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PubMed1995

Impairment of motor coordination, Purkinje cell synapse formation, and cerebellar long-term depression in GluR delta 2 mutant mice.

Of the six glutamate receptor (GluR) channel subunit families identified by molecular cloning, five have been shown to constitute either the AMPA, kainate, or NMDA receptor channel, whereas the function of the delta subunit family remains unknown. The selective localization of the delta 2 subunit of the GluR delta subfamily in cerebellar Purkinje cells prompted us to examine its possible physiological roles by the gene targeting technique. Analyses of the GluR delta 2 mutant mice reveal that the delta 2 subunit plays important roles in motor coordination, formation of parallel fiber-Purkinje cell synapses and climbing fiber-Purkinje cell synapses, and long-term depression of parallel fiber-Purkinje cell synaptic transmission. These results suggest a close relationship between synaptic plasticity and synapse formation in the cerebellum.

Animals↗
PubMed1991

Growth cone transduction: Go and GAP-43.

The neuronal growth cone plays a crucial role in forming the complex brain architecture achieved during development, and similar nerve terminal mechanisms may operate to modify synaptic structure during adulthood. The growth cone leads the elongating axon towards appropriate synaptic targets by altering motility in response to a variety of extracellular signals. Independently of extrinsic clues, neurons manifest intrinsic control of their growth and form (Banker and Cowan, 1979). Hence, there must be intracellular proteins which control nerve cell shape, so-called 'plasticity' or 'growth' genes. GAP-43 may be such a molecule (Skene and Willard, 1981; Benowitz and Lewis, 1983). For example, GAP-43 is localized to the growth cone membrane (Meiri et al. 1986; Skene et al. 1986) and can enhance filopodial formation even in non-neuronal cells (Zuber et al. 1989a). It includes a small region at the amino terminus for membrane association and perhaps growth cone targeting (Zuber et al. 1989b, Liu et al. 1991). We have found that Go, a member of the G protein family that links receptors and second messengers, is the major non-cytoskeletal protein in the growth cone membrane (Strittmatter et al. 1990). Double staining immunohistochemistry for GAP-43 and Go shows that the distributions of the two proteins are quite similar. Purified GAP-43 regulates the activity of purified Go (Strittmatter et al. 1990), a surprising observation since GAP-43 is an intracellular protein. We have compared the mechanism of GAP-43 activation of Go with that of G protein-linked receptors.2+ interactions between Go and GAP-43 suggest that Go plays a pivotal role in growth cone function, coordinating the effects of both extracellular signals and intracellular growth proteins.

Animals↗
PubMed2001

Plasticity of convergence-dependent variations of cyclovergence with vertical gaze.

Binocular alignment of foveal images is facilitated by cross-couplings of vergence eye movements with distance and direction of gaze. These couplings reduce horizontal, vertical and cyclodisparities at the fovea without using feedback from retinal image disparity. Horizontal vergence is coupled with accommodation. Vertical vergence that aligns tertiary targets in asymmetric convergence is thought to be coupled with convergence and horizontal gaze. Cyclovergence aligns the horizontal retinal meridians during gaze elevation in symmetrical convergence and is coupled with convergence and vertical gaze. The latter vergence-dependent changes of cyclovergence have been described in terms of the orientation of Listing's plane and have been referred to as the binocular extension of Listing's law. Can these couplings be modified? Plasticity has been demonstrated previously for two of the three dimensions of vergence (horizontal and vertical). The current study demonstrates that convergence-dependent changes of the orientation of Listing's plane can be adapted to either exaggerate or to reduce the cyclovergence that normally facilitates alignment of the horizontal meridians of the retinas with one another during gaze elevation in symmetrical convergence. The adaptability of cyclovergence demonstrates a neural mechanism that, in conjunction with the passive forces determined by biomechanical properties of the orbit, could play an active role in implementing Listing's extended law and provide a means for calibrating binocular eye alignment in three dimensions.

Accommodation, Ocular↗
PubMed1994

Laminar comparison of somatosensory cortical plasticity.

