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PubMed1999

The EGR family of transcription-regulatory factors: progress at the interface of molecular and systems neuroscience.

The EGR family of transcription regulatory factors, which is implicated in orchestrating the changes in gene expression that underlie neuronal plasticity, has attracted the attention of both molecular and systems neuroscientists. In this article, the advances made in both these fields of research are reviewed. Recent systems-based studies underscore the remarkable sensitivity and specificity of the induction of the expression of genes encoding EGR-family members in naturally occurring plasticity paradigms. However, they also challenge conventional views of the role of this family in plasticity. Recent molecular studies have identified the gonadotropin subunit, luteinizing hormone beta, as an EGR1-regulated gene in vivo and uncovered an essential role for EGR3 in muscle-spindle development. In addition, the discovery of novel proteins that are capable of suppressing EGR-mediated transcription cast doubt over the prevalent assumption that changes in EGR mRNA or protein levels provide an accurate measure of EGR-driven transcriptional activity.

Animals↗

PubMed1997

SNAP25 and GAP-43 behave differently in decentralized rat superior cervical ganglia.

The behaviour of synaptosome associated protein of mol. wt 25 kDa (SNAP25) in decentralized rat superior cervical ganglia (SCG) was investigated in order to observe its possible involvement in adrenergic postganglionic neuronal plasticity. Immunofluorescence and immunoblot results showed that the protein was increased in the nerve terminals in irides 8 days after operation. The intra-ganglionic nerve terminals and nerve fibres differed in their content of GAP-43 and SNAP25: GAP-43, which could not be observed at 1 day, appeared at 3 days after cutting the cervical sympathetic trunk, whilst SNAP25-immunoreactive material was still undetectable at this time. Immunoblot data also showed that SNAP25 did not reach control levels at 3 and 8 days after decentralization, in contrast to GAP-43. This observation may imply that SNAP25 is rapidly transported to its functional destinations immediately after synthesis and is possibly mainly involved in the remodelling of long projection pathways.

Animals↗

PubMed1998

KID-1, a protein kinase induced by depolarization in brain.

Membrane depolarization leads to changes in gene expression that modulate neuronal plasticity. Using representational difference analysis, we have identified a previously undiscovered cDNA, KID-1 (kinase induced by depolarization), that is induced by membrane depolarization or forskolin, but not by neurotrophins or growth factors, in PC12 pheochromocytoma cells. KID-1 is an immediate early gene that shares a high degree of sequence similarity with the family of PIM-1 serine/threonine protein kinases. Recombinant KID-1 fusion protein is able to catalyze both histone phosphorylation and autophosphorylation. KID-1 mRNA is present in a number of unstimulated tissues, including brain. In response to kainic acid and electroconvulsive shock-induced seizures, KID-1 is induced in specific regions of the hippocampus and cortex.

Amino Acid Sequence↗

PubMed2000

Ginkgo biloba extract (EGb 761) and CNS functions: basic studies and clinical applications.

The effects of EGb 761 on the CNS underlie one of its major therapeutic indications; i.e., individuals suffering from deteriorating cerebral mechanisms related to age-associated impairments of memory, attention and other cognitive functions. EGb 761 is currently used as symptomatic treatment for cerebral insufficiency that occurs during normal ageing or which may be due to degenerative dementia, vascular dementia or mixed forms of both, and for neurosensory disturbances. Depressive symptoms of patients with Alzheimer's disease (AD) and aged non-Alzheimer patients may also respond to treatment with EGb 761 since this extract has an "anti-stress" effect. Basic and clinical studies, conducted both in vitro and in vivo, support these beneficial neuroprotective effects of EGb 761. EGb 761 has several major actions; it enhances cognition, improves blood rheology and tissue metabolism, and opposes the detrimental effects of ischaemia. Several mechanisms of action are useful in explaining how EGb 761 benefits patients with AD and other age-related, neurodegenerative disorders. In animals, EGb 761 possesses antioxidant and free radical-scavenging activities, it reverses age-related losses in brain alpha 1-adrenergic, 5-HT1A and muscarinic receptors, protects against ischaemic neuronal death, preserves the function of the hippocampal mossy fiber system, increases hippocampal high-affinity choline uptake, inhibits the down-regulation of hippocampal glucocorticoid receptors, enhances neuronal plasticity, and counteracts the cognitive deficits that follow stress or traumatic brain injury. Identified chemical constituents of EGb 761 have been associated with certain actions. Both flavonoid and ginkgolide constituents are involved in the free radical-scavenging and antioxidant effects of EGb 761 which decrease tissue levels of reactive oxygen species (ROS) and inhibit membrane lipid peroxidation. Regarding EGb 761-induced regulation of cerebral glucose utilization, bilobalide increases the respiratory control ratio of mitochondria by protecting against uncoupling of oxidative phosphorylation, thereby increasing ATP levels, a result that is supported by the finding that bilobalide increases the expression of the mitochondrial DNA-encoded COX III subunit of cytochrome oxidase. With regard to its "anti-stress" effect, EGb 761 acts via its ginkgolide constituents to decrease the expression of the peripheral benzodiazepine receptor (PBR) of the adrenal cortex.

