Introductory remarks

In every day usage to say that something shows plasticity implies that it can be moulded or readily made to assume a new shape. In relation to the nervous system, we commonly imply a further restriction of meaning when using this term ; plasticity in the nervous system means an ordered or patterned alteration of organization - one which makes some sort of sense biologically. We do not mean just any alteration; for instance, a massive and disorganized malfunction associated with extensive injury would not be called plasticity. To qualify for this term an alteration has to show pattern or order, and we would normally imply that the structures or functions under discussion alter in some way to compensate for the deficit. When the plasticity takes the form of learning or memory, the functional alteration resulting from the input experience must also be organized, this time in a functional sense; functional or structural changes that were chaotic would qualify neither for the term plasticity nor the term learning. Plasticity of neural structure is discussed in several papers at this meeting. Horder, Keating, and Mark consider some of the very dramatic alterations that may be induced in the nervous systems of lower vertebrates, while Rakic, Raisman, and Wall describe structural changes in mammals. Some of the work discussed, notably that on amphibians and fishes, as well as the comparable mammalian work of Lund and Schneider which was unfortunately not represented at the meeting, merges at the edges into the sort of changes normally considered embryological. The question how closely mechanisms underlying structural plasticity are related to those underlying, for instance, embryological regulation, remains unanswered. The nature of neither phenomenon is yet understood.

1997 ◽  
Vol 136 (3) ◽  
pp. 679-692 ◽  
Author(s):  
Pico Caroni ◽  
Ludwig Aigner ◽  
Corinna Schneider

Long-term functional plasticity in the nervous system can involve structural changes in terminal arborization and synaptic connections. To determine whether the differential expression of intrinsic neuronal determinants affects structural plasticity, we produced and analyzed transgenic mice overexpressing the cytosolic proteins cortical cytoskeleton–associated protein 23 (CAP-23) and growth-associated protein 43 (GAP-43) in adult neurons. Like GAP-43, CAP-23 was downregulated in mouse motor nerves and neuromuscular junctions during the second postnatal week and reexpressed during regeneration. In transgenic mice, the expression of either protein in adult motoneurons induced spontaneous and greatly potentiated stimulus-induced nerve sprouting at the neuromuscular junction. This sprouting had transgene-specific features, with CAP-23 inducing longer, but less numerous sprouts than GAP-43. Crossing of the transgenic mice led to dramatic potentiation of the sprout-inducing activities of GAP-43 and CAP-23, indicating that these related proteins have complementary and synergistic activities. In addition to ultraterminal sprouting, substantial growth of synaptic structures was induced. Experiments with pre- and postsynaptic toxins revealed that in the presence of GAP-43 or CAP-23, sprouting was stimulated by a mechanism that responds to reduced transmitter release and may be independent of postsynaptic activation. These results demonstrate the importance of intrinsic determinants in structural plasticity and provide an experimental approach to study its role in nervous system function.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ben R. Cairns ◽  
Benjamin Jevans ◽  
Atchariya Chanpong ◽  
Dale Moulding ◽  
Conor J. McCann

AbstractNeuronal nitric oxide synthase (nNOS) neurons play a fundamental role in inhibitory neurotransmission, within the enteric nervous system (ENS), and in the establishment of gut motility patterns. Clinically, loss or disruption of nNOS neurons has been shown in a range of enteric neuropathies. However, the effects of nNOS loss on the composition and structure of the ENS remain poorly understood. The aim of this study was to assess the structural and transcriptional consequences of loss of nNOS neurons within the murine ENS. Expression analysis demonstrated compensatory transcriptional upregulation of pan neuronal and inhibitory neuronal subtype targets within the Nos1−/− colon, compared to control C57BL/6J mice. Conventional confocal imaging; combined with novel machine learning approaches, and automated computational analysis, revealed increased interconnectivity within the Nos1−/− ENS, compared to age-matched control mice, with increases in network density, neural projections and neuronal branching. These findings provide the first direct evidence of structural and molecular remodelling of the ENS, upon loss of nNOS signalling. Further, we demonstrate the utility of machine learning approaches, and automated computational image analysis, in revealing previously undetected; yet potentially clinically relevant, changes in ENS structure which could provide improved understanding of pathological mechanisms across a host of enteric neuropathies.