During tactile learning there is a transformation in the way the primary somatosensory cortex integrates, represents, and distributes information from the skin. To define this transformation, the site of earliest modification has been identified in rat somatosensory cortex after a change in sensory experience. Afferent activity was manipulated by clipping all except two whiskers on one side of the snout ("whisker pairing"), and the receptive fields of neurons at different cortical depths were mapped 24 hours later. Neurons in layer IV, the target of the primary thalamic pathway, were unaltered, whereas neurons located above and below layer IV showed significant changes. These changes were similar to those that occur in layer IV after longer periods of whisker pairing. The findings support the hypothesis that the layers of cortex contribute differently to plasticity. Neurons in the supragranular and infragranular layers respond rapidly to changes in sensory experience and may contribute to subsequent modification in layer IV.

Action Potentials↗
PubMed1998

Target neuron specification of short-term synaptic facilitation and depression in the cricket CNS.

We investigated the role of retrograde signals in the regulation of short-term synaptic depression and facilitation by characterizing the form of plasticity expressed at novel synapses on four giant interneurons in the cricket cercal sensory system. We induced the formation of novel synapses by transplanting a mesothoracic leg and its associated sensory neurons to the cricket terminal abdominal segment. Axons of ectopic leg sensory neurons regenerated and innervated the host terminal abdominal ganglion forming monosynaptic connections with the medial giant interneuron (MGI), lateral giant interneuron (LGI), and interneurons 7-1a and 9-2a. The plasticity expressed by these synapses was characterized by stimulating a sensory neuron with pairs of stimuli at various frequencies or with trains of 10 stimuli delivered at 100 Hz and measuring the change in excitatory postsynaptic potential amplitude recorded in the postsynaptic neuron. Novel synapses of a leg tactile hair on 7-1a depressed, as did control synapses of cercal sensory neurons on this interneuron. Novel synapses of leg campaniform sensilla (CS) sensory neurons on MGI, like MGI's control synapses, always facilitated. The form of plasticity expressed by novel synapses is thus consistent with that observed at control synapses. Leg CS synapses with 9-2a also facilitated; however, the plasticity expressed by these sensory neurons is dependent on the identity of the postsynaptic cell since the synapses these same sensory neurons formed with LGI always depressed. We conclude that the form of plasticity expressed at these synaptic connections is determined retrogradely by the postsynaptic cell.

Abdomen↗
PubMed1998

[Structure and function of neural plasticity-related gene products].

We have isolated novel immediate early genes (IEGs) from the hippocampus by differential cloning techniques. These mRNAs are induced by synaptic activity and translated into proteins that may affect neural function. We have analyzed a variety of "effector" immediate early genes. These mRNAs encode: 1) cytoplasmic proteins, such as cyclooxygenase-2, a small G protein, Rheb, and a cytoskeleton-associated protein, Arc; 2) membrane-bound proteins, such as the cell adhesion protein Arcadlin, and a neurite-outgrowth protein, Neuritin; and 3) a secreted protein, Narp. We hypothesize that physiological stimulation induces "effector" proteins that might strengthen synaptic connections of activated synapses. In contrast, pathological conditions such as epilepsy or drug addiction may accelerate overproduction of these gene products, which cause abnormal synapse formation. Gene targeting and in vivo gene transfer techniques are required to prove this hypothesis.

Animals↗
PubMed1994

Postsynaptic regulation of the development and long-term plasticity of Aplysia sensorimotor synapses in cell culture.

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, their 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 transmitter serotonin (5-HT) causes long-term facilitation of in vitro sensorimotor synapses due in part to growth of new presynaptic varicosities. But 5-HT applied to sensory neurons alone in culture 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 synapses 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 Hebbian mechanism in classical conditioning in Aplysia. They also indicate that Hebbian LTP is a phylogenetically ancient form of synaptic plasticity.

Animals↗
PubMed2006

Variations in clinical audit collection: a survey of plastic surgery units across the British Isles.