Alzheimer Disease↗

PubMed2003

Transcriptional regulation through glutamate receptors: Involvement of tyrosine kinases.

Glutamate receptors play a key role in neuronal plasticity, learning and memory, and in several neuropathologies. Short-term and long-term changes in synaptic efficacy are triggered by glutamate. Although an enhanced glutamate-dependent tyrosine phosphorylation has been described in several systems, its role in membrane-to-nuclei signaling is unclear. Taking advantage of the fact that the gene encoding the chick kainate-binding protein undergoes a glutamate-dependent transcriptional regulation via an activator protein-1 (AP-1) site, we evaluated the involvement of tyrosine kinases in this process. We describe here the participation of receptor and non-receptor tyrosine kinases in the signaling cascade triggered by glutamate. Our results suggest that in Bergmann glia cells, glutamate receptors transactivate receptor tyrosine kinases, favoring the idea of a complex network of signals activated by this excitatory neurotransmitter that results in regulation of gene expression.

Animals↗

PubMed2006

Enteric neuroplasticity evoked by inflammation.

Neuroplastic changes in the enteric nervous system (ENS) may be observed in physiological states, such as development and aging, or occur as a consequence of different pathological conditions, ranging from enteric neuropathies (e.g., Hirschsprung's disease) to intestinal (e.g., inflammatory bowel disease) or extra-intestinal diseases (e.g., Parkinson's disease). Studying ENS plasticity may help to elucidate the pathophysiology of several diseases and have a bearing on the development of new pharmacological interventions. In the present review, we would like to focus on neuronal plasticity evoked by gastrointestinal inflammation occurring in inflammatory bowel disease and in a subset of patients with severe derangement of gut motility due to an enteric neuropathy characterized by an inflammatory infiltrate of the enteric plexuses. Major features of neuroplasticity within the enteric microenvironment encompass structural abnormalities ranging from nerve re-arrangement (e.g., hypertrophy and hyperplasia) to degeneration and loss of enteric ganglion cells; altered synthesis, content and release of neurotransmitters as well as up- or down-regulation of receptor systems; gastrointestinal dysfunction characterized by sensory-motor and secretory impairment of the gut. Interestingly, neuronal changes may also occur in segments of the gastrointestinal tract remote from the site of the original inflammation, e.g. the ileum may show neuroplastic changes during colitis. Sometimes, the inflamed site may even be outside the gut. Among potential mechanisms underlying ENS plasticity, neurotrophins and enteric glia deserve special attention. A better comprehension of ENS plasticity during inflammation could be instrumental to develop new therapeutic options for patients with IBD and inflammatory enteric neuropathies.

Animals↗

PubMed1998

Acute functional tolerance to ethanol and fear conditioning are genetically correlated in mice.

