Neuronal plasticity in the adult invertebrate nervous system

This essay provides a brief overview of neuronal plasticity in adult invertebrate nervous systems. Our discussion focuses on the factors which influence sprouting by adult neurons, i.e., (1) the nature of the neuron itself, (2) axon integrity, (3) the presence of targets, (4) diffusible factors, and (5) ageing. Evidence that the neurites of some adult neurons exhibit a dynamic equilibrium of expansion and retraction is presented, a topic which prompted us to speculate on the significance of such plasticity in altered behavioral states. We conclude with some suggestions as to specific questions that need to be addressed by future studies in this challenging area.     

Structural bases of the plasticity of the nervous system

The present state of morphological study of variability in the nervous elements under conditions of adaptive change under the influence of afferent effects, age changes during different periods of ontogenesis, under conditions of de- and regeneration of synapses have been considered. A question on correlation between structure and the function of synapses during the change has been analysed. The tasks of subsequent study of this problem have been outlined.     

Calcium channels and channelopathies of the central nervous system

Several inherited human neurological disorders can be caused by mutations in genes encoding Ca²⁺ channel subunits. This review deals with known human and mouse calcium channelopathies of the central nervous system (CNS). The human diseases comprise: 1) a recessive retinal disorder, X-linked congenital stationary night blindness, associated with mutations in the CACNA1F gene, encoding α₁1.4 subunits of L-type channels; and 2) a group of rare allelic autosomal dominant human neurological disorders including familial hemiplegic migraine, episodic ataxia type 2, and spinocerebellar ataxia type 6, all associated with mutations in the CACNA1A gene, encoding α₁2.1 subunits of P/Q-type calcium channels. Mutations at the mouse orthologue of the CACNA1A gene cause a group of recessive neurological disorders, including the tottering, leaner, and rocker phenotypes with ataxia and absence epilepsy, and the rolling Nagoya phenotype with ataxia without seizures. Two other spontaneous mouse mutants with ataxia and absence epilepsy, lethargic and stargazer, have mutations in genes encoding a calcium channel auxiliary β subunit and a putative calcium channel auxiliary γ subunit. For each channelopathy, the review describes disease phenotype, channel genotype, and known functional consequences of the pathological mutations; in some cases, it also describes working hypothesis and/or speculations addressing the challenging question of how the alterations in channel function lead to selective cellular dysfunction and disease.     

Calcium channelopathies in the central nervous system.

The recent discovery that familial hemiplegic migraine, episodic ataxia type 2, and spinocerebellar ataxia type 6 are allelic disorders caused by different mutations in CACNA1A, a calcium-channel-encoding gene, adds to a growing list of channelopathies causing paroxysmal neurologic disturbance and progressive neurodegeneration. Calcium channelopathies in the central nervous system provide a model to study the important roles that calcium channels play in neuronal function.     

Enriched environments, experience-dependent plasticity and disorders of the nervous system

Behavioural, cellular and molecular studies have revealed significant effects of enriched environments on rodents and other species, and provided new insights into mechanisms of experience-dependent plasticity, including adult neurogenesis and synaptic plasticity. The demonstration that the onset and progression of Huntington's disease in transgenic mice is delayed by environmental enrichment has emphasized the importance of understanding both genetic and environmental factors in nervous system disorders, including those with Mendelian inheritance patterns. A range of rodent models of other brain disorders, including Alzheimer's disease and Parkinson's disease, fragile X and Down syndrome, as well as various forms of brain injury, have now been compared under enriched and standard housing conditions. Here, we review these findings on the environmental modulators of pathogenesis and gene-environment interactions in CNS disorders, and discuss their therapeutic implications.     

Polysialic acid in the plasticity of the developing and adult vertebrate nervous system

Polysialic acid (PSA) is a cell-surface glycan with an enormous hydrated volume that serves to modulate the distance between cells. This regulation has direct effects on several cellular mechanisms that underlie the formation of the vertebrate nervous system, most conspicuously in the migration and differentiation of progenitor cells and the growth and targeting of axons. PSA is also involved in a number of plasticity-related responses in the adult CNS, including changes in circadian and hormonal patterns, adaptations to pain and stress, and aspects of learning and memory. The ability of PSA to increase the plasticity of neural cells is being exploited to improve the repair of adult CNS tissue.     

Calcium stores and synaptic plasticity

Chemical transmission at central synapses is known to be highly plastic; the strength of synaptic connections can be modified bi-directionally as a result of activity at individual synapses. Long-term changes in synaptic efficacy, both increases and decreases, are thought to be involved in the development of the nervous system, and in ongoing changes in response to external cues such as during learning and addiction. Other, shorter lasting changes in synaptic transmission are also likely to be important in normal functioning of the CNS. Calcium mobilisation is an important step in multiple forms of plasticity and, although entry into neurones from the extracellular space is often the initial trigger for plasticity changes, release of calcium from intracellular stores also has an important part to play in a variety of forms of synaptic plasticity.     

Wnt signaling regulates experience-dependent synaptic plasticity in the adult nervous system

Comment on: Jensen M, et al. Cell 2012; 149:173-87.     

Wnt signaling regulates experience-dependent synaptic plasticity in the adult nervous system

Comment on: Jensen M, et al. Cell 2012; 149:173-87.     

钙依赖性突触的可塑性

突触前和突触后细胞内钙离子（[Ca^2 ]i)在短时程和长时程突触的可塑性中,发挥着重要的住处传递作用。兴奋后残留[Ca^2 ]i,可以激发短时程突触增强。突触前[Ca^2 ]i可以影响被抑制的突触前膜囊泡的更新,并准确编码突前和突触后信息,产生截然相反的长时程突触修（ＬＴＰ或ＬＴＤ）。