INTRODUCTION: Clinical audit is a requirement of good medical and surgical practice and is central to the UK Government's plans to modernise the NHS. MATERIALS AND METHODS: A survey was conducted to assess clinical audit data collection and collation within plastic surgery departments across the UK. The survey identified a variety of different data collection and collation methods, with extensive differences between plastic surgery departments. Those responsible for data collection and its funding were also identified by the survey. RESULTS: Results were obtained from 45 plastic surgery departments. Of the 45 departments surveyed, 12 collect data prospectively, whereas 26 units collect data retrospectively. The remaining departments collect data using a combination of methods. Of the units surveyed, 28 collect data on paper-based systems, with only 13 units using electronic applications. The personnel responsible for data collection were identified as being junior doctors. Departments collecting data prospectively do so from a greater number of sources than those collecting data retrospectively. CONCLUSIONS: This survey has focused on plastic surgery. The authors believe that similar results would be obtained from a survey of other surgical specialties. A huge variation in all parameters relating to the collection and collation of clinical audit data is seen. There are few standards within this specialty for data collection. Much work must be done in order to reach targets set by the UK Government.

Data Collection↗
PubMed2005

Site-specific phosphorylation of SCG10 in neuronal plasticity: role of Ser73 phosphorylation by N-methyl D-aspartic acid receptor activation in rat hippocampus.

Accumulated evidence suggests that actin and microtubule regulating proteins contribute to neuronal structural dynamics, which subsequently affect neuronal plasticity. SCG10 is a neuronal-specific stathmin protein with microtubule destabilizing activity that is affected by multiple phosphorylation, at least in vitro. SCG10 has four major phosphorylation sites: Ser50 and Ser97 targeted by protein kinase A (PKA), and Ser62 and Ser73 targeted by mitogen-activated protein kinase (MAPK). To explore the potential roles of site-specific phosphorylation in physiological models, we developed phosphorylation site-specific antibodies and examined the SCG10 status in primary cultured hippocampal neurons and tissues. Although SCG10 is concentrated in growth cones and the Golgi apparatus in primary cultured neurons, the phosphorylated form was also detected in both regions, suggesting that MT dynamics within the growth cone may be regulated by protein phosphorylation. In the adult hippocampus, an intense stimulus such as kainate treatment induced a rapid phosphorylation of Ser73 within 15 min that was sustained for at least 60 min. This response was mediated through the N-methyl D-aspartic acid (NMDA) receptor and was ablated by the antagonist MK-801. The MAPK enzyme Erk2 was simultaneously activated along a similar time course to SCG10, suggesting that Erk2 may directly phosphorylate Ser73. These results demonstrate that changes in the phosphorylation status of SCG10 in vivo, dependent upon neural activity and/or plasticity, could affect the microtubule dynamics in neuronal dendrites.

Amino Acid Sequence↗
PubMed1981

Cytotoxicity of human peripheral blood monocytes against Trichomonas vaginalis.

Human peripheral blood monocytes were purified by adherence on microexudate-coated plastic and detached by exposure to 1 mM ethylenediamine tetracetic acid. Lysis of Trichomonas vaginalis was measured as release of 3H-thymidine from prelabelled protozoa after 48 hr of incubation. Human blood monocytes had appreciable levels of spontaneous cytotoxicity against Trichomonas vaginalis at effector-to-target cell ratios ranging from 3:1 to 25:1. Cytotoxicity was expressed with fetal bovine serum and human AB serum. Unseparated mononuclear cells, containing 10-25% monocytes as assessed by staining with non-specific esterase, were significantly cytotoxic against Trichomonas vaginalis but cytolysis levels were lower than those of purified monocytes. Lymphoid cells depleted of adherent cells by repeated incubations on plastic (less than 2% esterase-positive cells) had little cytotoxicity against these protozoa. In vitro exposure to silica natural 40-75% inhibition of the cytotoxic capacity of monocytic preparations. The natural cytotoxic capacity of human monocytes against Trichomonas vaginalis could represent one line of resistance against these protozoa.

Adult↗
PubMed1995

Differential expression and distinct DNA-binding specificity of ME1a and ME2 suggest a unique role during differentiation and neuronal plasticity.

