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PubMed1995

Expression of molecules associated with neuronal plasticity in the striatum after aspiration and thermocoagulatory lesions of the cerebral cortex in adult rats.

Like the hippocampus, the striatum receives excitatory afferents from the cerebral cortex but, in the case of the striatum, very little is known about the molecular events associated with plasticity after lesions of this pathway. Using immunohistochemical techniques, we have examined the effects of cortical lesions induced either by aspiration of the frontoparietal cortex or by thermocoagulation of pial blood vessels on axonal and glial molecules associated with neuronal plasticity in the striatum. The growth associated protein GAP-43, a molecule present in axons and growth cones, decreased in the dorsolateral striatum after aspiration but not after thermocoagulatory lesions. In contrast, synaptophysin, a marker of synaptic vesicles, remained unchanged in the denervated striatum after both types of lesions. Immunostaining for basic fibroblast growth factor (bFGF) markedly decreased in striatal astrocytes after both lesions, despite an increased staining for glial fibrillary acidic protein (GFAP). The adhesion molecules tenascin, chondroitin sulfate proteoglycans, highly polysialylated neural cell adhesion molecule (PSA-NCAM), and laminin did not change significantly in the gray matter of the dorsolateral striatum after either type of lesion. These effects differed from those observed after partial denervation of the hippocampus and spinal cord, revealing marked regional differences in the response of axonal and glial proteins to afferent lesions. In addition, the results further indicate that cortical lesions have both similar and distinct consequences, depending on the procedure by which the lesions are induced, suggesting that cortical lesions associated with different types of pathology may differentially affect subcortical structures.

Animals↗
PubMed2001

Impaired neuronal plasticity in transgenic mice expressing human apolipoprotein E4 compared to E3 in a model of entorhinal cortex lesion.

The apolipoprotein E (APOE) epsilon 4 allele is a major risk factor for late-onset familial and sporadic Alzheimer's disease (AD) and is associated with a poor outcome after brain injury. Each apoE isoform is suggested to have differential effects on neuronal repair mechanisms within the CNS. In the present study, APOE genotype influence on the immediate response to injury and subsequent repair process was examined in a line of transgenic APOE mice possessing human APOE gene insertions (epsilon 3 and epsilon 4). Quantification of synaptophysin and GAP-43 immunoreactivity was used to measure the extent of degeneration and regeneration after entorhinal cortex lesion (ECL). Progressive neurodegenerative decline occurred in the ipsilateral dentate gyrus until day 28 post-ECL which was more severe in APOE epsilon 3 mice compared to APOE epsilon 4 mice. By day 90 post-ECL compensatory sprouting and reactive synaptogenesis had taken place in the dentate gyrus of APOE epsilon 3 mice such that GAP-43 and synaptophysin immunoreactivity had returned to prelesion levels. In contrast, APOE epsilon 4 mice displayed significant deficits in synaptophysin and GAP-43 immunostaining compared to the APOE epsilon 3 mice (P < 0.05). Expansion of the inner molecular layer (IML) was used as a measure of the sprouting index from the commissural-associational pathway and by day 90 post-ECL the IML width in APOE epsilon 3 mice had increased by 45% but only 20% in APOE epsilon 4 mice (P < 0.0001). ApoE immunoreactivity was increased within the neuropil and glia to the same extent in APOE epsilon 3 and APOE epsilon 4 mice post-ECL. There was no significant difference in the deposition and clearance of degeneration products between APOE epsilon 3 and epsilon 4 mice post-ECL. These results indicate that neuronal plasticity is impaired in transgenic mice possessing human APOE epsilon 4 alleles compared to APOE epsilon 3. These isoform-specific differences in plasticity may relate to the severity of AD and poor, long-term recovery after head injury in APOE epsilon 4 individuals.

Alzheimer Disease↗
PubMed2004

A gene for neuronal plasticity in the mammalian brain: Zif268/Egr-1/NGFI-A/Krox-24/TIS8/ZENK?

Zif268 is a transcription regulatory protein, the product of an immediate early gene. Zif268 was originally described as inducible in cell cultures; however, it was later shown to be activated by a variety of stimuli, including ongoing synaptic activity in the adult brain. Recently, mice with experimentally mutated zif268 gene have been obtained and employed in neurobiological research. In this review we present a critical overview of Zif268 expression patterns in the naive brain and following neuronal stimulation as well as functional data with Zif268 mutants. In conclusion, we suggest that Zif268 expression and function should be considered in a context of neuronal activity that is tightly linked to neuronal plasticity.