1983 ◽  
Vol 96 (5) ◽  
pp. 1337-1354 ◽  
Author(s):  
P De Camilli ◽  
R Cameron ◽  
P Greengard

Synapsin I (formerly referred to as protein I) is the collective name for two almost identical phosphoproteins, synapsin Ia and synapsin Ib (protein Ia and protein Ib), present in the nervous system. Synapsin I has previously been shown by immunoperoxidase studies (De Camilli, P., T. Ueda, F. E. Bloom, E. Battenberg, and P. Greengard, 1979, Proc. Natl. Acad. Sci. USA, 76:5977-5981; Bloom, F. E., T. Ueda, E. Battenberg, and P. Greengard, 1979, Proc. Natl. Acad. Sci. USA 76:5982-5986) to be a neuron-specific protein, present in both the central and peripheral nervous systems and concentrated in the synaptic region of nerve cells. In those preliminary studies, the occurrence of synapsin I could be demonstrated in only a portion of synapses. We have now carried out a detailed examination of the distribution of synapsin I immunoreactivity in the central and peripheral nervous systems. In this study we have attempted to maximize the level of resolution of immunohistochemical light microscopy images in order to estimate the proportion of immunoreactive synapses and to establish their precise distribution. Optimal results were obtained by the use of immunofluorescence in semithin sections (approximately 1 micron) prepared from Epon-embedded nonosmicated tissues after the Epon had been removed. Our results confirm the previous observations on the specific localization of synapsin I in nerve cells and synapses. In addition, the results strongly suggest that, with a few possible exceptions involving highly specialized neurons, all synapses contain synapsin I. Finally, immunocytochemical experiments indicate that synapsin I appearance in the various regions of the developing nervous system correlates topographically and temporally with the appearance of synapses. In two accompanying papers (De Camilli, P., S. M. Harris, Jr., W. B. Huttner, and P. Greengard, and Huttner, W. B., W. Schiebler, P. Greengard, and P. De Camilli, 1983, J. Cell Biol. 96:1355-1373 and 1374-1388, respectively), evidence is presented that synapsin I is specifically associated with synaptic vesicles in nerve endings.


2002 ◽  
Vol 13 (2) ◽  
pp. 698-710 ◽  
Author(s):  
Sylvie Ozon ◽  
Antoine Guichet ◽  
Olivier Gavet ◽  
Siegfried Roth ◽  
André Sobel

Stathmin is a ubiquitous regulatory phosphoprotein, the generic element of a family of neural phosphoproteins in vertebrates that possess the capacity to bind tubulin and interfere with microtubule dynamics. Although stathmin and the other proteins of the family have been associated with numerous cell regulations, their biological roles remain elusive, as in particular inactivation of the stathmin gene in the mouse resulted in no clear deleterious phenotype. We identified stathmin phosphoproteins inDrosophila, encoded by a unique gene sharing the intron/exon structure of the vertebrate stathmin andstathmin family genes. They interfere with microtubule assembly in vitro, and in vivo when expressed in HeLa cells. Drosophila stathmin expression is regulated during embryogenesis: it is high in the migrating germ cells and in the central and peripheral nervous systems, a pattern resembling that of mammalian stathmin. Furthermore, RNA interference inactivation ofDrosophila stathmin expression resulted in germ cell migration arrest at stage 14. It also induced important anomalies in nervous system development, such as loss of commissures and longitudinal connectives in the ventral cord, or abnormal chordotonal neuron organization. In conclusion, a single Drosophilagene encodes phosphoproteins homologous to the entire vertebrate stathmin family. We demonstrate for the first time their direct involvement in major biological processes such as development of the reproductive and nervous systems.


2020 ◽  
Author(s):  
Ivar S. Stein ◽  
Deborah K. Park ◽  
Nicole Claiborne ◽  
Karen Zito

SUMMARYExperience-dependent refinement of neuronal connections is critically important for brain development and learning. Here we show that ion flow-independent NMDAR signaling is required for the long-term dendritic spine growth that is a vital component of brain circuit plasticity. We found that inhibition of p38 MAPK, shown to be downstream of non-ionotropic NMDAR signaling in LTD and spine shrinkage, blocked LTP-induced spine growth but not LTP. We hypothesized that non-ionotropic NMDAR signaling drives the cytoskeletal changes that support bidirectional spine structural plasticity. Indeed, we found that key signaling components downstream of non-ionotropic NMDAR function in LTD-induced spine shrinkage also are necessary for LTP-induced spine growth. Furthermore, NMDAR conformational signaling with coincident Ca2+ influx is sufficient to drive CaMKII-dependent long-term spine growth, even when Ca2+ is artificially driven through voltage-gated Ca2+ channels. Our results support a model in which non-ionotropic NMDAR signaling gates the bidirectional spine structural changes vital for brain plasticity.