Class A basic-helix-loop-helix (bHLH) proteins have been referred to as ubiquitous and are believed to have redundant functions. They are involved in the control of several developmental pathways, such as neurogenesis and myogenesis. To rationalize the existence of multiple class A bHLH proteins, we evaluated the differences and similarities between ME1a and ME2, two class A bHLH proteins, highly expressed in differentiating neuronal cells. In situ hybridization analyses reveal that ME1a and ME2 are characterized by distinguishable patterns of expression in areas of the adult mouse brain where neuronal plasticity occurs. Also, DNA-binding assays show that both proteins bind to E-boxes as homodimers and heterodimers, and show differences in their DNA-binding specificities, which suggest selective interactions with different binding sites of target genes. In addition, in vitro DNA-binding assays demonstrate that Id2 forms heterodimers with ME1a and ME2. As a result of these interactions, their DNA-binding activity is abolished. Furthermore, overexpression of Id2 in neuronal cells suppresses ME1a and ME2 transcriptional activity. Based on our data, we hypothesize that ME1a and ME2 may activate gene expression of different target genes and therefore are likely to be differently involved during neurogenesis.

Animals↗
PubMed2003

Localizing synaptic mRNAs at the neuromuscular junction: it takes more than transcription.

The neuromuscular junction has been used for several decades as an excellent model system to examine the cellular and molecular events involved in the formation and maintenance of a differentiated chemical synapse. In this context, several laboratories have focused their efforts over the last 15 years on the important contribution of transcriptional mechanisms to the regulation of the development and plasticity of the postsynaptic apparatus in muscle fibers. Converging lines of evidence now indicate that post-transcriptional events, operating at the level of mRNA stability and targeting, are likely to also play key roles at the neuromuscular junction. Here, we present the recent findings highlighting the role of these additional molecular events and extend our review to include data showing that post-transcriptional events are also important in the control of the expression of genes encoding synaptic proteins in muscle cells placed under different conditions. Finally, we discuss the possibility that mis-regulation of post-transcriptional events can occur in certain neuromuscular diseases and cause abnormalities of the neuromuscular junction.

Animals↗
PubMed2002

Neurotrophins and their receptors in the primary olfactory neuraxis.

The primary olfactory pathway is an elegant and simple system in which to study neurogenesis and neuronal plasticity because of the simple fact that olfactory receptor neurons (ORNs) are continually generated throughout the adult lifetimes of vertebrates. Thus, neuronal birth, differentiation, survival, axon pathfinding, target recognition, synapse formation, and cell death are developmental events that can be examined in the mature olfactory epithelium (OE). Neurotrophins (nerve growth factor, brain-derived neurotrophic factor, and neurotrophin 3, and 4/5) are a family of bioactive peptides that exert their effects by interacting with high- and low-affinity receptors on the surfaces of responsive cells, and have been implicated in several stages of neuronal development throughout the central and peripheral nervous system (CNS and PNS). There has been significant interest within the olfactory community as to how these multifunctional peptides might regulate the cycle of degeneration and regeneration of olfactory receptor neurons. The focus of this review is to highlight what is known about the actions of neurotrophins in the primary olfactory pathway, and to pinpoint future directions that will enable us to further understand their role in olfactory receptor neuron development and turnover.

Animals↗
PubMed2000

Neurotrophic effects of central nicotinic receptor activation.

A growing number of data have shown that compounds interacting with neuronal nicotinic acetylcholine receptors (nAChRs) have, both in vivo and in vitro, the potential to be neuroprotective and that treatment with nAChR agonists elicit long-lasting improvement of cognitive performance in a variety of behavioural tests in rats, monkeys and humans. Epidemiological and clinical studies suggested also a potential neuroprotective/trophic role of (-)-nicotine in neurodegenerative disease, such as Alzheimer's disease and Parkinson's disease. This neuroprotective/trophic role of nAChR activation has been mainly mediated by alpha7 and alpha4beta2 nAChR subtypes, as evidenced using selective nAChR antagonists, and by potent nAChR agonists recently found displaying efficacy and/or larger selective affinities than (-)-nicotine for neuronal nAChR subtypes. A neurotrophic factor gene regulation by nAChR signalling has been taken into consideration as a possible mechanism involved in neuroprotective/trophic effects of nAChR activation and has given evidence that the fibroblast growth factor (FGF-2) gene is a target for nAChR signalling. These findings suggested that FGF-2 could be involved, in view of its neurotrophic functions, in nAChR mechanisms mediating neuronal survival, trophism and plasticity.