Animals↗
PubMed1988

The role of afferent activity in behavioral and neuronal plasticity in an insect.

Cockroaches (Periplaneta americana) have been shown to adapt behaviorally, in about 1 month, to ablation of one cercus. Additionally, those giant interneurons (GIs) that normally receive their major input from the lesioned cercus become more responsive to stimulation of the intact side (Vardi and Camhi 1982a, b). To investigate the role of afferent activity in the behavioral and neuronal plasticity, we silenced wind-evoked activity in the intact cercus by immobilizing the sensory hairs. This was carried out during the last nymphal stage which lasts for about one month. The animals were tested behaviorally and physiologically after they had molted to adults and a fresh set of mobile hairs had appeared. These animals showed no behavioral correction (Fig. 3). The responses of the GIs on the ablated side were somewhat enhanced, but they were also significantly smaller than those in animals with long-term cercal ablations and no sensory deprivation (Fig. 5). A variety of controls (Figs. 8, 9, and 10) were used to show that sensory deprivation by itself did not decrease the responsiveness of the afferents or the GIs. Thus elimination of wind-evoked activity specifically decreases enhancement of the responses in the GIs.

Afferent Pathways↗
PubMed2003

Expression of neuronal plasticity markers in hypoglycemia induced brain injury.

The expression of neuroplasticity markers was analyzed in four brain regions, namely cerebral hemispheres (CH), cerebellum (CB), brain stem (BS) and diencephalon (DC) from insulin-induced hypoglycemic young adult rats. Significant decrease in neural cell adhesion molecule (NCAM) isoforms and growth-associated protein-43 (GAP-43) was observed following hypoglycemic injury from majority of brain regions studied. The glial fibrillary acidic protein (GFAP) level increased significantly in cerebral hemispheres and diencephalon regions, whereas, synaptophysin level increased in cerebellum, brain stem and diencephalon regions. The selective downregulation of the neuronal plasticity marker proteins (GAP-43 and NCAM), and enhanced expression of GFAP and synaptophysin suggests that in acute hypoglycemia, mechanisms other than energy failure may also contribute to neuronal cell damage in the brain.

Animals↗
PubMed1992

Immediate-early genes, neuronal plasticity, and memory.

The demonstration that the immediate-early gene c-fos is rapidly and transiently expressed in brain following a variety of manipulations has led to intense study of these genes to determine what physiological role they play. The very wide range of stimuli which lead to induction of immediate-early genes (IEGs) in the brain has raised concerns for the specificity of their actions and the suggestion that they might merely be involved in housekeeping functions. On the other hand, there is evidence that these genes may play a role in the transmission of information from cell surface receptors to the genetic material in many instances of neuronal plasticity, including development of seizure susceptibility (kindling), long-term potentiation, drug-induced changes, the phase shift in circadian rhythms, and spreading neuronal depression. In addition to being a putative third (or fourth) messenger involved in transduction of signals to the genetic material, activation of IEGs has proven to be a useful tool for the study of transsynaptic activation of certain neuronal pathways in the brain. Thus, studies on the induction of IEGs are proving to be especially useful in understanding some important functions and properties of the mammalian brain.

Animals↗
PubMed1985

A species difference between Rana and Xenopus in the occurrence of intertectal neuronal plasticity.

In anuran amphibians, a system of neuronal connections links the two optic tecta and is involved in projections of the binocular visual field to the optic tecta. Electrophysiological studies have shown that in the frog, Xenopus laevis, the pattern of connections may be modified by procedures such as larval rotation of one eye. This modification appears to be effected by visual experience. Workers in other laboratories, however, found no evidence of such a modification in the related frog Rana pipiens. This difference in results may have been due to different rearing conditions and different recording techniques or may reflect a true species difference, in this respect, between Rana and Xenopus. In the present experiments, an attempt was made to distinguish between these possibilities by performing eye rotations in Rana and Xenopus, rearing them as identically as possible and recording from them under identical conditions. It was found that while Xenopus displayed the modification of intertectal connections, Rana did not. It is concluded that the different responses of the intertectal systems to larval eye rotation in Xenopus and Rana reflect a species difference.

Adaptation, Physiological↗
PubMed2006

Learning, aging and intrinsic neuronal plasticity.

