Mutations indeadly seven/notch1aReveal Developmental Plasticity in the Escape Response Circuit

Abstract

The relatively simple neural circuit driving the escape response in zebrafish offers an excellent opportunity to study properties of neural circuit formation. The hindbrain Mauthner cell is an essential component of this circuit. Mutations in the zebrafish deadly seven/notch1a (des) gene result in supernumerary Mauthner cells. We addressed whether and how these extra cells are incorporated into the escape-response circuit. Calcium imaging revealed that all Mauthner cells in desb420 mutants were active during an elicited escape response. However, the kinematic performance of the escape response in mutant larvae was very similar to wild-type fish. Analysis of the relationship between Mauthner axon collaterals and spinal neurons revealed that there was a decrease in the number of axon collaterals per Mauthner axon in mutant larvae compared with wild-type larvae, indicative of a decrease in the number of synapses formed with target spinal neurons. Moreover, we show that Mauthner axons projecting on the same side of the nervous system have primarily nonoverlapping collaterals. These data support the hypothesis that excess Mauthner cells are incorporated into the escape-response circuit, but they divide their target territory to maintain a normal response, thus demonstrating plasticity in the formation of the escape-response circuit. Such plasticity may be key to the evolution of the startle responses in mammals, which use larger populations of neurons in circuits similar to those in the fish escape response.

Potential Roles of Arnt2 in Zebrafish Larval Development

“…This reflex involves the integration of sensory input from Rohon-Beard neurons in the spinal cord and motor output from the hindbrain and a large number of interneurons. [37][38][39][40][41][42][43][44][45] Arnt2 À=À larvae were predominantly unreactive to vibrational or tactile stimuli, suggesting that Arnt2 is associated with a part of the neural network that coordinates this response. Neuromasts are present in the arnt2 À=À mutants, which together with the overall intact structure of the inner ear suggests that auditory sensation, as well as vibrational sensation (lateral line), is not affected by loss of Arnt2.…”

HoxGene Misexpression and Cell-Specific Lesions Reveal Functionality of Homeotically Transformed Neurons

“…Liu et al (2003) found that in the des b420 , all M-cells appear to respond to startle stimuli, and they respond simultaneously, suggesting that they are receiving similar sensory input. In addition, although multiple M-cells were active in response to a startle stimulus, the additional activity did not enhance behavioral performance (Liu et al, 2003). We found similar results for fish with ectopic M-cells generated by hoxb1b misexpression; although both r2 and r4 M-cells were active in response to startle stimuli, behavioral performance remained the same.…”

“…The live mounted fish was covered with HBSS to prevent drying. The dish was placed on the stage of an inverted confocal microscope (model 510; Zeiss, Thornwood, NY), and a fine glass tapper actuated with an electric current was positioned against the side of the body on the ipsilateral side to the M-cells being investigated, as described previously (Liu et al, 2003). A time series of images was recorded beginning before application of the startle stimulus and lasting until the fluorescence levels in the cell returned to baseline.…”

“…Startle behavior of individual fish was recorded before and after cell lesion. At 5 dpf, prelesion behavioral trials were performed, and at 6 dpf, postlesion trials were performed using the general protocol of Liu and Fetcho (1999) and Liu et al (2003). A touch to the side of the body was used as the startle stimulus.…”

The effect of temperature and thermal acclimation on the sustainable performance of swimming scup

“…More recently, Fetcho et al (1997) have been able to engineer certain classes of cells to express Ca 2C -sensitive dyes so that the development of complex connections between nerves can be determined (Higashijima et al 2003;Liu et al 2003). Finally, as the genetic approaches evolve, one would anticipate the ability to modify specific molecular aspects of muscle function (i.e.…”