Wiley
0022-3034
1097-4695
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Cellular and synaptic mechanisms of nicotine addiction Abstract The tragic health effects of nicotine addiction highlight the importance of investigating the cellular mechanisms of this complex behavioral phenomenon. The chain of cause and effect of nicotine addiction starts with the interaction of this tobacco alkaloid with nicotinic acetylcholine receptors (nAChRs). This interaction leads to activation of reward centers in the CNS, including the mesoaccumbens DA system, which ultimately leads to behavioral reinforcement and addiction. Recent findings from a number of laboratories have provided new insights into the biologic processes that contribute to nicotine self‐administration. Examination of the nAChR subtypes expressed within the reward centers has identified potential roles for these receptors in normal physiology, as well as the effects of nicotine exposure. The high nicotine sensitivity of some nAChR subtypes leads to rapid activation followed in many cases by rapid desensitization. Assessing the relative importance of these molecular phenomena in the behavioral effects of nicotine presents an exciting challenge for future research efforts. © 2002 Wiley Periodicals, Inc. J Neurobiol 53: 606–617, 2002
Tập 53 Số 4 - Trang 606-617 - 2002
Regulated <i>vnd</i> expression is required for both neural and glial specification in <i>Drosophila</i> Abstract The Drosophila embryonic CNS arises from the neuroectoderm, which is divided along the dorsal‐ventral axis into two halves by specialized mesectodermal cells at the ventral midline. The neuroectoderm is in turn divided into three longitudinal stripes—ventral, intermediate, and lateral. The ventral nervous system defective, or vnd, homeobox gene is expressed from cellularization throughout early neural development in ventral neuroectodermal cells, neuroblasts, and ganglion mother cells, and later in an unrelated pattern in neurons. Here, in the context of the dorsal‐ventral location of precursor cells, we reassess the vnd loss‐ and gain‐of‐function CNS phenotypes using cell specific markers. We find that over expression of vnd causes significantly more profound effects on CNS cell specification than vnd loss. The CNS defects seen in vnd mutants are partly caused by loss of progeny of ventral neuroblasts—the commissures are fused and the longitudinal connectives are aberrantly positioned close to the ventral midline. The commissural vnd phenotype is associated with defects in cells that arise from the mesectoderm, where the VUM neurons have pathfinding defects, the MP1 neurons are mis‐specified, and the midline glia are reduced in number. vnd over expression results in the mis‐specification of progeny arising from all regions of the neuroectoderm, including the ventral neuroblasts that normally express the gene. The CNS of embryos that over express vnd is highly disrupted, with weak longitudinal connectives that are placed too far from the ventral midline and severely reduced commissural formation. The commissural defects seen in vnd gain‐of‐function mutants correlate with midline glial defects, whereas the mislocalization of interneurons coincides with longitudinal glial mis‐specification. Thus, Drosophila neural and glial specification requires that vnd expression by tightly regulated. © 2002 Wiley Periodicals, Inc. J Neurobiol 50: 118–136, 2002; DOI 10.1002/neu.10022
Tập 50 Số 2 - Trang 118-136 - 2002
Members of the Dlx‐and NKx2‐gene families are regionally expressed in the developing forebrain Abstract Members of the vertebrate Dlx ‐ and NKx2 ‐homeobox‐containing gene families exhibit closely related, comple‐mentary areas of gene expression in the developing forebrain. The expression domains and onset of gene transcription indicate that these genes may play a role in forebrain patterning, particularly in the diencephalon. In some cases, gene expression borders coincide with mor‐phological boundaries separating functional and anatomical regions of the forebrain suggesting that the rostral region of the neural tube may indeed arise from a segmented structure. © 1993 John Wiley & Sons, Inc.
