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PubMed1994

Growth-associated protein-43 and protein gene-product 9.5 innervation in human pancreas: changes in chronic pancreatitis.

Growth-associated protein-43, an established marker of neuronal plasticity during development and in injury, was used to characterize innervation in the normal human pancreas and changes in chronic alcohol-induced pancreatitis by using light microscopic immunocytochemistry and computer-assisted image analysis. Immunostaining for the pan-neuronal marker protein gene-product 9.5 served as a reference for the characterization of total innervation in both groups. In normal human pancreas, strong protein gene-product 9.5 immunostaining revealed all nerve fibres in nerve trunks, all neuronal cell bodies and the entire parenchymal innervation. In contrast, growth-associated protein-43 immunoreactivity was restricted to a few nerve fibres in interlobular nerve trunks and to fine varicose nerve fibres supplying the parenchyma, blood vessels, pancreatic ducts and intrinsic ganglia. In cell bodies of intrinsic neurons, growth-associated protein-43 immunoreactivity was absent or extremely faint. In chronic pancreatitis, the protein gene-product 9.5 innervation exhibited region-specific changes. In areas with reduced parenchyma, the protein gene-product 9.5 innervation was sparse. In fibrotic regions, which are characteristic for advanced stages of chronic pancreatitis, enlarged nerve trunks showing neuroma-like formations were heavily stained for protein gene-product 9.5. In fibrotic tissue, protein gene-product 9.5-containing nerve fibres were extremely rare. The growth-associated protein-43 innervation in chronic pancreatitis was characterized by a dramatic increase, which was most pronounced in the enlarged nerve trunks. Such nerve trunks were frequently surrounded by infiltrates of immune cells, which in some cases formed follicle-like structures. Digital image analysis of adjacent sections and double fluorescence immunocytochemistry revealed that growth-associated protein-43 immunoreactivity was present in the vast majority of protein gene-product 9.5-immunoreactive nerve fibres. In contrast to the normal pancreas, a major subpopulation of intrinsic neurons immunostained for growth-associated protein-43. The expression of growth-associated protein-43 in the terminal fields of pancreatic nerve suggests that the innervation of the normal human pancreas undergoes continual and toposelective remodelling. The increase in the density of growth-associated protein-43 immunoreactive nerve fibres in enlarged nerve trunks paralleled by augmented expression of growth-associated protein-43 in intrinsic neurons and reduced parenchymal growth-associated protein-43-immunoreactive innervation underline the dramatic plasticity of pancreatic innervation in chronic pancreatitis.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1974

Plasticity in small neuronal assemblies.

When spike activity of two or more individual neurons is simultaneously recorded, it is possible to detect various types of neuronal connections to and between the observed neurons by making appropriate statistical analysis of the data. Such methods are reviewed. This approach is particularly useful in seeking changes of neuronal connectivity associated with behavioral plasticity. Examples from experiments with Aplysia and crayfish are given.

Animals↗
PubMed2005

Galanin plasticity in the cholinergic basal forebrain in Alzheimer's disease and transgenic mice.

Galanin (GAL) is a biologically active 29 amino acid (30 in humans) which participates in the modulation of several ascending neurotransmitter systems including cholinergic basal forebrain (CBF) neurons, which undergo extensive degeneration in Alzheimer's disease (AD). GAL immunoreactive fibers within the CBF display hypertrophy and hyperinnervate surviving CBF neurons in late AD. Over the years, this unique neuronal plasticity response has been an active area of research for our group. We have examined tissue from a clinically well characterized cohort of retired elderly clergy to determine whether people with mild cognitive impairment display GAL hyperinnervation upon CBF neurons. We found that GAL hyperinnervation is a late stage event and that CBF neuron reduction is not correlated with GAL over expression during prodromal AD. Interestingly, findings from our laboratory using tau immunohistochemistry and single cell gene array technologies suggest that GAL remodeling may influence neurofibrillary tangle formation by altering tau phosphorylation events in CBF neurons in AD. Studies using GAL-tg mice suggest that GAL over expression reduces the cholinergic phenotype but does not produce a frank loss of CBF cells. This phenotypic down regulation of ChAT is reminiscent of the lack of a frank CBF neuron loss in prodromal AD. Moreover, studies using mice transgenic for both the amyloid precursor protein (APP) and presenilin-1 (PS1) bearing AD-related mutations (APPswe/PS1delta9) displayed increased GAL immunoreactive fibers, neurities and plaques in cortex and hippocampus. These fin'dings provide evidence for a mechanistic relationship between amyloidosis and GAL over expression in AD. Understanding GALs role in the clinical and pathological features of AD, may lead to novel drug treatments for this disease.