It has been speculated that tolerance to alcohol involves some form of neuronal plasticity that is similar to or the same as that mediating learning and memory. To investigate this possibility further, we tested the hypothesis that acute functional tolerance (AFT) to alcohol is genetically correlated to a Pavlovian learning task: fear conditioning. Mice selectively bred for differences in ability to acquire AFT were tested for fear conditioning. Subjects received a mild footshock paired to a broadband clicker and were tested 24 hr later for their freezing response to the conditioning chamber (context), to an altered chamber, and to the clicker. Both the original and replicate lines selected for high AFT (HAFT) were found to freeze significantly more than those selected for low AFT (LAFT) in response to the context and to the clicker. In a second experiment, an F2 population derived from the C57BL/6 (B6) and DBA/2 (D2) mouse strains were tested first for fear conditioning, followed 3 weeks later by AFT testing. AFT was defined as the difference between blood alcohol levels determined at the time of regain balance on a dowel rod first after 1.75 g/kg of ethanol and again after a subsequent dose of 2.0 g/kg. Consistent with results from HAFT and LAFT, freezing to context was found to be significantly positively correlated to AFT (r = 0.38, p = 0.04) in the F2 mice. The results suggest that co-variation in fear conditioning and AFT may be mediated by one or more of the same or at least tightly linked genes. Further dissection of this correlation may reveal neuronal mechanisms common to both AFT and fear conditioning.

Alcoholism↗

PubMedDate not supplied

Amelioration of fetal alcohol-related neurodevelopmental disorders in rats: exploring pharmacological and environmental treatments.

Fetal alcohol syndrome (FAS) and alcohol-related neurodevelopmental disorders (ARNDs) in children are characterized by life-long compromises in learning, memory, and adaptive responses. Until the advent of effective prevention measures, it will remain necessary to seek ways to treat the life-long neurobehavioral consequences of prenatal alcohol exposure. To date, there are no clinical remedies to recommend for either specific or global fetal alcohol effects. This article reviews our basic research in animal models that assesses the potential of global environmental manipulations or specific psychopharmacological treatments to ameliorate the neurobehavioral effects of prenatal exposure to alcohol. Postweaning environmental enrichment can improve behavioral performance and ameliorate or even eliminate deficits in prenatal alcohol-exposed rats, although there is persistent impairment in neuronal plasticity, as indicated by the failure of hippocampal pyramidal cells to increase dendrite spine density. Behavioral and neural responses to CNS stimulants differ in rats exposed prenatally to alcohol, although it is not clear that these shifts in dose-response curves would predict benefit to children. Although the present results may sound a note of optimism for the development of effective treatment strategies for children with FAS or ARNDs, it is important to consider that application of these findings in rodents may not be straightforward. We also need to know the critical features of specific environments that influence brain development, and the limits of pharmacotherapy, as well as critical periods of exposure. Continued study of the beneficial, ameliorative effects of environmental enrichment, rehabilitative training, and of pharmacological therapies in animal models, will remain a valuable source of information for eventually devising treatments specific for children with FAS and ARNDs.

Animals↗

PubMed2005

Regulation of hippocampal gene expression is conserved in two species subjected to different stressors and antidepressant treatments.

BACKGROUND: Chronic stress has significant effects on hippocampal structure and function. We have previously identified nerve growth factor (NGF), membrane glycoprotein 6a (M6a), the guanine nucleotide binding protein (G protein) alpha q polypeptide (GNAQ), and CDC-like kinase 1 (CLK-1) as genes regulated by psychosocial stress and clomipramine treatment in the hippocampus of tree shrews. These genes encode proteins involved in neurite outgrowth. METHODS: To analyze whether regulation of the above-mentioned genes is conserved between different species, stressors, and antidepressant drugs, we subjected mice to repeated restraint stress and tianeptine treatment and measured hippocampal messenger RNA (mRNA) levels by real time reverse transcription polymerase chain reaction (RT-PCR). RESULTS: Chronically stressed mice displayed a reduction in transcript levels for NGF, M6a, GNAQ, and CLK-1. In addition, other genes implicated in neuronal plasticity, such as brain-derived neurotrophic factor (BDNF), cyclic adenosine monophosphate (cAMP) response element binding protein (CREB), protein kinase C (PKC), neural cell adhesion molecule (NCAM), and synapsin I were downregulated in stressed mice. Tianeptine treatment reversed the stress effects for the genes analyzed. Alterations in gene expression were dependent on the duration of the stress treatment and, in some cases, were only observed in male mice. CONCLUSIONS: These results suggest that genes involved in neurite remodeling are one of the main targets for regulation by chronic stress. The finding that this regulation is conserved in different stress models and antidepressant treatments highlights the biological relevance of the genes analyzed and suggests that they might be involved in stress-related disorders.