1992 ◽  
Vol 9 (3-4) ◽  
pp. 335-343 ◽  
Author(s):  
R. H. Douglas ◽  
H.-J. Wagner ◽  
M. Zaunreiter ◽  
U. D. Behrens ◽  
M. B. A. Djamgoz

AbstractThe retinae of lower vertebrates undergo a number of structural changes during light adaptation, including the photomechanical contraction of cone myoids and the dispersion of melanin granules within the epithelial pigment. Since the application of dopamine to dark-adapted retinae is known to produce morphological changes that are characteristic of light adaptation, dopamine is accepted as a causal mechanism for such retinomotor movements. However, we report here that in the teleost fish, Aequidens pulcher, the intraocular injection of 6-hydroxydopamine (6-OHDA), a substance known to destroy dopaminergic retinal cells, has no effect on the triggering of light-adaptive retinomotor movements of the cones and epithelial pigment and only slightly depresses the final level of light adaptation reached. Furthermore, the retina continues to show circadian retinomotor changes even after 48 h in continual darkness that are similar in both control and 6-OHDA injected fish. Biochemical assay and microscopic examination showed that 6-OHDA had destroyed dopaminergic retinal cells. We conclude, therefore, that although a dopaminergic mechanism is probably involved in the control of light-induced retinomotor movements, it cannot be the only control mechanism, nor can it be the cause of circadian retinomotor migrations. Interestingly, 6-OHDA injected eyes never reached full retinomotor dark adaptation, suggesting that dopamine has a role to play in the retina's response to darkness.


2018 ◽  
Vol 1 ◽  
Author(s):  
Sebastian Markett ◽  
Christian Montag ◽  
Martin Reuter

AbstractPersonality and individual differences originate from the brain. Despite major advances in the affective and cognitive neurosciences, however, it is still not well understood how personality and single personality traits are represented within the brain. Most research on brain-personality correlates has focused either on morphological aspects of the brain such as increases or decreases in local gray matter volume, or has investigated how personality traits can account for individual differences in activation differences in various tasks. Here, we propose that personality neuroscience can be advanced by adding a network perspective on brain structure and function, an endeavor that we label personality network neuroscience.With the rise of resting-state functional magnetic resonance imaging (MRI), the establishment of connectomics as a theoretical framework for structural and functional connectivity modeling, and recent advancements in the application of mathematical graph theory to brain connectivity data, several new tools and techniques are readily available to be applied in personality neuroscience. The present contribution introduces these concepts, reviews recent progress in their application to the study of individual differences, and explores their potential to advance our understanding of the neural implementation of personality.Trait theorists have long argued that personality traits are biophysical entities that are not mere abstractions of and metaphors for human behavior. Traits are thought to actually exist in the brain, presumably in the form of conceptual nervous systems. A conceptual nervous system refers to the attempt to describe parts of the central nervous system in functional terms with relevance to psychology and behavior. We contend that personality network neuroscience can characterize these conceptual nervous systems on a functional and anatomical level and has the potential do link dispositional neural correlates to actual behavior.


Author(s):  
Dale Purves

Although understanding neural functions has progressed at a remarkable pace in recent decades, a fundamental question remains: How does the nervous system relate the objective world to the subjective domain of perception? Everyday experience implies that the neural connections on which we and other animals depend link physical parameters in the environment with useful responses. But that interpretation won't work: biological sensory systems cannot measure the physical world. Whereas something is linking sensory inputs to useful responses, it is not the physical world that instruments measure. How, then, have we animals met this challenge, and what is it that we end up perceiving? The purpose of this chapter is to suggest how nervous systems have evolved to deal with the inability to convey the objective properties of the real world.


Author(s):  
Dale Purves

Definitions of the term “animals” in dictionaries and textbooks are surprisingly vague. The characteristics usually mentioned are eukaryotic, multicellular, heterotrophic, sexually reproducing, and capable of rapid and independent movement. But some or all of these properties are characteristic of many organisms in the other kingdoms of life on Earth. In fact, the major distinguishing feature of animals in most cases is the presence of a nervous system. But if nervous systems are indeed one of the main attributes that distinguish organisms in the animal kingdom, what exactly are nervous systems and what advantages do they bring? Without at least some provisional answers, seeking the operating principle of neural systems would be futile.


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