Acetylcholine↗
PubMed1995

Learning-induced expression of meningeal ependymin mRNA and demonstration of ependymin in neurons and glial cells.

The turnover of a CNS-specific cell adhesion glycoprotein, ependymin, has earlier been found to increase during periods of neuronal plasticity. Here, ependymin mRNA expression was analyzed by semiquantitative in situ hybridization in goldfish. Learning of an active avoidance response resulted in a significant increase in ependymin mRNA expression 20 min to 4 h after acquisition of the task. In contrast, yoked control animals that were exposed to the same numbers of conditioned and unconditioned stimuli in a random, unpaired manner exhibited a strong down-regulation of ependymin mRNA. Hybridization signals were also increased by injection of anti-ependymin antiserum into brain ventricles. Ependymin mRNA was exclusively localized to reticular-shaped fibroblasts of the inner endomeningeal cell layer. Immunoelectron microscopic investigation, however, revealed ependymin also in distinct neuronal and glial cell populations in which no ependymin mRNA had been detected. Uptake of meningeal protein factors into glial and neuronal cells may therefore be of functional importance for plastic adaptations of the CNS.

Animals↗
PubMedDate not supplied

[The analysis of the impulse activity of 2 neurons monosynaptically excitable by a 3rd using cross-correlation histograms and Cox's method. The potential for detecting neuronal and synaptic plasticity].

By a method of mathematical modelling exogenic stationary random single impulse activity was reproduced of two neurones (N1 and N2), monosynaptically excited by a third one (N3). Value P12, defined from cross-correlation histogram and Cox coefficient beta 12 were used to evaluate the degree of dependence of N1 and N2 impulse trains. Dynamics of P12, beta 12 and of values of P1*, P2* and P3* proportional to corresponding mean interimpulse intervals of N1, N2 and N3, was studied under changes of efficiency of interneuronal connections, neurones excitability and summate action on them of independent random afferent synaptic inflows. It has been shown that the increase (decrease) of P12 or beta 12 accompanied by decrease (increase) of P1* and P2* is a sign of plastic change or N3 discharges frequency, or a sign of plastic changes of the amplitude of excited postsynaptic potentials elicited by these discharges.

Animals↗
PubMed1992

Glutamate selectively increases the high-threshold Ca2+ channel current in sensory and hippocampal neurons.

Previous studies resulted in conflicting conclusions that glutamate application either decreases or increases the activity of Ca2+ channels in hippocampal neurons. We studied whole-cell Ca2+ currents (ICa) in chick dorsal root ganglion neurons and rat hippocampal cells. For both cell types glutamate (1-30 microM) increased high-threshold Ca2+ current. It was independent of the charge carriers, Ca2+ or Ba2+. Low-threshold Ca2+ channel current and the fast sodium current were not changed with glutamate application. The effect developed within 1-2 min and then further facilitated after washout of the agonist. A second application of glutamate produced no additional increase in ICa. No changes in the time-course of whole-cell currents were observed, suggesting that glutamate recruits 'sleepy' Ca2+ channels. Whatever its mechanism, overlasting increase of ICa by glutamate may be important in neuronal plasticity.

Animals↗
PubMed1995

Immunocytochemical study of phenotypic plasticity of cultured dorsal root ganglion neurons during development.

