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At least 289 records · Page 16Linked to original sources
PubMed2002

Mutation of Drosophila homer disrupts control of locomotor activity and behavioral plasticity.

Homer proteins have been proposed to play a role in synaptogenesis, synapse function, receptor trafficking, and axon pathfinding. Here we report the isolation and characterization of the Drosophila gene homer, the single Homer-related gene in fly. Using anti-Homer antibody we show that Homer is expressed in a broad range of tissues but is highly enriched in the CNS. Similarly to its mammalian counterpart, the Drosophila Homer localizes to the dendrites and the endoplasmic reticulum (ER). This subcellular distribution is dependent on an intact Enabled/Vasp homology 1 domain, suggesting that Homer must bind to one or more of its partners for proper localization. We have created a mutation of homer and show that flies homozygous for this mutation are viable and show coordinated locomotion, suggesting that Homer is not essential for basic neurotransmission. However, we found that homer mutants display defects in behavioral plasticity and the control of locomotor activity. Our results argue that in the CNS, Homer-related proteins operate in the ER and in dendrites to regulate the development and function of neural networks underlying locomotor control and behavioral plasticity.

Animals↗
PubMed2001

[Functional recuperation following lesions of the primary somatosensory fields. Study of compensatory mechanisms].

During a long time, lesions of the primary somatosensory area (S I) were considered as generating severe and definitive neurological sequelae. However, recent reports described a recovery following stroke and resective surgeries (for epilepsy or tumor). On the basis of these observations, of experimentations in animals, and of studies of the (re)organization of eloquent areas in man using new methods of functional mapping, brain plasticity phenomena underlying the recovery were analyzed. They seems to implicate the recruitment of local areas (sensory redundancies within S I), regional areas (primary motor area, secondary somatosensory area, posterior parietal cortex, insula), controlateral eloquent regions, and even learning of new compensatory strategies. Such data could allow us to extend surgical indications of resection of lesions located within S I. An improvement of our knowledge of these functional reshaping phenomena (unmasking of latent networks and/or participation of eloquent homologous and/or sprouting) and then their prediction remains mandatory, with the goal to optimize the surgical preplanning in functional regions, taking account of the individual dynamic spatiotemporal cortical organization. This better knowledge seems to be obtained by studying the correlations between pre- and post-operative functional neuroimaging (fMRI, MEG) data, and the intraoperative functional mapping results.

Animals↗
PubMed2002

Experience-dependent coincident expression of the effector immediate-early genes arc and Homer 1a in hippocampal and neocortical neuronal networks.

The transcription of the immediate-early genes Arc and Homer 1a (H1a) is dynamically regulated in response to synaptic activity; their protein products function at the postsynaptic sites of excitatory synapses. Previous studies demonstrate a role for Arc in the maintenance of long-term potentiation and in memory consolidation processes and indicate a role for H1a in modifying glutamatergic signaling pathways. Using double-label fluorescence in situ hybridization, we demonstrate that Arc and H1a RNA expression is induced strongly in the same neurons of rat hippocampus and neocortex after exploration of a novel environment. These findings support the view that novel experience activates a cell-specific genomic program and that Arc and H1a may function in concert in the structural and functional modifications of dendrites that lead to long-term changes in synaptic efficacy.

3' Untranslated Regions↗
PubMed2003

Semaphorin 3F is critical for development of limbic system circuitry and is required in neurons for selective CNS axon guidance events.

Little is known about the role of class 3 semaphorins in the development of CNS circuitry. Several class 3 semaphorins, including semaphorin 3F (Sema3F) bind to the receptor neuropilin-2 to confer chemorepulsive responses in vitro. To understand the role of Sema3F in the establishment of neural circuitry in vivo, we have generated sema3F null and sema3F conditional mutant mice. Inspection of the peripheral nervous system in sema3F null mice reveals that Sema3F is essential for the proper organization of specific cranial nerve projections. Analysis of the CNS in sema3F null mice reveals a crucial role for Sema3F in the rostral forebrain, midbrain, and hippocampus in establishing specific Npn-2 (neuropilin-2)-expressing limbic tracts. Furthermore, we identify Sema3F and Npn-2 as the first guidance cue-receptor pair shown to be essential for controlling the development of amygdaloid circuitry. In addition, we provide genetic evidence in vertebrates for a neuronal requirement of a soluble axon guidance cue in CNS axon guidance. Our data reveal a requirement for neuronal Sema3F in the normal development of the anterior commissure in the ventral forebrain and infrapyramidal tract in the hippocampus. Thus, our results show that Sema3F is the principal ligand for Npn-2-mediated axon guidance events in vivo and is a critical determinant of limbic and peripheral nervous system circuitry.

Amygdala↗
PubMed2003

Mutations in deadly seven/notch1a reveal developmental plasticity in the escape response circuit.

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.

Animals↗
PubMed1992

Regeneration of an interneuronal network in Helisoma: re-establishment of synaptic contacts.

