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PubMedDate not supplied

Receptor-receptor interactions as an integrative mechanism in nerve cells.

Several lines of evidence indicate that interactions among transmission lines can take place at the level of the cell membrane via interactions among macromolecules, integral or associated to the cell membrane, involved in signal recognition and transduction. The present view will focus on this last subject, i.e., on the interactions between receptors for chemical signals at the level of the neuronal membrane (receptor-receptor interaction). By receptor-receptor interaction we mean that a neurotransmitter or modulator, by binding to its receptor, modifies the characteristics of the receptor for another transmitter or modulator. Four types of interactions among transmission lines may be considered, but mainly intramembrane receptor-receptor interactions have been dealt with in this article, exemplified by the heteroregulation of D2 receptors via neuropeptide receptors and A2 receptors. The role of receptor-receptor interactions in the integration of signals is discussed, especially in terms of filtration of incoming signals, of integration of coincident signals, and of neuronal plasticity.

Animals↗

PubMed2002

Immediate early gene expression in the visual cortex of normal and dark reared cats: differences between fos and egr-1.

Northern blotting indicated that the level of induced fos was higher in normal than dark reared cat visual cortex (VC) at 5 weeks of age, comparable at 10 weeks, and higher in dark reared than normal cat visual cortex at 20 weeks. Fos egr-1, induction was higher in dark reared visual cortex at all ages. Thus, dark rearing has similar effects on fos, but not egr-1, expression as it has on physiological neuronal plasticity during the VC critical period.

Animals↗

PubMedDate not supplied

[The serine proteases and their function in neuronal death processes].

AIMS: In this review we analyse the role played by the serine proteases in the nervous system and we focus on the role they play in degenerative processes. DEVELOPMENT: These proteolytic enzymes, together with the caspases, play a vital role in the processes regulating cell functioning, both in the development stages and following the response to a harmful stimulus. This family of proteases includes the granzymes and thrombin (TR). The former, which are closely related to proteases I and II and cathepsin G, are situated in the cytoplasmic granules of the activated T lymphocytes, together with other proteins such as perforin or cytolysin. Granzymes A and B are linked to degenerative processes. These enter the target cells thanks to the action of perforin and once inside they are translocated to the nucleus. Granzyme A has been isolated and identified as the agent responsible for the immediate and complete retraction of neurites in different models. Its physiological substrates include fibronectin, type IV collagen and the proteoglycans. Granzyme B is characterised by its being a cysteine protease with substrates such as prointerleukin 1 beta, TR receptor and poly(ADP ribose) polymerase. The family of TR type proteases includes proteases such as TR itself, plasmin, kallikrein, urokinase plasminogen activator and tissue plasminogen activator. TR is considered to be an early modulator in damaged tissues which acts as an extracellular signal of death, leading to the activation of intracellular mechanisms that appear to be mediated by calcium. Serine protease activity is regulated by endogenous inhibitors, such as plasminogen activator inhibitor, protease nexin 1 and neuroserpin. CONCLUSIONS: Upsets in the protease inhibitor balance are crucial in the processes involved in the neuronal plasticity and death induced by ischemia in the brain and by excitotoxins.

Animals↗

PubMed1987

Reduced binocularity in the noradrenaline-infused striate cortex of acutely anesthetized and paralyzed, otherwise normal cats.

In anesthetized and paralyzed cats, the normal alignment of the visual axes is disturbed by paralysis of the eye muscles. Thus, the separation between paired receptive fields of binocular cells in visual cortex is increased (paralysis squint). This increased separation is normally tolerated by the majority of visuocortical cells, about 80% of them being binocularly driven (Hubel and Wiesel 1962). It was shown previously that neuronal plasticity in visual cortex can be enhanced in both normal adult cats (Kasamatsu et al. 1979) and kittens (Kuppermann and Kasamatsu 1984) by intracortical microinfusion of noradrenaline (NA). In the present study we tested whether the usual range of disparity produced by the paralysis squint is sufficient to induce ocular dominance changes in visual cortex of adult cats when the neuronal plasticity is enhanced by NA. NA was continuously infused into visual cortex throughout the experiments. The period of the paralysis squint varied from experiment to experiment between 9 and 47 h. We found: (1) These short periods were sufficient to produce a marked reduction in the proportion of binocular cells. (2) The proportion decreased linearly with increasing the duration of the squint period at a rate of 0.17 per 10 h up to about 22 h. (3) At longer durations the average binocularity remained at about 0.30 and could not be further reduced in the present paradigm. (4) The binocularity seemed to decrease with increasing separation of paired receptive fields. (5) Binocularity increased again toward the normal value after optical correction of the squint. (6) The amount of increased binocularity was linearly correlated with the duration of the period after the squint correction. (7) The binocularity increased at a rate of 0.18 per 10 h, reaching the normal value in less than 30 h. We thus concluded that if visuocortical plasticity is maintained at a high level through the continuous infusion of NA it is possible to change the ocular dominance distribution in the mature visual cortex by manipulations of the alignment of the visual axes even in the acutely anesthetized and paralyzed condition.

Anesthesia↗

PubMed2000

"Impoverished" and "enriched" living conditions influence the proliferation and survival of neurons in crayfish brain.

