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Results for “Neuronal Plasticity”

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PubMed2004

[Vital investigation of the genome activity and neuronal synaptic plasticity in snail in the course of learning].

Vital investigation of genome activity and its role in mechanisms of long-term synaptic plasticity formation were studied in LP11 neuron (command neurone of defence behaviour) during sensitisation (simple form of learning) in semi-intact preparation of snail Helix lucorum. Genome activity was investigate by means of specific fluorescent dye SYTO 16 and image analysis system. It was found that application of sensitizing stimulation (10% quinine solution) onto the snail head initiate two-phase changes in neural responses evoked by tactile or chemical stimulation. Depression of neural responses was obtained during short-term phase (during 1 hour after sensitization) and facilitation of neural responses--during long-term phases (over 1 hour). At the same time (15-20 min after learning), a significant increase in SYTO 16 fluorescent level was found in nucleus site LP11 neurone. Initial SYTO 16 fluorescence level was registered in 4-5 hours after sensitization. If the sensitization was produced during actinomycin D application (inhibitor of RNA synthesis, 20 microM) then facilitation of neural responses evoked by sensory stimulation were suppressed during long-term phase of sensitization and was the same as in control sensitized snails during short-term phase of learning. Increase in SYTO 16 fluorescence level in nucleus region site of LP11 neurone was completely prevented in sensitization during actinomycin D application. If actinomycin D was applied 30 min after sensitization (1 hour after first sensitizing stimulation) then synaptic facilitation and fluorescent dynamics was the same as in control sensitized snails. Our experimental data showed that nociceptive sensitization development was followed by quick (15-20 min) DNA activation and long-term synaptic facilitation (1 hour after sensitization), while induction of the processes was suppressed by inhibitor of RNA synthesis during short time interval (during 1 hour of learning).

Animals↗

PubMed2002

Diabetes, but not stress, reduces neuronal nitric oxide synthase expression in rat hippocampus: implications for hippocampal synaptic plasticity.

Neuronal nitric oxide synthase (nNOS) plays an important role in synaptic plasticity and learning and memory. Since deficits in long-term potentiation (LTP) and learning are observed in diabetic rats and following stress, we examined the expression of nNOS mRNA and protein in the hippocampus of streptozotocin (STZ) diabetic rats and rats subjected to restraint stress. Stress did not modulate nNOS expression, while nNOS mRNA and protein levels were significantly decreased in the hippocampus of STZ diabetic rats. These results suggest that: (1) decreased expression of nNOS mRNA and protein may contribute to deficits in hippocampal dependent learning and LTP in diabetic rats; and (2) other mechanisms may be involved in stress mediated decreases in hippocampal synaptic plasticity.

Animals↗

PubMed2000

The neuron as a dynamic electrogenic machine: modulation of sodium-channel expression as a basis for functional plasticity in neurons.

Neurons signal each other via regenerative electrical impulses (action potentials) and thus can be thought of as electrogenic machines. Voltage-gated sodium channels produce the depolarizations necessary for action potential activity in most neurons and, in this respect, lie close to the heart of the electrogenic machinery. Although classical neurophysiological doctrine accorded 'the' sodium channel a crucial role in electrogenesis, it is now clear that nearly a dozen genes encode distinct sodium channels with different molecular structures and functional properties, and the majority of these channels are expressed within the mammalian nervous system. The transcription of these sodium-channel genes, and the deployment of the channels that they encode, can change significantly within neurons following various injuries. Moreover, the transcription of these genes and the deployment of various types of sodium channels within neurons of the normal nervous system can change markedly as neurons respond to changing milieus or physiological inputs. As a result of these changes in sodium-channel expression, the membranes of neurons may be retuned so as to alter their transductive and/or encoding properties. Neurons within the normal and injured nervous system can thus function as dynamic electrogenic machines with electroresponsive properties that change not only in response to pathological insults, but also in response to shifting functional needs.

Action Potentials↗

PubMed2005

The pathogenesis of clinical depression: stressor- and cytokine-induced alterations of neuroplasticity.

