance of pathological pain.
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Impaired presynaptic long-term potentiation in the anterior cingulate cortex of Fmr1 knock-out mice.
Fragile X syndrome is a common inherited form of mental impairment. Fragile X mental retardation protein (FMRP) plays important roles in the regulation of synaptic protein synthesis, and loss of FMRP leads to deficits in learning-related synaptic plasticity and behavioral disability. Previous studies mostly focus on postsynaptic long-term potentiation (LTP) in Fmr1 knock-out (KO) mice. ⋯ This potentiation was blocked in Fmr1 KO mice. Biochemical experiments showed that Fmr1 KO mice displayed altered translocation of protein kinase A subunits in the ACC. Our results demonstrate that FMRP plays an important role in pre-LTP in the adult mouse ACC, and loss of this pre-LTP may explain some of the behavioral deficits in Fmr1 KO mice.
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Adolescence is often described as a period of increased risk taking relative to both childhood and adulthood. This inflection in risky choice behavior has been attributed to a neurobiological imbalance between earlier developing motivational systems and later developing top-down control regions. Yet few studies have decomposed risky choice to investigate the underlying mechanisms or tracked their differential developmental trajectory. ⋯ Return sensitivity, on the other hand, increased monotonically across age groups and was associated with increased activation in the ventral medial PFC and posterior cingulate cortex with age. Our results implicate adolescence as a developmental phase of increased neural risk sensitivity. Importantly, this work shows that using a behaviorally validated decision-making framework allows a precise operationalization of key constructs underlying risky choice that inform the interpretation of results.