In vitro experiments indicate that intrinsic neuronal excitability, as evidenced by changes in the post-burst afterhyperpolarization (AHP) and spike-frequency accommodation, is altered during learning and normal aging in the brain. Here we review these studies, highlighting two consistent findings: (i) that AHP and accommodation are reduced in pyramidal neurons from animals that have learned a task; and (ii) that AHP and accommodation are enhanced in pyramidal neurons from aging subjects, a cellular change that might contribute to age-related learning impairments. Findings from in vivo single-neuron recording studies complement the in vitro data. From these consistently reproduced findings, we propose that the intrinsic AHP level might determine the degree of synaptic plasticity and learning. Furthermore, it seems that reductions in the AHP must occur before learning if young and aging subjects are to learn a task successfully.

Aging↗
PubMed2003

Inducible cAMP early repressor (ICER) in the nervous system--a transcriptional regulator of neuronal plasticity and programmed cell death.

The acronym ICER (inducible cAMP early repressor) refers to a group of four proteins produced from the CREM/ICER gene due to use of an internal promoter (P2) placed in an intron of the CREM (cAMP responsive element modulator) gene. The ICER proteins contain DNA binding/leucine zipper domains that make them endogenous inhibitors of transcription driven by CREB (cAMP responsive element binding protein) and its cognates, CREM and ATF-1 (activating transcription factor-1). ICER expression is inducible in the brain and in neuronal culture by a variety of stimuli. As a CREB antagonist, ICER appears to be of pivotal importance in neuronal plasticity and programmed cell death.

Animals↗
PubMed2004

Does the neuronal plasticity exist in elderly patients? report of an unusual clinical case.

STUDY DESIGN: Case report. OBJECTIVE: To report complete recovery after paraplegia in an elderly patient after removal of meningioma at C7-T1 level. SETTING: Department of Neurosurgery, Reggio Calabria, Italy. METHODS: An 82-year-old lady with 48 months of progressive weakness and numbness was admitted with complete paraplegia lasting 15 days. Investigations (magnetic resonance imaging (MRI)) demonstrated a meningioma at C7-T1. The tumour compressed the extremely thinned spinal cord. MRI after surgery showed no evidence of residual tumour and the spinal cord was of normal dimensions. The patient recovered fully and locomotion was restored. CONCLUSION: Surgical decompression gave an excellent result. The result raises the possibility of neuronal plasticity.

Aged↗
PubMed2000

Hebb and homeostasis in neuronal plasticity.

The positive-feedback nature of Hebbian plasticity can destabilize the properties of neuronal networks. Recent work has demonstrated that this destabilizing influence is counteracted by a number of homeostatic plasticity mechanisms that stabilize neuronal activity. Such mechanisms include global changes in synaptic strengths, changes in neuronal excitability, and the regulation of synapse number. These recent studies suggest that Hebbian and homeostatic plasticity often target the same molecular substrates, and have opposing effects on synaptic or neuronal properties. These advances significantly broaden our framework for understanding the effects of activity on synaptic function and neuronal excitability.

Animals↗
PubMedDate not supplied

Are there differences between the secretion characteristics of NGF and BDNF? Implications for the modulatory role of neurotrophins in activity-dependent neuronal plasticity.

In previous experiments the activity-dependent secretion of nerve growth factor (NGF) from native hippocampal slices and from NGF-cDNA transfected hippocampal neurons showed unusual characteristics [Blochl and Thoenen (1995) Eur J Neurosci 7:1220-1228; (1996) Mol Cell Neurosci 7:173-190]. In both hippocampal slices and cultured hippocampal neurons the activity-dependent secretion proved to be independent of extracellular calcium, but dependent on the release of calcium from intracellular stores. Under different experimental conditions, Goodman et al. [(1996) Mol Cell Neurosci 7:222-238] reported that the high potassium-mediated secretion of brain-derived neurotrophic factor (BDNF) from hippocampal cultures was dependent on extracellular calcium. Mowla et al. [(1997) Proc 27th Annu Meet Soc Neurosci New Orleans 875.10] reported on even further-reaching differences between NGF and BDNF secretion, namely, that in hippocampal neurons and in pituitary cell lines NGF was secreted exclusively according to the constitutive pathway, whereas BDNF was exclusively sorted according to the activity-dependent regulated pathway. In view of the crucial importance of such potential differences between the processing, sorting, and secretory mechanisms of different neurotrophins for their modulatory roles in activity-dependent neuronal plasticity, a thorough analysis under comparable experimental conditions was mandatory. We demonstrate that in native hippocampal slices and adenoviral-transduced hippocampal neurons there are no differences between NGF and BDNF with respect to the subcellular distribution and mechanism of secretion; that the activity-dependent secretion of both NGF and BDNF is dependent on intact intracellular calcium stores; and that the differences between our own observations and those of Goodman et al. (ibid.) regarding the dependence on extracellular calcium do not reflect differences between NGF and BDNF sorting and secretion, but reflect the differing experimental conditions used.