Stressful events promote neurochemical changes that may be involved in the provocation of depressive disorder. In addition to neuroendocrine substrates (e.g. corticotropin releasing hormone, and corticoids) and central neurotransmitters (serotonin and GABA), alterations of neuronal plasticity or even neuronal survival may play a role in depression. Indeed, depression and chronic stressor exposure typically reduce levels of growth factors, including brain-derived neurotrophic factor and anti-apoptotic factors (e.g. bcl-2), as well as impair processes of neuronal branching and neurogenesis. Although such effects may result from elevated corticoids, they may also stem from activation of the inflammatory immune system, particularly the immune signaling cytokines. In fact, several proinflammatory cytokines, such as interleukin-1, tumor necrosis factor-alpha and interferon-gamma, influence neuronal functioning through processes involving apoptosis, excitotoxicity, oxidative stress and metabolic derangement. Support for the involvement of cytokines in depression comes from studies showing their elevation in severe depressive illness and following stressor exposure, and that cytokine immunotherapy (e.g. interferon-alpha) elicited depressive symptoms that were amenable to antidepressant treatment. It is suggested that stressors and cytokines share a common ability to impair neuronal plasticity and at the same time altering neurotransmission, ultimately contributing to depression. Thus, depressive illness may be considered a disorder of neuroplasticity as well as one of neurochemical imbalances, and cytokines may act as mediators of both aspects of this illness.

Animals↗

PubMed1987

Expression of tyrosine hydroxylase in neurons of cultured cerebral cortex: evidence for phenotypic plasticity in neurons of the CNS.

In vivo, neurons of the cerebral cortex of rat embryos did not stain with antibodies to the catecholamine (CA) biosynthetic enzyme tyrosine hydroxylase (TH) even when examined using a highly sensitive technique for radioimmunocytochemistry. However, when embryonic day (E) 13 cortex was grown 1 d in culture, several thousand cells expressed immunoreactive and catalytically active TH. All TH cells simultaneously labeled with the neuronal enzyme, neuronal specific enolase, indicating that the TH was exclusively localized in neurons. Moreover, all TH neurons were postmitotic since they did not incorporate 3H-thymidine. With time in culture, the number of TH cells selectively declined from nearly 3000 cells at 2 d to several cells at 14 d. Similarly, the number of neurons competent to express TH in culture declined with advancing age of the donor embryo. Thus, by E18, very few cortical neurons had the capacity to express TH. We conclude that during a critical period of development, postmitotic cerebral cortical neurons can express catecholamine traits in vitro but not in vivo. Thus, the neurotransmitter phenotype of certain classes of central neurons is not fixed but can be influenced by epigenetic factors found in their environment, thereby providing evidence of phenotypic plasticity in the central nervous system (CNS).

Animals↗

PubMedDate not supplied

[Pacemaker plasticity of the command neuron of a defensive reflex in the snail].

In an identified command neurone, a linear dependence has been found of the amplitude of the pneumostome muscles' contraction on the number of APs generated by the neurone. The adaptive nature of the motor reaction is confirmed by the existence of elementary motor acts triggered by each AP. During a series of repetitive application of intracellular rectangular electric pulses, habituation is developing in the shape of a gradual reduction of APs number and a corresponding gradual decrease of the amplitude of the pneumostome muscles' contraction. It has been shown that neuronal plasticity in response to repetitive action of the intracellular depolarizing current develops due to a change in the excitability of the pacemaker mechanism.

Animals↗

PubMed1997

BDNF potentiates spontaneous Ca2+ oscillations in cultured hippocampal neurons.

Brain-derived neurotrophic factor (BDNF) is thought to regulate neuronal plasticity in developing and matured neurons, although the molecular mechanisms are less well characterized. We monitored changes in the intracellular calcium (Ca2+) levels induced by BDNF using a fluorescence Ca2+ indicator (Fluo-3) by means of confocal laser microscopy in rat cultured hippocampal neurons. BDNF acutely potentiated spontaneous Ca2+ oscillations in dendrites and also in the soma of several neurons, although it increased intracellular Ca2+ in only selective proportion of resting neurons without Ca2+ oscillations. The potentiation was observed both in the frequency and the amplitude of Ca2+ oscillations, completely blocked by K-252a, and significantly reduced by 2-aminophosphonovaleric acid. These findings suggest that BDNF increases glutamate release and N-methyl-D-aspartate (NMDA) channel-gated Ca2+ influx via TrkB and regulates the frequency and the amplitude of Ca2+ oscillations. BDNF may have the potential to modulate spontaneous Ca2+ oscillations to regulate neuronal plasticity in developing hippocampal neurons.

2-Amino-5-phosphonovalerate↗

PubMed1995

Collateral sprouting and responsiveness to nerve growth factor of ageing neurons.