Animals↗

PubMed1994

Regulation of 1,4,5-IP3, 1,3,4,5-IP4 and IP6 binding sites following entorhinal cortex lesions in rat brain.

A lesion of the entorhinal cortex produces a loss of more than 80% of the synapses in the outer molecular layer of the hippocampus in the rat. However, this synaptic loss is transient. Beginning a few days after denervation, new synapses are formed, virtually replacing the lost inputs within two months. Synaptic remodelling induced by entorhinal cortex lesion is associated with specific modifications of various neurotransmitters, hormones and growth factors. Many of these substances act at membrane bound-receptors to induce the hydrolysis of phosphatidylinositols generating various inositol phosphates. Some of the key members of this family include inositol 1,4,5-trisphosphate, inositol 1,3,4,5-tetrakisphosphate and inositol hexakisphosphate which are all associated with the maintenance Ca2+ homeostasis. To investigate the potential roles and/or alterations of inositol phosphates in entorhinal cortex lesions-induced neuronal plasticity, we quantified specific receptor sites for inositol 1,4,5-trisphosphate, inositol 1,3,4,5-tetrakisphosphate and inositol hexakisphosphate using their respective tritiated ligands, at different periods post-lesion corresponding to the degenerative and subsequent reinnervation phases. [3H]inositol 1,4,5-trisphosphate binding sites are maximally increased (30%) between two and eight days post-lesion in the hippocampal formation on both sides of the lesion. In the cortex, [3H]inositol 1,4,5-trisphosphate binding increased also bilaterally following the lesion. Changes in [3H]inositol 1,3,4,5-tetrakisphosphate binding are delayed and reduced (20% increase) in magnitude compared to these seen for [3H]inositol 1,4,5-trisphosphate binding. The maximal peak in [3H]inositol 1,3,4,5-tetrakisphosphate binding is observed between eight and 14 days after the lesion in the hippocampal formation and the cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Degree of adaptability of the somatosensory cortex to change: prospects for integration of bone-mounted dental prostheses.

1. The topographic representation of the body surface in the somatosensory cortex provides an important model system for the in vivo study of neuronal plasticity, induced changes in somatotopy providing a direct measure of plasticity not available in most parts of the central nervous system. 2. Over the past two decades, animal experimentation in a number of laboratories has shown a remarkable degree of adaptability of the cortical representation following peripheral lesions and has had a widespread influence by challenging the once-accepted dogma that the brain is a structurally fixed organ. 3. Although some aspects of original stimulation will be missing, it is likely that receptors stimulated through bone conduction and compression by bone-mounted dental prostheses preserve some of the geometric and temporal relationships of original stimulation. By analogy with data obtained from the forearm representations, it would be expected that many features of the original cortical representations will be recreated. 4. There are also examples in the literature of perceptual learning without gross changes to the cortical representation (some being within a class of adaptability known as gain control) and it is likely that perceptual integration of many dental prostheses occurs within the limits of these neural adaptation mechanisms.

Adaptation, Physiological↗

PubMed2004

Neural cell adhesion molecule in human serum. Increased levels in dementia of the Alzheimer type.

Memory impairment is a process associated with alterations in neuronal plasticity, synapses formation, and stabilization. As the neural cell adhesion molecule (NCAM) plays a key role in synaptic bond stabilization, we analyzed the usefulness of soluble NCAM isoforms in the diagnosis of patients with dementia of the Alzheimer type (DAT). NCAM was measured in the sera of 70 control subjects and 43 DAT patients (with different severity of cognitive impairment, GDS), employing Western blot and densitometric quantification. LMW-NCAM bands (100-130 kDa) decreased significantly with age independently of sex. DAT patients presented values of LMW-NCAM and HMW-NCAM significantly higher than healthy controls of similar age (higher than 130 kDa). Only LMW-NCAM was associated with GDS. Our results suggest that NCAM could be involved in the pathogenesis of DAT disorder and that serum NCAM levels could be useful as differential diagnostic markers of the disease.

