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PubMed1997

Chronic haloperidol treatment differentially affects the expression of synaptic and neuronal plasticity-associated genes.

Synaptophysin is a protein used as a marker of presynaptic terminals. We previously showed that, in dorsolateral striatum of the rat, 2 weeks' haloperidol treatment up-regulated synaptophysin mRNA. We have now investigated the effects of 16 weeks' treatment with haloperidol on synaptophysin expression in dorsolateral striatum, frontoparietal cortex and hippocampus, in order to see if the implied haloperidol-induced synaptic plasticity persists. For comparison, in both the 2- and 16-week treatment groups we determined the mRNA abundance of the neuronal plasticity-associated gene GAP-43, and the housekeeping gene cyclophilin. Sixteen weeks' haloperidol administration increased synaptophysin mRNA in striatum and frontoparietal cortex but not in hippocampus. The increase was demonstrable both regionally and per neuron. A similar trend was seen for synaptophysin protein using immunoautoradiography-GAP-43 mRNA was elevated in frontoparietal cortex by 2 weeks' haloperidol but was not significantly changed in any area in the 16-week treatment group. Cyclophilin mRNA, a marker of overall gene expression, was unaffected by haloperidol. The persistent increase in synaptophysin expression supports the evidence that chronic antipsychotic drug treatment induces synaptic reorganisation in some striatal and cortical neuron populations, whereas the GAP-43 mRNA data suggest that haloperidol does not produce a sustained alteration of neuronal plasticity. Further study of plasticity-associated gene expression may be valuable in clarifying the long-term neuronal and synaptic changes produced by antipsychotics, and how these are related to the neurochemical effects of the drugs.

Amino Acid Isomerases↗
PubMed1986

Ganglioside enhancement of neuronal differentiation, plasticity, and repair.

Gangliosides are carbohydrate-rich complex lipids of large size and great complexity which are found in cell membranes, especially neuronal cell membranes. They are present in the external leaflet of the membrane. The hydrophobic moiety, consisting of sphingosine and fatty acid (stearic acid, 95%), is inserted into the membrane, while the hydrophilic moiety, consisting of sialic acid (NANA) and other carbohydrates, protrudes towards the extracellular fluid. Although gangliosides were discovered some 50 years ago, their potential role in neuronal functions has been appreciated only recently. During development, their composition and concentration change in a variety of animal species. Their role is indicated from studies which have shown that abnormalities in ganglioside metabolism can have a severe impairing effect on normal development. The mouse mutant weaver is characterized by cerebellar granule cell death, which is correlated by the lack of GM1 expression on the neuronal surface. On the other hand, inborn metabolic errors causing ganglioside accumulation in neurons (GM1 gangliosides) are correlated to an aberrant neurite outgrowth. A further appreciation of ganglioside action has been obtained either by adding gangliosides to neurons in culture or by treating animals during neuronal regeneration. It was found that these agents increased the rate and extent of sprouting of regenerating axons and enhanced neuronal differentiation and sprouting in vitro. Such effects were dependent upon the presence of the growth factor in the bathing medium; ganglioside incorporation, however, did not alter nerve growth factor (NGF) binding and internalization, indicating that some membrane events triggered by ganglioside incorporation may be relevant in neuronal differentiation and sprouting. More recently, we have obtained evidence showing that neurons from animals treated with gangliosides are more resistant to anoxia and ionic unbalances. It seems that ganglioside treatment prevents the decay of some key enzyme activity, such as Na+-K+-ATPase occurring after trauma. Indeed, the recent literature suggests that gangliosides may play an important role during development and, when injected into animals, enhance reparatory events in the central and peripheral nervous system.

Animals↗
PubMed2004

An engram found? Evaluating the evidence from fruit flies.

Is it possible to localize a memory trace to a subset of cells in the brain? If so, it should be possible to show: first, that neuronal plasticity occurs in these cells. Second, that neuronal plasticity in these cells is sufficient for memory. Third, that neuronal plasticity in these cells is necessary for memory. Fourth, that memory is abolished if these cells cannot provide output during testing. And fifth, that memory is abolished if these cells cannot receive input during training. With regard to olfactory learning in flies, we argue that the notion of the olfactory memory trace being localized to the Kenyon cells of the mushroom bodies is a reasonable working hypothesis.