Loss of neuronal plasticity and/or alterations in neuronal targets with ageing can induce degenerative phenomena in the nervous system. To study the possible contribution of reduced neuronal plasticity to age-related neurodegeneration, we examined the sprouting response to aged rat iridial nerves on in oculo grafts of peripheral tissues taken from young and old animals. Contrary to previous observations in young hosts, both young and old transplants became re-innervated by host nerves to a similar extent, with a nerve density which was typical of old target tissue in situ. Nerve growth factor treatment increased the innervation density on all transplants. However, the increase was significant only on young target tissues.

Aging↗

PubMed2002

Neuronal responses of the rat amygdala during extinction and reassociation learning in elementary and configural associative tasks.

To investigate functional heterogeneity within the amygdala in appetitive conditioned instrumental behaviours, neuronal activity was recorded from the amygdala of behaving rats during learning and discrimination of conditioned sensory stimuli associated with or without reinforcement [sucrose solution, intracranial self-stimulation (ICSS)]. Sensory stimuli included auditory (tone), visual (light) and configural (simultaneous presentation of tone and light) stimuli. The rat was trained to lick a spout protruded close to its mouth just after a conditioned sensory stimulus to obtain a reward. Of the 609 neurons recorded from the amygdala and amygdalostriatal transition area, 154 responded to one or more sensory stimuli. The 62 amygdalar neurons responded strongly to certain conditioned sensory stimuli associated with rewards. Of these 62 neurons, 45 were tested with the extinction trials. Responses of 31 neurons to conditioned stimuli were finally extinguished, and those of the remaining 14 were not extinguished. Furthermore, responses of 26 of these 31 neurons resumed in the relearning trials (plastic neurons), suggesting that these sensory responses were associative rather than just responses to physical properties of the stimuli. These plastic neurons were located mainly in the basolateral nucleus of the amygdala, and responses of the plastic neurons were correlated with behavioural responses. These results suggest that the basolateral nucleus is crucial in associative learning between sensory information and affective significance for behavioural outputs in appetitive conditioned instrumental behaviours.

Acoustic Stimulation↗

PubMed1988

A cellular analogue of visual cortical plasticity.

Neuronal activity plays an important role in the development of the visual pathway. The modulation of synaptic transmission by temporal correlation between pre- and postsynaptic activity is one mechanism which could underly visual cortical plasticity. We report here that functional changes in single neurons of area 17, analogous to those known to take place during epigenesis of visual cortex, can be induced experimentally during the time of recording. This was done by a differential pairing procedure, during which iontophoresis was used to artificially increase the visual response for a given stimulus, and to decrease (or block) the response for a second stimulus which differed in ocularity or orientation. Long-term modifications in ocular dominance and orientation selectivity were produced in 33% and 43% of recorded cells respectively. Neuronal selectivity was nearly always displaced towards the stimulus paired with the reinforced visual response. The largest changes were obtained at the peak of the critical period in normally reared and visually deprived kittens, but changes were also observed in adults. Our findings support the role of temporal correlation between pre- and postsynaptic activity in the induction of long-lasting modifications of synaptic transmission during development, and in associative learning.

Afferent Pathways↗

PubMed2003

Mitochondrial potassium channels and uncoupling proteins in synaptic plasticity and neuronal cell death.

The function of the nervous system relies upon synaptic transmission, a process in which a neurotransmitter released from pre-synaptic terminals of one neuron (in response to membrane depolarization and calcium influx) activates post-synaptic receptors on dendrites of another neuron. Synapses are subjected to repeated bouts of oxidative and metabolic stress as the result of changing ion gradients and ATP usage. Mitochondria play central roles in meeting the demands of synapses for ATP and in regulating calcium homeostasis, and mitochondrial dysfunction can cause dysfunction and degeneration of synapses, and can trigger cell death. We have identified two types of mitochondrial proteins that serve the function of protecting synapses and neurons against dysfunction and death. Mitochondrial ATP-sensitive potassium (MitoKATP) channels modulate inner membrane potential and oxyradical production; mitochondrial potassium fluxes can affect cytochrome c release and caspase activation and may determine whether neurons live or die in experimental models of stroke and Alzheimer's disease. Uncoupling proteins (UCPs) are a family of mitochondrial membrane proteins that uncouple electron transport from ATP production by transporting protons across the inner membrane. Neurons express at least three UCPs including the widely expressed UCP-2 and the neuron-specific UCP-4 and UCP-5 (BMCP-1). We have found that UCP-4 protects neurons against apoptosis by a mechanism involving suppression of oxyradical production and stabilization of cellular calcium homeostasis. The expression of UCP-4 is itself regulated by changes in energy metabolism. In addition to their roles in neuronal cell survival and death, MitoKATP channels and UCPs may play roles in regulating neuronal differentiation during development and synaptic plasticity in the adult.