Animals↗
PubMed1998

Profound neuronal plasticity in response to inactivation of the dopamine transporter.

The dopamine transporter (DAT) plays an important role in calibrating the duration and intensity of dopamine neurotransmission in the central nervous system. We have used a strain of mice in which the gene for the DAT has been genetically deleted to identify the DAT's homeostatic role. We find that removal of the DAT dramatically prolongs the lifetime (300 times) of extracellular dopamine. Within the time frame of neurotransmission, no other processes besides diffusion can compensate for the lack of the DAT, and the absence of the DAT produces extensive adaptive changes to control dopamine neurotransmission. Despite the absence of a clearance mechanism, dopamine extracellular levels were only 5 times greater than control animals due to a 95% reduction in content and a 75% reduction in release. Paradoxically, dopamine synthesis rates are doubled despite a decrease of 90% in the levels of tyrosine hydroxylase and degradation is markedly enhanced. Thus, the DAT not only controls the duration of extracellular dopamine signals but also plays a critical role in regulating presynaptic dopamine homeostasis. It is interesting to consider that the switch to a dopamine-deficient, but functionally hyperactive, mode of neurotransmission observed in mice lacking the DAT may represent an extreme example of neuronal plasticity resulting from long-term psychostimulant abuse.

Animals↗
PubMed2002

[Neuronal plasticity and the scientific bases of neurohabilitation].

INTRODUCTION: The validity of methods of neurological habilitation and rehabilitation has long been questioned by a large proportion of the medical profession. This sceptical attitude was partly due to lack of scientific confirmation of the theories on which methods of habilitation-rehabilitation were based, and the absence of reliable studies of the follow-up of such treatment, designed on strict statistical criteria. DEVELOPMENT: Advances in recent years in understanding neuronal plasticity have permitted better understanding of the mechanisms which come into action following brain damage and the factors which help or hinder recovery, and the various possible patterns involved in the reorganization of neuronal circuits. A review of studies of animal experiments, and recently in humans (using techniques of functional imaging and magnetic exploration) show that by sensory stimulation and exercise it is possible to modify the structure and function of the brain, after its somatotopical organization, increase synaptic connections, influence the orientation of the dendrites, number of receptors etc. There are critical periods in development during which these plastic properties of the brain become fully developed and subsequently the possibility of recovery is considerably less. CONCLUSIONS: The findings of neurobiological investigation show that there are good prospects for the recovery of a damaged nervous system by means of embryonic neurone implantation, axon bridges, transference of genes producing trophic factor, enzymes, neurotransmitters etc. In any case, therapeutic intervention and rehabilitation teaching continue to be useful for the functional recovery of these patients.

Animals↗
PubMed1990

c-fos protooncogene expression and neuronal plasticity.

Protooncogene c-fos is a nuclear protein repeatedly implicated in regulation of gene expression. The elevated expression of the c-fos protooncogene in neurons has been observed in many instances of neuronal activation both in vitro and in vivo. The increase of c-fos mRNA and/or protein levels has been shown to result from the action of neurotransmitters on membrane receptors and seems to be induced by physiological stimuli. We suggest that the elevated expression of c-fos protooncogene couples stimulation of the neurons by extracellular ligands with intracellular long term effector responses including long lasting memory formation.

Animals↗
PubMed1999

CRE-mediated gene transcription in neocortical neuronal plasticity during the developmental critical period.

Neuronal activity-dependent processes are believed to mediate the formation of synaptic connections during neocortical development, but the underlying intracellular mechanisms are not known. In the visual system, altering the pattern of visually driven neuronal activity by monocular deprivation induces cortical synaptic rearrangement during a postnatal developmental window, the critical period. Here, using transgenic mice carrying a CRE-lacZ reporter, we demonstrate that a calcium- and cAMP-regulated signaling pathway is activated following monocular deprivation. We find that monocular deprivation leads to an induction of CRE-mediated lacZ expression in the visual cortex preceding the onset of physiologic plasticity, and this induction is dramatically downregulated following the end of the critical period. These results suggest that CRE-dependent coordinate regulation of a network of genes may control physiologic plasticity during postnatal neocortical development.

Aging↗