Animals↗
PubMed1992

Dependence of cortical plasticity on correlated activity of single neurons and on behavioral context.

It has not been possible to analyze the cellular mechanisms underlying learning in behaving mammals because of the difficulties in recording intracellularly from awake animals. Therefore, in the present study of neuronal plasticity in behaving monkeys, the net effect of a single neuron on another neuron (the "functional connection") was evaluated by cross-correlating the times of firing of the two neurons. When two neurons were induced to fire together within a short time window, the functional connection between them was potentiated, and when simultaneous firing was prevented, the connection was depressed. These modifications were strongly dependent on the behavioral context of the stimuli that induced them. The results indicate that changes in the temporal contingency between neurons are often necessary, but not sufficient, for cortical plasticity in the adult monkey: behavioral relevance is required.

Acoustic Stimulation↗
PubMed2006

Adult neurogenesis and functional plasticity in neuronal circuits.

The adult brain is a plastic place. To ensure that the mature nervous system's control of behaviour is flexible in the face of a varying environment, morphological and physiological changes are possible at many levels, including that of the entire cell. In two areas of the adult brain - the olfactory bulb and the dentate gyrus - new neurons are generated throughout life and form an integral part of the normal functional circuitry. This process is not fixed, but highly modulated, revealing a plastic mechanism by which the brain's performance can be optimized for a given environment. The functional benefits of this whole-cell plasticity, however, remain a matter for debate.

Animals↗
PubMed1995

Regulation of neuron cholinoreceptor plasticity of Helix lucorum by second messengers and opioids.

The rhythmical local ionophoretic applications of acetylcholine (ACh) to the somatic membrane of Helix lucorum identified neurons evokes the reversible depression of the ACh-induced response which shows cholinoreceptor (ChR) desensitization. ChR desensitization is regulated not by one but by several known second messengers and G-proteins. The endogenous opioids perform the excitation or inhibitory tonic control of the membrane potential in some neurons constantly activating the ionotropic opiate receptors. The direction of neuron ChR desensitization modulation by opioids depends on the type of the activated modulatory opiate receptors (mu or kappa) on the neuron membrane. Second messengers are involved in intracellular mechanism of modulation of the ChR desensitization by opiate kappa-agonist bremazocine.

Acetylcholine↗
PubMed2003

Making the brain plastic: early neuroanatomical staining techniques and the pursuit of structural plasticity, 1910-1970.

The concept of neuronal plasticity is widely used, but seldom defined in the neurosciences. It can signify many different occurrences, such as structural alterations of axons and dendrites (Cotman & Nadler, 1978), behavioural adaptations (Rosenzweig & Bennett, 1996), or physiological changes in synapse formation (Martin et al., 2000) at different stages of health and disease. Although there is such a wealth of research from many disciplines, the neuroanatomical aspects of plasticity are the focus of this paper. It seeks to illuminate the evolution of different concepts of plasticity concerning the structure and circuitry of the central nervous system (CNS). Early modern morphological research on de- and regeneration phenomena in the 19th- and early 20th-century is well documented. These studies, however, almost exclusively concentrated on the peripheral nervous system (PNS). It was one of the major contributions of Santiago Ramón y Cajal (1852-1934), that he applied the concept of regenerative capacities to the CNS. But the term plasticity seemed to have disappeared for about two decades after his death. The ensuing comeback of the expression may be attributed, at least in part, to new neuroanatomical staining and tracing methods. The pursuit of these techniques will serve as a guidepost through varying approaches in different times: It was the 1950s which seemed to spawn the time for new departures in structural investigations of neuronal plasticity.

History, 19th Century↗
PubMed2005

REST and its corepressors mediate plasticity of neuronal gene chromatin throughout neurogenesis.