Apoptosis↗

PubMed2006

Methyl-CpG binding proteins are involved in restricting differentiation plasticity in neurons.

Neurons and astrocytes are generated from common neural precursors, yet neurogenesis precedes astrocytogenesis, which normally commences at later stages of development. We have previously reported that a particular cytosine residue within a STAT3-binding site in the astrocyte-specific marker glial fibrillary acidic protein (GFAP) gene promoter becomes demethylated in neuroepithelial cells as gestation proceeds. This demethylation correlates tightly with the onset of astrocyte differentiation, suggesting that a change in DNA methylation at cell-type-specific gene promoters controls the switch from neurogenesis to astrocytogenesis in the developing brain. Here, we show that late-gestation neuroepithelial cells, which have already lost the methylation in the STAT3-binding site within the GFAP promoter, can still give rise to neurons and that these neurons do not respond to a STAT3-activating cytokine to express GFAP. Members of a transcriptional repressor family, the methylated-CpG binding proteins (MBDs), including MeCP2, are predominantly expressed in neurons, and ectopic MeCP2 expression inhibited astrocyte differentiation of neuroepithelial cells. Moreover, we found that exon 1 of the GFAP gene remains hypermethylated even in neuroepithelial cells at a late developmental stage and in neurons differentiated from such neuroepithelial cells. We further demonstrate that MeCP2 actually binds to the highly methylated exon 1 of the GFAP gene in neurons. These results suggest that region-specific DNA methylation and MBDs play an important role in the regulation of differentiation plasticity in neurons.

Animals↗

PubMed1996

Impaired plasticity of neurons in aging. Biochemical, biophysical, and behavioral studies.

Age-related correlation of impaired plasticity of neurons (biochemical and biophysical aspects) and behavioral alterations were investigated in young (3.5 months) and extremely aged (approximately 40 months) female Wistar rats. Age-dependent significant differences in second messenger (cAMP and Ins (1,4,5)P3) concentration and signal transduction via muscarinic and dopaminergic receptors were found. The results point to the specifically impaired coupling between dopamine D1 receptor and GS protein, which underlies normal brain aging. However, cholinergic neurotransmission may be modulated at another level in extremely aged rats. Thus, it appears that the site of affection in coupling of receptor and G protein and/or G protein-dependent signal transduction in aging cannot be generalized. This indicates that alterations in the coupling of signal transduction depend on diverse neurotransmitter receptors with advanced age. The age-dependent alterations in the cAMP and PI signal pathways could be due to changes in the physical properties of the membranes. To support this hypothesis, age-dependent changes in the physical state and the biochemical composition of synaptosomal membranes from the cortex, cerebellum, and striatum were examined by measuring the steady-state fluorescence amisotropy of the membrane probes 1,6-diphenyl-1,3,5-hexatriene (DPH), trimethylammonium-DPH (TMA-DPH), and trimethylammoniumpropyl-DPH (TMAP-DPH). Significant differences in the physical properties of the synaptosomal membranes existed between young and very aged rats, expressed by a higher anisotropy in the 40-month-old rat brain tissue. The changes in the physical properties of the membranes were in line with the determined age-dependent alterations in the chemical composition, e.g., the increase in cholesterol content of the aged membranes.

Age Factors↗

PubMed2005

Neuronal-glial plasticity in gonadotropin-releasing hormone release in adult female rats: role of the polysialylated form of the neural cell adhesion molecule.

