The giant Mauthner (M) cell is the largest neuron known in the vertebrate brain. It has enabled major breakthroughs in neuroscience but its ultimate function remains surprisingly unclear: An actual survival value of M cell-mediated escapes has never been supported experimentally and ablating the cell repeatedly failed to eliminate all rapid escapes, suggesting that escapes can equally well be driven by smaller neurons. Here we applied techniques to simultaneously measure escape performance and the state of the giant M axon over an extended period following ablation of its soma. We discovered that the axon survives remarkably long and remains still fully capable of driving rapid escape behavior. By unilaterally removing one of the two M axons and comparing escapes in the same individual that could or could not recruit an M axon, we show that the giant M axon is essential for rapid escapes and that its loss means that rapid escapes are also lost forever. This allowed us to directly test the survival value of the M cell-mediated escapes and to show that the absence of this giant neuron directly affects survival in encounters with a natural predator. These findings not only offer a surprising solution to an old puzzle but demonstrate that even complex brains can trust vital functions to individual neurons. Our findings suggest that mechanisms must have evolved in parallel with the unique significance of these neurons to keep their axons alive and connected.
In non-mammalian vertebrates, some neurons can regenerate after spinal cord injury. One of these, the giant Mauthner (M-) neuron shows a uniquely direct link to a robust survivalcritical escape behavior but appears to regenerate poorly. Here we use two-photon microscopy in parallel with behavioral assays in zebrafish to show that the M-axon can regenerate very rapidly and that the recovery of functionality lags by just days. However, we also find that the site of the injury is critical: While regeneration is poor both close and far from the soma, rapid regeneration and recovery of function occurs for injuries between 10% and 50% of total axon length. Our findings show that rapid regeneration and the recovery of function can be studied at remarkable temporal resolution after targeted injury of one single M-axon and that the decision between poor and rapid regeneration can be studied in this one axon.
Abstract. The ladybird Coccinella magnifica is typically considered to be myrmecophilous, and primarily associated with the For mica rufa group of wood ants. It is regularly associated with ants of the F. rufa group in north-western Europe. The very limited data on the habitat preference of C. magnifica in the southern and eastern parts of its range indicate that its ant-associations change and that it may even be non-myrmecophilous in this region. C. magnifica might consist of geographically restricted species or semispe cies, on the basis of its geographical variation in ant-association. Laboratory and field observations on north-western myrmecophi lous populations C. magnifica appear to indicate it is a generalist predator of aphids. Coccinella magnifica's potential dietary breadth is similar to that of its congener Coccinella septempunctata, which has been used as a model of C. magnifica's non-myrmecophilous ancestor in evolutionary studies.
The parallel occurrence in archerfish of fine-tuned and yet powerful predictive C-starts as well as of kinematically identical escape C-starts makes archerfish an interesting system to test hypotheses on the roles played by the Mauthner cells, a pair of giant reticulospinal neurons. In this study, we show that the archerfish Mauthner cell shares all hallmark physiological properties with that of goldfish. Visual and acoustic inputs are received by the ventral and lateral dendrite, respectively, and cause complex postsynaptic potentials (PSPs) even in surgically anaesthetised fish. PSP shape did not indicate major differences between the species, but simple light flashes caused larger PSPs in archerfish, often driving the cell to fire an action potential. Probing archerfish in the classical tests for feedback inhibition, established in the Mauthner-associated networks in goldfish, revealed no differences between the two species, including the indications for electrical and chemical synaptic components. Also, the established hallmark experiments on feed-forward inhibition showed no differences between the goldfish and archerfish Mauthner system. Extending these experiments to visual stimuli also failed to detect any differences between the two species and suggested that acoustical and visual input cause feed-forward inhibition, the magnitude, time course and duration of which match that of the respective PSPs in both archerfish and goldfish. Our findings question simple views on the role of the Mauthner cell and suggest that the archerfish Mauthner cell should be a good system to explore the function of these giant neurons in more sophisticated C-start behaviours.
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