Adult↗

PubMed1992

Organization and plasticity of GABA neurons and receptors in monkey visual cortex.

The GABA neurons of monkey area 17 are a morphologically and chemically heterogeneous population of interneurons that are normally distributed most densely within the geniculocortical recipient zones of the visual cortex. In adult monkeys deprived of visual input from one eye, the levels of immunoreactivity for GABA and GAD within neurons of these geniculocortical zones is reduced. Similar changes are seen in the levels of proteins that make up the GABAA receptor sub-type. The effects of monocular deprivation on other substances suggest that specific types of GABA neurons, such as those in which the tachykinin neuropeptide family and parvalbumin coexist with GABA, are greatly influenced by changes in visual input. That some proteins remain normal within deprived-eye neurons and that other proteins are increased indicates the changes in the GABA cells of the cortex are not the result of a general reduction in protein synthesis. Comparisons of what is known about the morphological and synaptic features of GABA cells in area 17 and the characteristics of cells affected by monocular deprivation suggests that certain classes, such as the clutch cell, may be preferential targets of deprivation. Such a selective loss of certain GABA neurons would have broad implications for the possible physiological plasticity of cortical cells, for if ongoing studies determine that specific receptive field properties are affected by monocular deprivation in adults, the correlation of functional properties and classes of GABA cells would be possible.

Animals↗

PubMed2006

[Functional reorganization of language in a case of cortical development disorder with continuous spike and wave during sleep].

INTRODUCTION: Left cerebral hemisphere dominance for language is a well known fact. However, this typical lateralization may be affected when left hemisphere is damaged at an early age. In this case, neuronal plasticity allows language to be totally or partially transferred to another area within the ipsilateral or contralateral hemisphere. CASE REPORT: 21 year old woman. Congenital right hemiparesis. Focal epilepsy and continuous spike and wave during NREM sleep at 4 years old. Magnetic resonance imaging: extensive malformation of cortical development in the left hemisphere. From 7 years old, seizures were controlled and the continuous spike and wave discharges disappeared. TREATMENT: Valproic acid, 500 mg/day. Neuropsychological assessment showed that basic language functions were well preserved, while there were signs of non-dominant hemisphere dysfunction. These paradoxical results, together with the fact that the patient was left-handed, established the possibility of functional reorganization of language to the right hemisphere. A functional magnetic resonance imaging (fMRI) study for language lateralization demonstrated preferential right hemisphere activation on Broca's and Wernicke's areas. CONCLUSIONS: This case shows the brain's potential for functional reorganization, especially if, according to Kennard's principle, the injury is produced at an early age.

Adult↗

PubMed1987

Behavioral stress impairs long-term potentiation in rodent hippocampus.

A number of hormones secreted from the pituitary-adrenal system during stress affect learning and memory processes. The phenomenon of hippocampal long-term potentiation (LTP) is viewed by many as a putative mechanism of memory storage and has proved a most valuable model for study of neuronal plasticity at the cellular level. The present study was conducted to investigate the possibility that stressful events which occur prior (in vivo) to the preparation of brain slices may influence the electrophysiology of the in vitro hippocampal explant when tested for LTP. Adult male rats (Long-Evans male X Sprague-Dawley female) were pair-housed 1 week prior to testing. One animal in each pair was either placed in a restraining tube for 30 min and received no tail shocks (Restraint) or placed in a restraining tube and received tail shocks (1 microA, 1 s) every minute for 30 min (Restraint + Shock). The other animal in each pair was taken directly from the home cage and received no restraint or tail shock (Control). In vitro hippocampal slices were then prepared immediately from these animals according to standard methods. Our results demonstrate a marked impairment of LTP in hippocampal explants taken from rats exposed to stress. The significance of this result with respect to cellular mechanisms underlying the relationship between stress, cognition, and learning is discussed.