Animals↗
PubMed1985

Extensive target cell loss during development results in mossy fibers in the regio superior (CA1) of the rat hippocampal formation.

The axons of dentate granule cells (mossy fibers) have been reported to appear in the regio superior (CA1) of the rat hippocampal formation following destruction of the pyramidal cells in the regio inferior (CA3). We undertook the present experiments to confirm this finding and to determine the requirements for this dramatic neuronal rearrangement. We found that extensive (greater than 80%) loss of CA3 cells, as well as the presence of surviving CA1 neurons within a narrow period of development (postnatal days 3-5) is necessary, however apparently not sufficient, for the appearance of CA1 mossy fibers. That the absence of normal target cells during a restricted period of mossy fiber development will lead to their association with novel targets suggests that much of the specificity of this developing connection depends on the presence of normal targets during a critical period.

Animals↗
PubMed1991

Immobilization techniques and dosimetric aspects for pituitary tumors.

Twelve percent of all intracranial tumors arise in the pituitary fossa. The management of pituitary tumors is a complex process that may combine several treatment modalities including radiation therapy. Minimizing patient movement during the course of radiation therapy treatment is imperative to ensure both the delivery of the prescribed dose to the small target volume and to minimize the radiation dose to critical structures. Several alternative types of immobilization devices are being used for this purpose; these include biteblocks, thermal plastics, and polyurethane molds (Alpha Cradle). The advantages and disadvantages of each of these devices are reviewed and the fabrication process of the pituitary immobilization mold that we are currently using is described. Dosimetric aspects of the treatments using these devices is addressed.

Humans↗
PubMed1998

Reutilization of trigeminal motoneurons during amphibian metamorphosis.

Indirect evidence suggests that trigeminal motoneurons (Vmns) in Rana pipiens innervate distinct myofiber populations in tadpoles and adult frogs. Redeployment occurs when the larval myofibers die and are replaced during metamorphosis. To directly test this hypothesis, DiI was injected into the larval muscle and Fast Blue into the replacement myofiber population. Over 95% of the Vmns contained both tracers, providing support for the innervation of sequential targets by the same motoneurons.

Animals↗
PubMed2003

Interactions of norepinephrine and galanin in the central amygdala and lateral bed nucleus of the stria terminalis modulate the behavioral response to acute stress.

Many aspects of drug abuse and addiction share neurobiological substrates with the modulatory processes underlying the response and adaptation to acute stress. In particular, the ascending noradrenergic system has been implicated in facilitating the response to stress, and in stress-induced reinstatement of drug seeking behavior. Thus, to better understand the link between stress and addictive behaviors, it would be informative to understand better the modulatory function of the ascending noradrenergic system, and its interaction with other neurotransmitters with which it is closely associated or co-localized, such as the neuropeptide galanin. In this paper, we review a series of studies investigating the functional interactions of norepinephrine and galanin in modulating the behavioral response to acute stress in two components of the extended amygdala, the central nucleus of the amygdala and the lateral bed nucleus of the stria terminalis. We showed that norepinephrine facilitates behavioral reactivity to stress on the elevated plus-maze and social interaction tests. However, when stress-induced activation of the noradrenergic system was enhanced by blocking inhibitory adrenergic autoreceptors, galanin release was recruited in the central amygdala, acting to attenuate the behavioral response to stress. By contrast, stress-induced galanin release in the lateral bed nucleus appeared to be independent of enhanced noradrenergic activation, and unlike the central amygdala, both galanin and norepinephrine facilitated behavioral stress reactivity in the bed nucleus. The different modes of interaction and differential region- and response-specificity of galanin and norepinephrine suggest that a complex neural circuit interconnecting these two regions is involved in the modulatory effects of norepinephrine and galanin on the behavioral response to stress. Such complexity may allow for flexibility and plasticity in stress adaptation, and may also contribute to behavioral changes induced by chronic drug administration. Thus, the interaction of galanin and norepinephrine may be a viable target for the future development of novel therapeutic strategies for treating behavioral disorders related to stress or drug abuse.

Acute Disease↗