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I H Brivanlou

Publications and source records attributed to I H Brivanlou.

4 recordsLinked to original sources

Anticipation of moving stimuli by the retina.

A flash of light evokes neural activity in the brain with a delay of 30-100 milliseconds, much of which is due to the slow process of visual transduction in photoreceptors. A moving object can cover a considerable distance in this time, and should therefore be seen noticeably behind its actual location. As this conflicts with everyday experience, it has been suggested that the visual cortex uses the delayed visual data from the eye to extrapolate the trajectory of a moving object, so that it is perceived at its actual location. Here we report that such anticipation of moving stimuli begins in the retina. A moving bar elicits a moving wave of spiking activity in the population of retinal ganglion cells. Rather than lagging behind the visual image, the population activity travels near the leading edge of the moving bar. This response is observed over a wide range of speeds and apparently compensates for the visual response latency. We show how this anticipation follows from known mechanisms of retinal processing.

Animals↗

Mechanisms of concerted firing among retinal ganglion cells.

Nearby retinal ganglion cells often fire action potentials in near synchrony. We have investigated the circuit mechanisms that underlie these correlations by recording simultaneously from many ganglion cells in the salamander retina. During spontaneous activity in darkness, three types of correlations were distinguished: broad (firing synchrony within 40-100 ms), medium (10-50 ms), and narrow (<1 ms). When chemical synaptic transmission was blocked, the broad correlations disappeared, but the medium and narrow correlations persisted. Further analysis of the strength and time course of synchronous firing suggests that nearby ganglion cells share inputs from photoreceptors conveyed through interneurons via chemical synapses (broad correlations), share excitation from amacrine cells via electrical junctions (medium), and excite each other via electrical junctions (narrow). It appears that the firing patterns in the optic nerve are strongly shaped by electrical coupling in the inner retina.

Action Potentials↗

BMP-4-responsive regulation of dorsal-ventral patterning by the homeobox protein Mix.1.

In an expression screen for factors that pattern or induce ventral mesoderm, we isolated a complementary DNA encoding Mix.1, a paired class homeobox gene with no previously known function. Injection of Mix.1 messenger RNA results in extensive blood formation in the whole embryo and transforms dorsal mesoderm to a ventral fate. Mix.1 expression is induced by bone morphogenetic protein-4 (BMP-4), and a dominant inhibitory mutant of Mix.1 can restore a dorsal axis in embryos ventralized by ectopic BMP-4 expression. Mix.1 can form heterodimers with the dorsalizing gene siamois, which encodes a homeodomain protein that is structurally similar to Mix.1. Furthermore, Mix.1 blocks the duplicated axis induced by ectopic siamois expression. Our findings indicate that Mix.1 participates in a BMP-4 signalling pathway to pattern ventral mesoderm, and suggest a model whereby dimerization of homeodomain proteins regulates dorsal-ventral patterning.

Animals↗

TGF-beta signals and a pattern in Xenopus laevis endodermal development.

We have analyzed two gene products expressed in the early endoderm of Xenopus laevis: Xlhbox-8, a pancreas-specific transcription factor and intestinal fatty acid binding protein (IFABP), a marker of small intestinal epithelium. Expression of the pancreas marker relies on cell signaling mediated by both the TGF-beta and FGF classes of secreted peptide growth factors, whereas, expression of the more posterior small intestinal marker does not. Endodermal explants devoid of mesoderm express both markers in a regionalized manner. Cortical rotation is required for the expression of the more anterior marker, Xlhbox-8, but not for the small intestinal marker, IFABP. These findings suggest that endodermal patterning is dependent, in part, on the same events and signals known to play important roles in mesodermal development. Furthermore, inhibition of TGF-beta signaling in the endoderm leads to ectopic expression of both mesodermal and ectodermal markers, suggesting the TGF-beta signaling may play a general role in the segregation of the three embryonic germ layers.

Animals↗