We have identified a network of three interneurons located in the central ring ganglia of Helisoma. Two of these interneurons, designated Left Pedal Dorsal 1 (LPeD1) and Right Pedal Dorsal 1 (RPeD1), are the largest neurons of the pedal ganglia and appear to contain dopamine and serotonin, respectively. A third interneuron, identified as Visceral Dorsal 4 (VD4), is a small FMRFamide immunoreactive cell located on the dorsal surface of the visceral ganglion. Monosynaptic chemical connections exist between all these interneurons. For instance, a reciprocal inhibitory connection exists between LPeD1 and RPeD1, whereas VD4 has inhibitory effects on both LPeD1 and RPeD1. Furthermore, LPeD1, but not RPeD1, has an excitatory connection with VD4. We demonstrate that following axotomy these interneurons not only regenerate their axons but re-establish their appropriate synaptic connections.

Animals↗
PubMed1992

Long-term potentiation and sprouting of mossy fibers produced by brief episodes of hyperactivity.

A brief application of high K+ or excitatory amino acids (i.e. kainic acid) generated repetitive synchronized burst that persisted for the duration of the application, in the CA3 field. Once excitability has been enhanced, further stimulation of various inputs evoked burst instead the typical excitatory postsynaptic potential--inhibitory postsynaptic potential sequence evoked in control conditions. These long-lasting changes in synaptic efficacy involved the activation of glutamate receptors of N-methyl-D-aspartate (NMDA) subtype. A brief period of hyperactivity (i.e. kindling of limbic pathways or administration of kainic acid) also resulted in a more delayed synaptic remodeling, notably of hippocampal mossy fibers (i.e. the axons of granule cells that mostly contact the apical dendrites of CA3 pyramidal neurons). Thus mossy fibers sprouted and made multiple ectopic asymmetrical synapses with spines of both granule cells dendrites and basilar dendrites of CA3 pyramidal cells. Finally, sprouting of mossy fibers was associated with a significant rise in the density of kainic acid binding sites (fmol/mg tissue) in the aberrantly innervated zones: the inner third of molecular layer and the stratum oriens of CA3. Saturation studies revealed that this rise did not significantly affect the affinity (Kd values) but the Bmax. In conclusion, brief seizure episodes produced in the hippocampus remarkably long-lasting changes in synaptic efficacy; synaptic density and the mean density of excitatory amino acid receptors of non-NMDA subtype. The role that such plastic changes may play in the permanence of the epilepsy is finally discussed.

Afferent Pathways↗
PubMed1992

The dentate gyrus as a control point for seizures in the hippocampus and beyond.

Considerable in vitro work has pointed to a resistance of dentate gyrus granule cells for expressing epileptiform paroxysms. However, in vivo work has shown that these neurons, under appropriate conditions, support and sustain seizure discharges. This range of activity of granule cells, along with their location in the middle of a pathway that connects hippocampal regions with high propensities for generating seizures, allows the dentate gyrus to act as a critical regulator of seizures. In the following report we review experiments on a stereotyped, robust paroxysmal discharge, maximal dentate activation (MDA), that occurs in granule cells, and we examine the role of MDA in reinforcing seizures in hippocampal circuits. In addition, work is presented that indicates MDA regulates seizures at sites beyond the hippocampus and its connections. Other studies that examine morphological and functional changes in the local circuits of granule cells and other neurons in the dentate gyrus in different models of epilepsy are discussed. We conclude that the dentate gyrus functions in several modes during seizures, even in the naive brain, and that in chronic epilepsy alterations take place that provide an even greater diversity of functional capabilities. Explicating these heterogeneous conditions will provide important insight into basic mechanisms of seizures and epileptogenesis.

Afferent Pathways↗
PubMed2004

[Roles of semaphorins in neuron network formation].

A secreted semaphorin, Sema3A, is an axon guidance molecule that induces collapse of growth cones and repels axons in vitro. Neuropilin-1 (Nrp-1) is a receptor for Sema3A. To clarify the function of the semaphorin in vivo, we generated Sema3A mutant mice and Nrp-1 mutant mice by targeted disruption of the Sema3A and Nrp-1 genes, respectively. These mutant mouse embryos showed a severe defect in the trajectory and projection of PNS efferent, suggesting that the Nrp-1-mediated Sema3A signals play crucial roles in the directional guidance of nerve fibers and the establishment of PNS networks. The deprivation of Nrp-1-mediated Sema3A signals also induced disorganization of the sympathetic nervous system. In the Nrp-1 and Sema3A mutant mouse embryos, more than half of the TH-positive SG neurons were distributed at ectopic positions. As a whole, the sympathetic trunk was severely disorganized. Sema3 A recombinant proteins inhibited migration of the wild-type (Nrp-1-expressing) but not Nrp-1-deficient SG neurons in culture, suggesting that Nrp-1-mediated Sema3A inhibitory signals are essential in precise migration of SG neurons, as well as directional guidance of axons.