Regulation of neuronal gene expression is critical to central nervous system development. Here, we show that REST regulates the transitions from pluripotent to neural stem/progenitor cell and from progenitor to mature neuron. In the transition to progenitor cell, REST is degraded to levels just sufficient to maintain neuronal gene chromatin in an inactive state that is nonetheless poised for expression. As progenitors differentiate into neurons, REST and its co-repressors dissociate from the RE1 site, triggering activation of neuronal genes. In some genes, the level of expression is adjusted further in neurons by CoREST/MeCP2 repressor complexes that remain bound to a site of methylated DNA distinct from the RE1 site. Expression profiling based on this mechanism indicates that REST defines a gene set subject to plasticity in mature neurons. Thus, a multistage repressor mechanism controls the orderly expression of genes during development while still permitting fine tuning in response to specific stimuli.

Animals↗
PubMed1992

The role of microtubule-associated protein 2 (MAP-2) in neuronal growth, plasticity, and degeneration.

Microtubule associated protein 2 (MAP-2) historically has been perceived primarily as a static, structural protein, necessary along with other cytoskeletal proteins to maintain neuroarchitecture but somewhat removed from the "mainstream" of neuronal response mechanisms. Quite to the contrary, MAP-2 is exquisitely sensitive to many inputs and recent investigations have revealed dynamic functions for MAP-2 in the growth, differentiation, and plasticity of neurons, with key roles in neuronal responses to growth factors, neurotransmitters, synaptic activity, and neurotoxins. These discoveries indicate that modification and rearrangement of MAP-2 is an early obligatory step in many processes which modify neuronal function.

Aging↗
PubMed1996

Hebb's concept of synaptic plasticity and neuronal cell assemblies.

Both in vertebrates and in invertebrates the study of processes of plasticity in nervous systems have led to consistent models of molecular mechanisms for the so-called Hebb's synapse. Changes of synaptic efficacy will lead to changes in the properties of assemblies of nerve cells--as seen today the correlates of purport. Donald Hebb's view of the characteristics of such assemblies appears farsighted.

History, 20th Century↗
PubMed2000

Searching for depolarization-induced genes that modulate synaptic plasticity and neurotrophin-induced genes that mediate neuronal differentiation.

We identify and characterize two classes of immediate-early genes: (i) genes, induced by depolarization in neurons, that play a role in depolarization-induced neuronal plasticity and (ii) genes, induced in neuronal precursors by neurotrophins, that play a causal role in neurotrophin-directed neuronal differentiation. We use rat PC12 pheochromocytoma cells to identify (i) genes preferentially induced by [depolarization or forskolin] versus [Nerve Growth Factor (NGF) or Epidermal Growth Factor (EGF)] and (ii) genes preferentially induced by NGF versus EGF. We describe (i) a collection of genes preferentially induced by depolarization/forskolin in PC12 cells and by kainic acid in vivo, and (ii) a collection of genes preferentially induced by NGF. The synaptotagmin IV gene encodes a synaptic vesicle protein whose level is modulated by depolarization. NGF preferentially induces the urokinase-plasminogen activator receptor in PC12 cells. Antisense oligonucleotide and anti-UPAR antibody experiments demonstrate that NGF-induced UPAR expression is required for NGF-driven PC12 cell differentiation.

Adrenal Gland Neoplasms↗
PubMed2007

A role for reactive oxygen/nitrogen species and iron on neuronal synaptic plasticity.

A great body of experimental evidence collected over many years indicates that calcium has a central role in a variety of neuronal functions. In particular, calcium participates in synaptic plasticity, a neuronal process presumably correlated with cognitive brain functions such as learning and memory. In contrast, only recently, evidence has begun to emerge supporting a physiological role of reactive oxygen (ROS) and nitrogen (RNS) species in synaptic plasticity. This subject will be the central topic of this review. The authors also present recent results showing that, in hippocampal neurons, ROS/RNS, including ROS generated by iron through the Fenton reaction, stimulate ryanodine receptor-mediated calcium release, and how the resulting calcium signals activate the signaling cascades that lead to the transcription of genes known to participate in synaptic plasticity. They discuss the possible participation of ryanodine receptors jointly stimulated by calcium and ROS/RNS in the normal signaling cascades needed for synaptic plasticity, and how too much ROS production may contribute to neurodegeneration via excessive calcium release. In addition, the dual role of iron as a necessary, but potentially toxic, element for normal neuronal function is discussed.