Rat dorsal root ganglia (DRG) were cultured from different stages of development ranging from embryonic day-14 to adult. The expression of eight neurotransmitter phenotypes was examined with immunocytochemical detection and the percentages of each phenotype were calculated with reference to the whole neuronal population defined by the expression of neuron-specific enolase (NSE). The expression of peptides, calcitonin gene-related peptide (CGRP), substance P (SP), cholecystokinin (CCK) and neuropeptide Y (NPY) was always present whatever the age at onset of the cultures. Although the percentage of CGRP remained stable, that of the other peptides declined progressively. Their in-vitro expression did not differ markedly from that found in vivo. Another group of neurotransmitters, including 5-hydroxytryptamine (5-HT), thyrotropin-releasing hormone (TRH) and gamma-aminobutyric acid (GABA) was never expressed in situ in DRG neurons. In culture, they were expressed in a high percentage of neurons, especially for 5-HT and TRH, and they showed a similar evolution, with a decrease at early postnatal ages followed by a further increase. This profile suggests that the expression of these transmitters is strongly environment-dependent and may be repressed in situ. Finally, somatostatin (SOM) was found only in cultures prepared from adult tissues, whereas it was present in situ from the embryo onwards. The expression of this peptide would thus require a stabilization by a long exposure to environmental factors. We can conclude that the great diversity of phenotypic expression found in DRG neurons in situ is the result of a wide variety of influences occurring at different stages of development in a large potential repertory present in these neurons.

Animals↗
PubMed2005

Interference with activity-dependent transcriptional activation of BDNF gene depending upon the expanded polyglutamines in neurons.

Expanded polyglutamines (polyQ) have been demonstrated to impair the CREB-dependent transcription in established cell lines. Since activity-dependent transcription in neurons, which plays an important role in forming neuronal plasticity, is largely controlled by CREB, it is important to study whether polyQ interferes with the activity-dependent transcriptional activation of genes in neurons. In cultured rat cortical neurons, over-expression of truncated dentatorubral-pallidoluysian atrophy proteins containing expanded polyQ, which form aggregation bodies in nucleus, reduced the calcium (Ca(2+)) signal-mediated transcriptional activation of brain-derived neurotrophic factor, c-fos, and pituitary adenylate cyclase-activating polypeptide gene promoters in a dose-dependent manner. The interference with the transcriptional activation was dependent upon the presence of polyQ, the strength of which was increased as the length of polyQ stretches was expanded. Thus, polyQ interferes with the activity-dependent transcription in a polyQ-length-dependent manner, which may correspond to the severity of polyglutamine diseases.

Animals↗
PubMed2005

Theta bursts set up glutamatergic as well as GABA-ergic plasticity in neonatal rat hippocampal CA1 neurons.

gamma-Aminobutyric acid (GABA) is inhibitory in adult, but excitatory in neonatal, neurons. The switch from excitatory to inhibitory action is due to a negative shift in the equilibrium potential for the GABA(A) receptor-mediated postsynaptic current (E(GABA-PSC)). Here, we report that, in neonatal rat hippocampal CA1 neurons, presynaptic theta-burst activation induces not only a shift in E(GABA-PSC) towards that in adult neurons, but also a recruitment of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-receptor-mediated postsynaptic currents.

2-Amino-5-phosphonovalerate↗
PubMed1997

De novo protein synthesis in isolated axons of identified neurons.

Neurons are highly polarized cells that contain a wealth of cytoplasmic and membrane proteins required for neurotransmission, synapse formation and various forms of neuronal plasticity. Typically, these proteins are differentially distributed over somatic, dendritic and axonal compartments. Until recently, it was believed that all proteins destined for various neuronal sites were synthesized exclusively in the somata and were subsequently targeted to appropriate extrasomal compartments. The discovery of various messenger RNA molecules in both dendrites and axons is suggestive of de novo protein synthesis in extrasomatic regions. The latter process has been demonstrated in few neuronal svrstems, but direct proof for the axonal transcription of a specific protein from a given messenger RNA is still lacking. This lack of fundamental knowledge in the field of cellular and molecular neurobiology is due primarily to both anatomical and experimental difficulties encountered in most animal preparations studied thus far. In this study we developed a neuronal experimental system comprising of individually identified neurons and their isolated axons from the mollusc Lymnaea stagnalis. We injected a foreign messenger RNA encoding a peptide precursor into the isolated axons of cultured neurons; and utilizing cellular, molecular and immunocytochemical techniques, we provide direct evidence for specific protein synthesis in isolated axons. The Lymnaea model provides us with an opportunity to examine the role and specificity of de novo protein synthesis in the extrasomal regions.

