Neuroscience
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Until now, cortical crossmodal plasticity has largely been regarded as the effect of early and complete sensory loss. Recently, massive crossmodal cortical reorganization was demonstrated to result from profound hearing loss in adult ferrets (Allman et al., 2009a). Moderate adult hearing loss, on the other hand, induced not just crossmodal reorganization, but also merged new crossmodal inputs with residual auditory function to generate multisensory neurons. ⋯ When compared with hearing controls, partially-deaf animals revealed elevated spontaneous levels and a dramatic increase (∼2 times) in the proportion of multisensory cortical neurons, but few of which showed multisensory integration. Moreover, a large proportion (68%) of neurons with somatosensory and/or visual inputs was vigorously active in core auditory cortex in the absence of auditory stimulation. Collectively, these results not only demonstrate multisensory dysfunction in core auditory cortical neurons from hearing impaired adults but also reveal a potential cortical substrate for maladaptive perceptual effects such as tinnitus.
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A number of studies have demonstrated that the relative timing of audiovisual stimuli is especially important for multisensory integration of speech signals although the neuronal mechanisms underlying this complex behavior are unknown. Temporal coincidence and congruency are thought to underlie the successful merging of two intermodal stimuli into a coherent perceptual representation. It has been previously shown that single neurons in the non-human primate prefrontal cortex integrate face and vocalization information. ⋯ When tested with a dynamic face-vocalization stimulus that had been temporally offset (asynchronous) one-third of multisensory cells in VLPFC demonstrated a change in response compared to the response to the natural, synchronous face-vocalization movie. Our results indicate that prefrontal neurons are sensitive to the temporal properties of audiovisual stimuli. A disruption in the temporal synchrony of an audiovisual signal which results in a change in the firing of communication related prefrontal neurons could underlie the loss in intelligibility which occurs with asynchronous speech stimuli.
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Xenon (Xe) and other inert gases produce anesthesia via an inhibitory mechanism in neuronal networks. To better understand this mechanism, we measured the electrical signals from cultured rat cortical neuronal networks in a multi-electrode array (MEA) under an applied Xe pressure. We used the MEA to measure the firing of the neuronal network with and without Xe gas pressurized to 0.3MPa. ⋯ The Xe-induced inhibition-recovery of neuronal network firing was reversible: after purging Xe from the system, the synchronized bursts gradually resumed. Thus, Xe did not inhibit single neuron firing, yet reversibly inhibited the synaptic transmission. This finding agrees with the channel-blocker and a modified-hydrate hypothesis of anesthesia, but not the lipid-solubility hypothesis.
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Previous studies have indicated that Müller glia in chick and fish retinas can re-enter the cell cycle, express progenitor genes, and regenerate neurons via the Notch signaling pathway in response to retinal damage or growth factors. Here, we investigated the role of Notch signaling and the effect of hypoxia, as a means to induce retinal damage, on the proliferation of an immortalized Müller cell line (rMC-1 cells). Our data showed that rMC-1 cells expressed Müller glia and neural and retinal progenitor markers but did not express neuronal or retinal markers. ⋯ Blockade of the Notch signaling pathway by DAPT after hypoxia promoted the differentiation of rMC-1 cells to neurons, as demonstrated by the induction of neural marker (Tuj1), retinal amacrine (Syntaxin1), and retinal ganglion cell (Brn3b) markers, although the expression of the latter marker was low. Taken together, our data indicate that Notch signaling is required for proliferation under hypoxic conditions either by activating the positive cell-cycle regulators or by skewing their de-differentiation towards a neural progenitor lineage. These findings indicate that the Notch signaling pathway regulates hypoxia-induced proliferation and differentiation of Müller glia.