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Segmentation of the vertebrate hindbrain into rhombomeres is a key step in the development of a complex pattern of differentiated neurons from a homogeneous neuroepithelium. Many of the transcription factors important for establishing the segmental plan and assigning rhombomere identity are now known. However, the downstream effectors that bring about the formation of rhombomere boundaries are only just being characterized. Here we discuss molecules that could be responsible for segregating populations of cells from different rhombomeres. We focus on recent work demonstrating that the Eph family of receptor tyrosine kinases and their ligands, the ephrins, function in rhombomere-specific cell sorting and initiation of a structural boundary. We discuss the contributions of two mechanisms -- cell sorting and plasticity -- to the formation of rhombomere boundaries.

Radial glia are specialized cells in the developing nervous system of all vertebrates, and are characterized by long radial processes. These processes facilitate the best known function of radial glia: guiding the radial migration of newborn neurons from the ventricular zone to the mantle regions. Recent data indicate further important roles for these cells as ubiquitous precursors that generate neurons and glia, and as key elements in patterning and region-specific differentiation of the CNS. Thus, from being regarded mainly as support cells, radial glia have emerged as multi-purpose cells involved in most aspects of brain development.

Vertebrate rod photoreceptors adjust their sensitivity as they adapt during exposure to steady light. Light adaptation prevents the rod from saturating and significantly extends its dynamic range. We examined the time course of the onset of light adaptation in bullfrog rods and compared it with the projected onset of feedback reactions thought to underlie light adaptation on the molecular level. We found that adaptation developed in two distinct temporal phases: (1) a fast phase that operated within seconds after the onset of illumination, which is consistent with most previous reports of a 1-2-s time constant for the onset of adaptation; and (2) a slow phase that engaged over tens of seconds of continuous illumination. The fast phase desensitized the rods as much as 80-fold, and was observed at every light intensity tested. The slow phase was observed only at light intensities that suppressed more than half of the dark current. It provided an additional sensitivity loss of up to 40-fold before the rod saturated. Thus, rods achieved a total degree of adaptation of ~3,000-fold. Although the fast adaptation is likely to originate from the well characterized [Ca.sup.2+]-dependent feedback mechanisms regulating the activities of several phototransduction cascade components, the molecular mechanism underlying slow adaptation is unclear. We tested the hypothesis that the slow adaptation phase is mediated by cGMP dissociation from noncatalytic binding sites on the cGMP phosphodiesterase, which has been shown to reduce the lifetime of activated phosphodiesterase in vitro. Although cGMP dissociated from the noncatalytic binding sites in intact rods with kinetics approximating that for the slow adaptation phase, this hypothesis was ruled out because the intensity of light required for cGMP dissociation far exceeded that required to evoke the slow phase. Other possible mechanisms are discussed. KEYWORDS: photoreceptors * phototransduction * adaptation * calcium * cGMP

I. INTRODUCTION This review explores the mechanisms of central control and coordination of the respiratory and cardiovascular systems in vertebrates. Animals have evolved sophisticated control mechanisms enabling them to match [...]

The kinetic consequences of the N217K mutation in the M1 site of the acetylcholine receptor alpha subunit causing slow channel congenital myasthenic syndrome, is described. A study uses single channel kinetic analysis to show that prolonged activation episodes are mainly due to the slower rate of acetylcholine dissociation from the binding site. Results found that the mutation in the amino-terminal part of the M1 site leads to localized perturbation, stabilizing agonists linked to the resting state of the acetylcholine receptor.

Neurons become dependent on a supply of target-derived neurotrophins for survival when their axons reach their targets in development. Because the distance axons have to grow varies from one population of neurons to another, the timing of dependence on neurotrophins likewise varies. Although it would be expected that the simplest way of getting the timing right would be for the target to provide a suitable signal to the arriving axons, detailed studies on developing cranial sensory neurons suggest that these neurons are programmed, before differentiation, to acquire dependence at the correct time independently of external signals. Neurons not only partly compensate for different target distances by extending axons more rapidly the further they have to grow, but possess an intrinsic clock that switches on dependence at the right time in accordance with the time it normally takes their axons to reach their targets. Here the experimental evidence for these intrinsic programmes of growth and survival is reviewed, the rationale that might have favoured their evolution is discussed, and parallels are drawn with other developing neuronal systems.