Animals↗
PubMed2006

RNA binding proteins and the regulation of neuronal synaptic plasticity.

Cognitive function and memory rely on synaptic plasticity - the ability of synapses to modify their strength in response to stimulation. Emerging evidence indicates that post-transcriptional gene regulation is necessary for synaptic plasticity at several levels: by increasing proteome diversity through alternative splicing, or by enabling activity-dependent regulation of mRNA localization, translation or degradation in the dendrite. Mouse knockout studies have linked three RNA-binding proteins, fragile X mental retardation protein, cytoplasmic polyadenylation element binding factor and neuro-oncological ventral antigen to specific aspects of synaptic plasticity. Specificity in the regulation of synaptic plasticity might, in part, relate to the functional coherence of proteins encoded by the RNA targets of each RNA-binding protein.

Alternative Splicing↗
PubMedDate not supplied

Analysis of spike activity of two neurons monosynaptically excited by a third, using cross-correlation histograms and Cos' method. Possibility of detecting plasticity of neurons and synapses.

Exogenous stationary random single spike activity of two neurons (N1 and N2), monosynaptically excited by a third (N3), was reproduced by a mathematical model. The degree of dependence of spike trains of N1 and N2 was assessed by the value of P12, determined by cross-correlation histogram, and Cox' coefficient B12. The dynamics of P12 and beta 12 and also values of P1*, P2*, and P3*, proportional to the mean interspike intervals of N1, N2, and N3 were investigated during changes in the efficiency of synaptic connections, excitability of the neurons, and their response to afferent synaptic bombardment. It was shown that an increase (decrease) in P12 or beta 12, accompanied by a decrease (increase) in P1' and P2', is a sign of a plastic change either in the discharge frequency of N3 (not always recorded experimentally) or of the amplitudes of excitatory postsynaptic potentials of N1 and (or) N2, evoked by these discharges.

Models, Neurological↗
PubMedDate not supplied

Ca(2+)/CREB/CBP-dependent gene regulation: a shared mechanism critical in long-term synaptic plasticity and neuronal survival.

CREB is a transcription factor critical for long-term synaptic plasticity. Intriguingly, recent work has elucidated a role for CREB, as well as upstream CREB kinases, in the control of activity-dependent neuronal survival. Additionally, analysis of the molecular pathology of polyglutamine-repeat diseases suggest that alteration of pCREB-CBP function may underlie, at least in part, the neurodegenerative process. Taken together, these new findings support the idea that Ca(2+)/CREB/CBP-dependent gene regulation might be a shared mechanism critical in both long-term synaptic plasticity and neuronal survival.

Amino Acid Sequence↗
PubMed2006

Odorant deprivation reversibly modulates transsynaptic changes in the NR2B-mediated CREB pathway in mouse piriform cortex.

The olfactory system is an outstanding model for understanding activity-dependent neuronal plasticity in mammals. Olfactory sensory neurons (OSNs) in the periphery project onto mitral/tufted cells in the olfactory bulb (OB) and these mitral/tufted cells in turn project to piriform cortex (PC). Numerous studies have examined changes in OB after a permanent OSN ablation, but little is known about "trans-transsynaptic" changes taking place in the PC. Permanent zinc sulfate lesion of the olfactory epithelium resulted in a selective loss of the NMDA receptor NR2B protein and mRNA expression in pyramidal cells in layer IIb of PC after 2-7 d. Regulatory elements affected by NR2B signaling, namely the phosphorylation of CREB, were also downregulated only in layer IIb neurons. These changes could be caused by OSN axon loss in the zinc sulfate lesion, or to a reduced activity. To test this hypothesis, we performed both permanent and reversible naris occlusion, which blocks odorant access to the nasal cavities and OSN activity. The expression of NR2B and phospho-CREB were downregulated 5 d after occlusion and this reduction was fully restored 10 d after reopening of the naris. Subsequently, we identified the subset of pyramidal cells in layer IIb that are especially sensitive to the loss of odor-evoked activity using double retrograde tracers. In summary, the present study provides an initial characterization of the molecular mechanisms associated with odor stimulation on second order neuronal plasticity and phenotype in the olfactory system.

Animals↗