Tập 24 Số 10 - Trang 1385-1399 - 1993
Neuronal circuit reorganization in mammalian agranular cerebellar cortex Abstract Morphological and electrophysiological studies of the agranular cerebellar cortex of ferret after infection with panleukopenia virus have led to the following conclusions:
At light microscopic level this agranular cerebellar cortex is shown to be totally disorganized when compared to its normal lamination. From an ultrastructural point of view, Purkinje cells are present throughout the thickness of the cerebellar cortex, demonstrating dendritic branches studded with unwed spines. Purkinje cells receive four different types of inputs‐climbing fibers, mossy fibers, stellate cell terminals, and Purkinje cell axon collateral terminals. The mossy fiber contacts which are generally not present in mammals are made in some cases to elongated, “dolichoderic” spines. Stellate, basket, and Golgi cell interneurons are present, and receive inputs from mossy and climbing fiber terminals, and probably from axon collaterals of Purkinje cells. The mossy fiber input to these neurons represents a true reorganization of the cerebellar circuit, since it has never been observed in any other vertebrate. Stellate and basket cells terminate in contact with dendrites and somata from Purkinje cells, while the Golgi cell terminals seem to be restricted to somata and dendrites of other Golgi cells. Electrophysiologically, Purkinje cells can show normal excitability following antidromic invasion, and may be activated by the mossy and climbing fiber afferent systems. Intra‐and extracellular recording from Purkinje cells demonstrates that the mossy fiber afferent system activates Purkinje cells with a latency of approximately 1 msec and its excitatory action is graded with relation to the amplitude of the white matter stimulation. Following an initial excitation, this input generates a longlasting inhibition (50 msec), which is attributed to mossy and climbing fiber activation of inhibitory interneurons. Climbing fiber activation generates the typical all‐or‐none burst response in Purkinje cells extracellularly. Intracellularly, large unitary EPSPs characteristic of this form of activation may be recorded with a latency of 1.5 to 3 msec. This large unitary EPSP seems to behave in the usual one‐to‐one relation (one climbing fiber to one Purkinje cell). Double climbing fiber activation reveals that a conditioning white matter stimulation produces a total inhibition of a climbing fiber burst at 15 msec interval, which indicates a rather strong inhibitory action on Purkinje cells following this form of activation. Climbing fiber activation is followed in most cases by a so‐called climbing fiber reflex, suggesting that the inferior olive in this agranular condition is functioning in a normal manner. Finally, some of the neurobiological implications of these findings are considered in the discussion.
Tập 4 Số 1 - Trang 69-94 - 1973
Establishment of neuronal connectivity during development of the <i>Drosophila</i> larval visual system Abstract We used confocal microscopy in conjunction with specific antibodies and enhancer trap strains to investigate the development of specific neuronal connections in a simple model system, the larval visual system of Drosophila . We find that the establishment of axonal projections from the larval photoreceptor neurons to their central nervous system targets involves a series of discrete steps. During embryogenesis, the larval optic nerve contacts several different cell types, including optic lobe pioneer (OLP) neurons and a number of glial cells. We demonstrate that OLP neurons are present and project normally in glass (gl ) mutant embryos in which the larval optic nerve fails to develop, suggesting that they do not depend on interactions with the larval optic nerve for differentiation and proper axonal projection. The OLPs fail to differentiate properly in disconnected (disco ) mutant embryos, where appropriate connections between the larval optic nerve and its targets in the brain are not formed. The disco gene is expressed in the OLPs and may therefore act autonomously to direct the differentiation of these cells. Taken together, our results suggest that the OLPs act as an intermediate target required for the establishment of normal optic nerve projection and connectivity. © 1995 John Wiley & Sons, Inc.
Tập 28 Số 3 - Trang 313-329 - 1995
Postsynaptic regulation of the development and long‐term plasticity of <i>Aplysia</i> sensorimotor synapses in cell culture Abstract The monosynaptic component of the neuronal circuit that mediates the withdrawal reflex of Aplysia californica can be reconstituted in dissociated cell culture. Study of these in vitro monosynaptic connections has yielded insights into the basic cellular mechanisms of synaptogenesis and long‐term synaptic plasticity. One such insight has been that the development of the presynaptic sensory neurons is strongly regulated by the postsynaptic motor neuron. Sensory neurons which have been cocultured with a target motor neuron have more elaborate structures—characterized by neurites with more branches and varicosities—than do sensory neurons grown alone in culture or sensory neurons that have been cocultured with an inappropriate target cell. Another way in which the motor neuron regulates the development of sensory neurons is apparent when sensorimotor cocultures with two presynaptic cells are examined. In such cocultures the outgrowth from the different presynaptic cells is obviously segregated on the processes of the postsynaptic cell. By contrast, when two sensory neurons are placed into cell culture without a motor neuron, thier processes readily grow together. In addition to regulating the in vitro development of sensory neurons, the motor neuron also regulates learning‐related changes in the structure of sensory neurons. Application of the endogenous facilitatory trasmitter serotonin (5‐HT) causes long‐term facilitation of in vitro sensorimotor synapses due in part to growth of new presynatpic varicosities. But 5‐HT applied to sensory neurons alone in cultuer does not produce structural changes in these cells. More recently it has been found that sensorimotor synapses in cell culture can exhibit long‐term potentiation (LTP). Like LTP of some hippocampal synapses, LTP of in vitro Aplysia syanpses is regulated by the voltage of the postsynaptic cell. Pairing high‐frequency stimulation of sensory neurons with strong hyperpolarization of the motor neuron blocks the induction of LTP. Moreover, LTP of sensorimotor synapses can be induced in Hebbian fashion by pairing weak presynaptic stimulation with strong postsynaptic depolarization. These findings implicate a Habbian mechanism in classical conditioning in Aplysia . They also indicate that Hebbian LTP is a phylogenetically ancient form of synaptic plasticity. 1994 John Wiley & Sons, Inc.