Animals↗
PubMed1997

Plasticity of Na+ channels in afferent neurones innervating rat urinary bladder following spinal cord injury.

1. Whole-cell patch-clamp recordings in combination with axonal tracing techniques were used to investigate the effects of chronic spinal cord injury on the electrical properties of dorsal root ganglion neurones innervating the urinary bladder or colon of the adult rat. 2. In spinal intact animals, the majority (73-74%) of bladder and colon neurones which were small in size exhibited high-threshold humped spikes mediated by tetrodotoxin (TTX)-resistant Na+ channels, whereas large neurones had low-threshold narrow spikes mediated by TTX-sensitive Na+ channels. 3. In chronic spinal transected animals, 60% of bladder afferent neurones exhibited TTX-sensitive low-threshold spikes. The average diameter and input capacitance of the cells were significantly larger than those of cells obtained from spinal intact animals. 4. In bladder afferent neurones from chronic spinal transected rats, the density of TTX-resistant Na+ currents significantly decreased from 60.5 to 17.9 pA pF-1, whereas that of TTX-sensitive currents increased from 32.1 to 80.6 pA pF-1. 5. These changes in action potential and Na+ current characteristics were not detected in colon afferent neurones following spinal cord injury. 6. The results indicate that spinal cord injury increases bladder afferent neurone excitability by shifting the expression of Na+ channels from a high-threshold TTX-resistant type to a low-threshold TTX-sensitive type. This change in properties may occur in response to alterations in neurotrophic signals originating in the hypertrophied bladder.

Action Potentials↗
PubMed2003

Long-term plasticity of ipsilesional medial vestibular nucleus neurons after unilateral labyrinthectomy.

Unilateral labyrinthectomy results in oculomotor and postural disturbances that regress in a few days during vestibular compensation. The long-term (after 1 mo) consequences of unilateral labyrinthectomy were investigated by characterizing the static and dynamic membrane properties of the ipsilesional vestibular neurons recorded intracellularly in guinea pig brain stem slices. We compared the responses of type A and type B medial vestibular nucleus neurons identified in vitro to current steps and ramps and to sinusoidal currents of various frequencies. All ipsilesional vestibular neurons were depolarized by 6-10 mV at rest compared with the cells recorded from control slices. Both their average membrane potential and firing threshold were more depolarized, which suggests that changes in active conductances compensated for the loss of excitatory afferents. The afterhyperpolarization and discharge regularity of type B but not type A neurons were increased. All ipsilesional vestibular cells became more sensitive to current injections over a large range of frequencies (0.2-30 Hz), but this increase in sensitivity was greater for type B than for type A neurons. This was associated with an increase of the peak frequency of linear response restricted to type B neurons, from 4-6 to 12-14 Hz. Altogether, we show that long-term vestibular compensation involves major changes in the membrane properties of vestibular neurons on the deafferented side. Many of the static and dynamic membrane properties of type B neurons became more similar to those of type A neurons than in control slices, leading to an increase in the overall homogeneity of medial vestibular nucleus neurons.

Action Potentials↗
PubMed2000

Seasonal plasticity of synaptic connections between identified neurones in Lymnaea.

Here we investigate the synaptic connectivity of the giant dopamine containing neurone (RPeDI) of Lymnaea stagnalis during the winter months, in wild and laboratory bred animals. RPeD1 is one of the three neurones forming the respiratory central pattern generator (CPG) in Lymnaea and initiates ventilation under normal circumstances. Many of the follower cells of RPeD1 are ventilatory motor neurones. The connections of RPeD1 to its follower cells were investigated using standard intracellular recording techniques and dopamine was applied to the follower cells using a puffer pipette. During February and early March, RPeD1 was functionally disconnected from its follower cells, but connections reappeared towards the end of March. Most functionally disconnected cells failed to respond to applied dopamine, consistent with the hypothesis that there is down regulation of dopamine receptors in the follower cells of RPeD1 in the winter months. Behaviourally, Lymnaea that survive the winter, are not active at this time and do not indulge in lung ventilation, but stay quiescent. Thus functional disconnection of neurones from the CPG may be either a cause or a consequence of this change in behaviour.