Animals↗

PubMed2005

NR1, NR2A and NR2C subunits expression after cervical spinal cord transplant and section in dogs.

This paper served to evaluate the expression levels of subunits NR1, NR2A and NR2C which are implicated in neuronal plasticity events. A 50% (right half) 4 mm longitudinal resection of the spinal cord was done at the C5-C6 level with preservation of the anterior spinal artery. This was effected in a dog model after either a homologous transplant or a pure spinal cord section. In this study we used two groups of dogs with four individuals each, as well as a control group. The transplant group (n=4) was analyzed at days 3 and 28 post surgery. The section group (n=4) was also analyzed at days 3 and 28 post op. All three groups (transplant, section and control) were evaluated as to the subunit expression in each of the segments corresponding to the transplanted or sectioned sites, the site contralateral to the transplanted or sectioned sites at levels half a centimeter both proximal and distal to the site of transplant and section. The results showed a variety of changes in each of the subunits depending on the group, the segment and the time of evaluation (acute versus chronic). This could be closely related to mechanisms which participate in regeneration and functional recuperation.

Animals↗

PubMed2005

Voxel-based analysis of MRI detects abnormal visual cortex in children and adults with amblyopia.

Amblyopia, sometimes called "lazy eye," is a relatively common developmental visual disorder well characterized behaviorally; however, the neural substrates associated with amblyopia in humans remain unclear. We hypothesized that abnormalities in the cerebral cortex of subjects with amblyopia exist, possibly as a result of experience-dependent neuronal plasticity. Anatomic magnetic resonance imaging (MRI) and psychophysical vision testing was carried out on 74 subjects divided into two age ranges, 7-12 years and 18-35 years, and three diagnoses, strabismic amblyopia, anisometropic amblyopia, and normal vision. We report a behavioral impairment in contrast sensitivity for subjects with amblyopia, consistent with previous reports. When the high-resolution MRI brain images were analyzed quantitatively with optimized voxel-based morphometry, results indicated that adults and children with amblyopia have decreased gray matter volume in visual cortical regions, including the calcarine sulcus, known to contain primary visual cortex. This finding was confirmed with a separate region-of-interest analysis. For the children with amblyopia, additional gray matter reductions in parietal-occipital areas and ventral temporal cortex were detected, consistent with recent reports that amblyopia can result in spatial location and object processing deficits. These data are the first to provide possible neuroanatomic bases for the loss of binocularity and visual sensitivity in children and adults with amblyopia.

Adolescent↗

PubMed2006

MAP2 and synaptophysin protein expression following motor learning suggests dynamic regulation and distinct alterations coinciding with synaptogenesis.

Learning a new motor skill can induce neuronal plasticity in rats. Within motor cortex, learning-induced plasticity includes dendritic reorganization, synaptogenesis, and changes in synapse morphology. Behavioral studies have demonstrated that learning requires protein synthesis. It is likely that some of the proteins synthesized during learning are involved in, or the result of, learning-induced structural plasticity. We predicted the expression of proteins involved in neural plasticity would be altered in a learning dependent fashion. Long-Evans rats were trained on a series of motor tasks that varied in complexity, so that the effects of activity could be teased apart from the effects of learning. The motor cortices were examined for MAP2 and synaptophysin protein using Western blotting and immunohistochemistry. Western blotting revealed that expression of MAP2 was not detectably influenced by learning, whereas synaptophysin expression increased on day 1, 3, and 5 of complex motor skill learning. Expression of MAP2 does not seem to indicate difficulty of task or duration of training time, whereas increases in synaptophysin expression, which appear diffusely across the cortex, seem to be correlated with the first 5 days of motor skill learning. Similar findings with GAP-43 suggest the change in synaptophysin may coincide with synapse formation. Immunohistochemistry did not reveal any localized changes in protein expression. These data indicate a difference in learning-induced expression in the mammalian brain compared to reports in the literature, which have often focused on stimulation to induce alterations in protein expression.

Adaptation, Physiological↗