The gonadotropin-releasing hormone (GnRH) neurosecretory system undergoes marked structural and functional changes during the ovarian cycle. The aim of this study was to examine the neuroanatomical relationship between GnRH neurons and a polysialylated form of neural cell adhesion molecule (PSA-NCAM), a known marker of neuronal plasticity. Using immunohistofluorescent dual labeling, we determined that axon terminals of GnRH in the median arcuate nucleus (ME-ARC) region of the hypothalamus in the proestrous phase of the estrous cycle were intimately associated with PSA-NCAM. To further examine whether PSA-NCAM expression associated with GnRH neuron terminals varies in conjugation with cyclic changes in ovarian steroid hormone levels, we examined GnRH and PSA-NCAM dual expression in ovariectomized (OVX) and estrogen-progesterone-primed OVX (EBP-OVX) rats. The expression of PSA-NCAM immunoreactivity associated with the GnRH neurons in the proestrous phase and EBP-OVX rats was significantly higher than during the diestrous phase and in OVX rats where GnRH secretion declines. We further examined whether the structural changes in GnRH axon terminals in the ME-ARC region are also associated with glial plasticity. By extension and retraction of the glial processes, the GnRH neuron terminals in the ME-ARC region could undergo dynamic plastic changes that control GnRH release during the proestrous phase. PSA-NCAM expression was also seen on glial cells in the ME-ARC region. The close association between PSA-NCAM on GnRH and glial cells in the ME-ARC region of the hypothalamus in the rat showed dynamic structural changes in GnRH neuron terminals during the estrous cycle. These observations suggested that PSA-NCAM may act as a molecular substrate to promote neuroplastic changes in the GnRH neurosecretory system.

Animals↗

PubMed2006

Organelles and trafficking machinery for postsynaptic plasticity.

Neurons are among the largest and most complex cells in the body. Their immense size and intricate geometry pose many unique cell-biological problems. How is dendritic architecture established and maintained? How do neurons traffic newly synthesized integral membrane proteins over such long distances to synapses? Functionally, protein trafficking to and from the postsynaptic membrane has emerged as a key mechanism underlying various forms of synaptic plasticity. Which organelles are involved in postsynaptic trafficking, and how do they integrate and respond to activity at individual synapses? Here we review what is currently known about long-range trafficking of newly synthesized postsynaptic proteins as well as the local rules that govern postsynaptic trafficking at individual synapses.

Animals↗

PubMed2006

Extensive enriched environments protect old rats from the aging dependent impairment of spatial cognition, synaptic plasticity and nitric oxide production.

In aged rodents, neuronal plasticity decreases while spatial learning and working memory (WM) deficits increase. As it is well known, rats reared in enriched environments (EE) show better cognitive performances and an increased neuronal plasticity than rats reared in standard environments (SE). We hypothesized that EE could preserve the aged animals from cognitive impairment through NO dependent mechanisms of neuronal plasticity. WM performance and plasticity were measured in 27-month-old rats from EE and SE. EE animals showed a better spatial WM performance (66% increase) than SE ones. Cytosolic NOS activity was 128 and 155% higher in EE male and female rats, respectively. Mitochondrial NOS activity and expression were also significantly higher in EE male and female rats. Mitochondrial NOS protein expression was higher in brain submitochondrial membranes from EE reared rats. Complex I activity was 70-80% increased in EE as compared to SE rats. A significant increase in the area of NADPH-d reactive neurons was observed in the parietotemporal cortex and CA1 hippocampal region of EE animals.

Aging↗

PubMed1986

Central nervous system repair and nerve cell cultures.

Is anatomical and functional repair following injury or disease in the adult brain and spinal cord possible, and to what extent? Current evidence concerning neuronal plasticity of mature neurons suggests that opportunities may exist provided the variables are understood. Highly informative are the cellular and molecular processes regulated, in the mature CNS, by growth-promoting molecules directed to neurons. In this field neuronal cell culture methodology has proven to be indispensable and its application may in the future contribute significantly to the development of novel therapeutical strategies.

Animals↗

PubMed1997

Differential changes in the expression of AMPA receptors genes in rat brain after chronic exposure to ethanol: an in situ hybridization study.

Chronic treatment with ethanol of adult rat was used as an experimental paradigm to investigate changes in the expression of glutamate receptor genes under the condition of a slowly progressing neurodegeneration that is associated with a plastic neuronal growth response. Effects of chronic oral ethanol exposure (20% v/v, 28 weeks) on the expression of the AMPA receptor mRNA subtypes GluR-A, GluR-B and GluR-C (flip variants) were analysed in the rat hippocampus by in situ hybridization and subsequent quantitative autoradiography. In both controls and ethanol treated animals strong hybridization signals could be detected over pyramidal neurones and dentate gyrus cells. GluR-C mRNA was elevated by 15% to 30%, while expression of the AMPA receptor transcripts GluR-A and GluR-B were not significantly altered after ethanol treatment. The present findings demonstrate that chronic ethanol exposure affects gene expression of AMPA receptor subtypes differentially. Differential influences of distinct AMPA-receptor subtypes on neuronal survival and plastic neuronal response under conditions of chronic neuronal degeneration might, therefore, be suggested.

Alcoholism↗