Animals↗
PubMed2002

Stability and plasticity of developing synapses in hippocampal neuronal cultures.

To explore mechanisms governing the formation, stability, and elimination of synapses during neuronal development, we used FM 1-43 fluorescence imaging to track vesicle turnover at >7000 individually identified developing synapses between embryonic rat hippocampal neurons in culture. The majority of presynaptic boutons were stable in efficacy and position over a period of 1.5 hr. Activity, evoked by burst-patterned field stimulation, decreased presynaptic function across the population of boutons, an effect that required NMDA receptor activation. Decreased FM 1-43 staining correlated with low synapsin-I and synaptophysin immunoreactivities, suggesting that decreased presynaptic function was commensurate with synaptic disassembly. These observations provide new information on the stability of developing presynaptic function and suggest that NMDA receptor activation may regulate the stability of developing synapses.

Animals↗
PubMedDate not supplied

[The effect of leukotrienes B4, C4, 12-hydroxyeicosatetraenoic acid and of the threo- and erythro-epimers of hepoxilin B3 on the plasticity of the neuronal cholinoreceptors in the snail].

Effects of several acyclic eicosanoids (which are formed from arachidonic acid under the action of 5- and 12-lipoxygenases) on desensitization of somatic cholinoreceptors of Helix lucorum RPa3 and LPa3 neurons were studied by means of two-electrode voltage clamp technique. The substances under study were: leukotrienes B4, C4, 12(S)-hydroxy-(5Z,8Z,10E,14Z)-eicosatetraenoic acid (12-HETE), threo- and erythro-epimers of hepoxilin B3. Cholinoreceptor plasticity was evaluated by a degree of depression of inward current, induced by rhythmical local ACh applications on the soma with intervals 55-180 sec. Leukotrienes B4 and C4 intensified cholinoreceptor plasticity. Inhibitor of inositol-1,4,5-trisphosphate-dependent (IP3-d) mobilization of deposited Ca2+, TMB-8, prevented the effect of leukotriene C4. 12-HETE, threo- and erythro-epimers of hepoxilin B3 did not change plasticity. A conclusion is made that cholinoreceptor plasticity is controlled by leukotrienes B4 and C4. One of the regulatory pathways includes IP3-d Ca-mobilization. Eicosanoids from 12-lipoxygenase pathway (12-HETE, threo- and erythro-epimers of hepoxilin B3) do not participate in this intracellular regulatory mechanism.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed2001

Changes in NMDA-receptor gene expression are associated with neurotoxicity induced neonatally by glutamate in the rat brain.

The N-methyl-D-aspartate receptor (NMDA-R) is fully functional in the rat early in embryogenesis, and diverse neuronal plasticity events are regulated through its activation later in postnatal development. On the other hand, systemic administration of glutamate (Glu) to rats at birth induces neuronal degeneration in glutamatergic central nervous system regions via Glu receptor activation. However, it is not known whether an increase in neonatal Glu levels modifies the gene expression of NMDA-R subunits, or if these putative changes are related to gamma-aminobutyric acid-mediated (GABAergic) neurotransmission. We measured, by means of semi-quantitative reverse transcriptase polymerase chain reaction, changes in gene expression of the NMDA-R subunits: NMDA-R1, NMDA-R 2A and NMDA-R 2B in cerebral cortex (CC), striatum (ST) and hippocampus (HP) in the brains of rats treated neonatally with monosodium L-glutamate (MSG). These studies were supported by histological and quantitative analysis of the glia. Our results showed histological evidence of neuronal damage, and increased glial cell number and activity were detected. This was seen mainly in the ST and HP of MSG-treated animals. Significant increases in NMDA-R1, 2A and 2B subunits gene expression was also observed in ST and HP but not in CC, where only NMDA-R 2B was increased in MSG-treated rats. Our data suggest that increases in Glu levels and activation of Glu-receptors after neonatal administration of MSG induce an increase in glial cell reactivity and important changes in NMDA-R molecular composition, with signs of neuronal damage.

Animals↗