Animals↗
PubMed2004

The role of the hippocampus in the pathophysiology of major depression.

Converging lines of research suggest that the hippocampal complex (HC) may have a role in the pathophysiology of major depressive disorder (MDD). Although postmortem studies show little cellular death in the HC of depressed patients, animal studies suggest that elevated glucocorticoid levels associated with MDD may negatively affect neurogenesis, cause excitotoxic damage or be associated with reduced levels of key neurotrophins in the HC. Antidepressant medications may counter these effects, having been shown to increase HC neurogenesis and levels of brain-derived neurotrophic factor in animal studies. Neuropsychological studies have identified deficits in hippocampus-dependent recollection memory that may not abate with euthymia, and such memory impairment has been the most reliably documented cognitive abnormality in patients with MDD. Finally, data from imaging studies suggest both structural changes in the volume of the HC and functional alterations in frontotemporal and limbic circuits that may be critical for mood regulation. The extent to which such functional and structural changes determine clinical outcome in MDD remains unknown; a related, but also currently unanswered, question is whether the changes in HC function and structure observed in MDD are preventable or modifiable with effective treatment for the depressive illness.

Animals↗
PubMed2005

[Effects of selenium and B-27 supplements on viability and differentiation of neural stem cell in newborn rat].

OBJECTIVE: To assess how trace element selenium and B27 supplements affect the neural stem cell (NSc) differentiation in vitro. METHODS: The development and differentiation of NSc from the newborn rat were observed with primary culture and subculture during treating by sodium-selenite, and selenium-methyl-cysteine (SMC). The immunocytochemistry techniques were used to identify the NSc and mature protein expression with neuron marker beta-tubulin, astrocyte marker GFAP, and oligodendrocyte marker CNPase. The neurosphere morphology and neurite outgrowth were observed. RESULTS: Adding the complete B-27 serum-free supplement, Selenium could promote the neurosphere viability, development and differentiation. Without selenium and B-27, neurosphere could not survive and differentiate. Without B-27 in the medium but there containing selenium, the neurosphere could promote the viability and development into neuron, astrocyte and oligodendrocyte, as compared with the no-containing B-27 and selenium groups, these differentiated cells might have more quantity, more branches and better morphological nerve net. The count of the neuron, astrocyte and oligodendrocyte was 11.2/Hp, 16.1/Hp and 9.3/Hp. CONCLUSIONS: The selenium should be very important for neural stem cells' survival. Selenium could promote the neurosphere cells differentiation and development.

Animals↗
PubMed2006

Translational and developmental perspective on N-methyl-D-aspartate synaptic deficits in schizophrenia.

Schizophrenia has long been approached from a translational perspective; however, new findings from the past decade have radically affected the dominant accounts of this illness. It is now possible to derive a consistent account of one contributing cause of schizophrenia across multiple levels of analysis, from genes to receptors, functional neuroanatomy, cognition, and symptoms. To this end, we summarize the data attributing the disorganization symptoms of schizophrenia to a failure of executive, prefrontal cortical processes. We describe the hypothesis that this failure reflects an impairment in N-methyl-D-aspartate (NMDA) glutamatergic neurotransmission, that is likely to involve both the dysregulated function of NMDA synapses, as well as the physical loss of NMDA synapses, particularly in prefrontal cortex. Dysregulation in NMDA synaptic function can be in turn attributed to polymorphisms in a variety of genes (regulator of G-protein signaling 4, dystrobrevin binding protein I, neuregulin-1, D-amino acid oxidase activator, and others) that have been linked to schizophrenia and are likely to impact NMDA-mediated synaptic neuroplasticity. Although the science of schizophrenia is not yet at a point where any domain or set of findings provides strong constraints across other levels of analysis, the further development of evidence for this chain of causation can provide increasingly strong tests of the NMDA synapse deficit theory.

Carrier Proteins↗
PubMedDate not supplied

Improvement after cerebellar injury achieved by coordination dynamics therapy.

Coordination dynamics therapy of changing intensity was administered at home for nearly 8 years (at the beginning at low intensity) to a patient who had suffered a severe injury of the cerebellum (and of the cerebrum). Motor functions improved markedly during the first year of rather intensive therapy (by 42%), but there was but little improvement in the 5 following years (by 27%). An intensive 3-week coordination dynamics therapy was administered after 4 years of quantified therapy at an up-to-date therapy place under optimal conditions. The motor functions improved strongly (by 29% in 13 days). Therapy under professional conditions was shown to be much more efficient (by the factor of 150 as quantified by low-load coordination dynamics values) than that at home. A comparable patient with a brain (cerebral) injury improved slightly more under optimal conditions (by the factor of 390). In the patient with the injury of the cerebellum, the largest improvement concerned speech and higher mental functions. The strong improvement during the 3-weeks of optimal therapy may have partly been due to the enhanced training of CNS symmetries. It thus seems that not only phase and frequency coordination between neuron firings has to be improved by the therapy, but also symmetries in CNS organization.

Ataxia↗