Tập 25 Số 6 - Trang 666-693 - 1994
Neuroanatomical specificity in the co‐localization of aromatase and estrogen receptors Abstract The relative distributions of aromatase and of estrogen receptors were studied in the brain of the Japanese quail by a double‐label immunocytochemical technique. Aromatase immunoreactive cells (ARO‐ir) were found in the medial preoptic nucleus, in the septal region, and in a large cell cluster extending from the dorso‐lateral aspect of the ventromedial nucleus of the hypothalamus to the tuber at the level of the nucleus inferioris hypothalami. Immunoreactive estrogen receptors (ER) were also found in each of these brain areas but their distribution was much broader and included larger parts of the preoptic, spetal, and tuberal regions. In the ventromedial and tuberal hypothalamus, the majority of the ARO‐ir cells (over 75%) also contained immunoreactive ER. By contrast, very few of the ARO‐ir cells were double‐labeled in the preoptic area and in the septum. More than 80% of the aromatase‐containing cells contained no ER in these regions. This suggests that the estrogens, which are formed centrally by aromatization of testosterone, might not exert their biological effects through binding with the classical nuclear ER. The fact that significant amounts of aromatase activity are found in synaptosomes purified by differential centrifugation and that aromatase immunoreactivity is observed at the electron microscope level in synaptic boutons suggests that aromatase might produce estrogens that act at the synaptic level as neurohomones or neuromodulators.
Tập 22 Số 2 - Trang 143-157 - 1991
Effects of axonal injury on norepinephrine, tyrosine hydroxylase and monoamine oxidase levels in sympathetic ganglia Abstract A combined morphological and biochemical study was made of the responses of lumbar sympathetic ganglion cells to ligation of their axons in the sciatic nerve of the rat. There was a progressive accumulation of norepinephrine proximal to the ligature for the first few days without detectable changes in the ganglion cells. However, three days after ligation there was a decrease in the axoplasmic accumulation of norepinephrine, accompanied by pronounced falls in ganglion norepinephrine, tyrosine hydroxylase, and monoamine oxidase. These changes, that coincided with the development of signs of chromatolysis in the light and electron microscope, were fully developed one week after ligation and by one month were almost reversed. Proteolysis and death of chromatolytic cells may have made some contribution to the observed changes, but there were no significant changes in the soluble protein content of the lumbar ganglia, presumably because of the counter‐balancing increase in protein synthesis known to occur during chromatolysis and regeneration. It is suggested that axotomy caused a reordering of the priorities of protein synthesis in sympathetic neurones to favor the production of proteins necessary for regenerative rather than transmitter functions.
Tập 4 Số 5 - Trang 443-452 - 1973
Mechanisms of Hedgehog gradient formation and interpretation Abstract Morphogens are molecules that spread from localized sites of production, specifying distinct cell outcomes at different concentrations. Members of the Hedgehog (Hh) family of signaling molecules act as morphogens in different developmental systems. If we are to understand how Hh elicits multiple responses in a temporally and spatially specific manner, the molecular mechanism of Hh gradient formation needs to be established. Moreover, understanding the mechanisms of Hh signaling is a central issue in biology, not only because of the role of Hh in morphogenesis, but also because of its involvement in a wide range of human diseases. Here, we review the mechanisms affecting the dynamics of Hh gradient formation, mostly in the context of Drosophila wing development, although parallel findings in vertebrate systems are also discussed. © 2005 Wiley Periodicals, Inc. J Neurobiol 64: 334–356, 2005
Tập 64 Số 4 - Trang 334-356 - 2005
Injury‐associated induction of GAP‐43 expression displays axon branch specificity in rat dorsal root ganglion neurons Abstract Peripheral nerve injury results in the increased synthesis and axonal trasnport of the growth‐associated protein GAP‐43 in dorsal root ganglion (DRG) neurons, coincident with regenerative growth of the injured peripheral axon branches. To determine wheter the injury‐associated signalling mechanism which leads to GAP‐43 induction also operates through the central branches of DRG axons, we used immunocytochemistry to compare the expression of GAP‐43 in adult rat DRG neurons 2 weeks after dorsal root crush lesions (central axotomy) or peripheral nerve crush lesions (peripheral axotomy). In uninjured ganglia, a subpopulation of smaller DRG neurons expresses moderate levels of GAP‐43, whereas larger neurons generally do not. At 2 weeks following peripheral axotomy, virtually all axotomized neurons, large and small, express high levels of GAP‐43. At 2 weeks following dorsal root lesions, no increase in GAP‐43 expression is detected. Thus, the injury‐associated up‐regulation of GAP‐43 expression in DRG neurons is triggered by a mechanism that is responsive to injury of only the peripheral, and not the central, axon branches. These findings support the hypothesis that GAP‐43 induction in DRG neurons is caused by disconnection from peripheral target tissue, not by axon injury per se. © 1993 John Wiley & Sons, Inc.
Tập 24 Số 7 - Trang 959-970 - 1993