New neurons are added to two bilateral clusters of neurons in crayfish brain throughout their lives. These interneurons are associated with the olfactory and accessory lobes, areas of the brain that receive primary olfactory information and higher order inputs from the visual and tactile receptor systems. The rate of cell proliferation in these four clusters, revealed by BrdU labeling, is sensitive to the living conditions of the animals: individuals isolated in small spaces (impoverished condition) exhibit a lower rate of cell proliferation in comparison to their siblings living together in larger areas (enriched condition), although both groups were fed to satiation. Reduction in the rate of proliferation can be measured 1 to 2 weeks after the animals are subjected to the impoverished condition. Counts of the labeled neurons that survive after 4 weeks of subjection to the two conditions show that fewer new neurons survive in the brains of animals that have lived for 2 weeks in the impoverished condition in comparison to their siblings living in the enriched conditions. Factors such as surface area, depth of water, and social interaction can all play a role in determining both the rate of new neuron production and the incorporation of the new neurons into the brain of freshwater crayfish. The results indicate a high degree of neuronal plasticity in the crayfish brain that is highly sensitive to the conditions under which the animals are kept.

Animals↗

PubMed1994

Synaptic facilitation at connections of Hermissenda type B photoreceptors.

The enhancement of excitability in type B photoreceptors is an important neural mechanism underlying classically conditioned suppression of phototaxis in the marine mollusk Hermissenda crassicornis. However, the possibility that type B photoreceptors also exhibit synaptic plasticity has not previously been explored. We now report that connections of type B photoreceptors onto type A photoreceptors exhibit synaptic facilitation, and that this facilitation involves the same first messenger (5-HT) and second messenger (protein kinase C) previously implicated in the learning-produced excitability changes. In brief, we found that application of 5-HT dramatically facilitates synaptic potentials evoked by type B cells in type A cell cells, and that this facilitation is blocked by preincubation with staurosporine, a protein kinase inhibitor. Furthermore, activation of protein kinase C also induces synaptic facilitation, whereas activation of the cAMP-dependent protein kinase has no effect. Changes in synaptic strength produced by these manipulations are paralleled by changes in type B cell input resistance (a simple index of cellular excitability), whereas type A cell input resistance is unaffected. These findings indicate a previously unrecognized form of neuronal plasticity in Hermissenda that may contribute importantly to the learned changes in behavior, and thereby highlight general principles of learning-related neuronal plasticity shared by different preparations and species.

Alkaloids↗

PubMed2004

Gene expression analysis of the critical period in the visual cortex.

The development of the primary visual cortex in animals possessing binocular vision is a classical paradigm for the study of activity-dependent neuronal plasticity. To elucidate the genetic determinants of this period of substantial plasticity, we conducted an unbiased and comprehensive transcript profiling analysis with differential display and DNA array techniques. We characterized the transcripts that change significantly between the critical and postcritical periods in the rat binocular visual cortex. We determined if these changes are specific for the visual cortex by simultaneously profiling the hippocampus and examined the impact of sensory experience on the accumulation of the identified transcripts. Our results uncover visual cortex-specific and unspecific transcription programs. Transcripts for protein kinases and phosphatases are particularly regulated. The identified transcripts support the notion that the critical period provides a permissive state for plasticity.

Animals↗

PubMed1995

Receptor endocytosis and dendrite reshaping in spinal neurons after somatosensory stimulation.

In vivo somatosensory stimuli evoked the release of substance P from primary afferent neurons that terminate in the spinal cord and stimulated endocytosis of substance P receptors in rat spinal cord neurons. The distal dendrites that showed substance P receptor internalization underwent morphological reorganization, changing from a tubular structure to one characterized by swollen varicosities connected by thin segments. This internalization and dendritic structural reorganization provided a specific image of neurons activated by substance P. Thus receptor internalization can drive reversible structural changes in central nervous system neurons in vivo. Both of these processes may be involved in neuronal plasticity.

Animals↗

PubMed2006

Profile of immediate early gene expression in the lumbar spinal cord of low-thoracic paraplegic mice.

Induction of immediate early gene (IEG) expression is believed to constitute one of the earliest steps in plasticity and long-term modification of neuronal properties. Although behavioral evidence of neuronal plasticity at the sublesional level after spinal cord injury exists, spatiotemporal changes of IEGs in spinal segments located caudally to such an injury have never been examined. Here, the authors studied spatiotemporal changes of c-fos, nor-1, nur77, nurr1, and retinoid x receptor (rxr) messenger RNA expression in the lumbar segments L1-L2 after low-thoracic spinal transection (Tx). C-fos expression generally increased in the dorsal horn with significant levels reached at 3 days and 14 days post-Tx. Basal nor-1 transcript levels decreased in the intermediate zone and dorsal horn areas at 7 days. Nur77 levels were nonsignificantly depressed throughout that period of time, whereas nurr1 and rxr transcripts were not detected before or after Tx. In conclusion, the results provide evidence of distinct roles for c-fos and nor-1 in reorganization and plasticity of neuronal networks typically involved in sensorimotor integration and locomotor control.

Animals↗

PubMed1998

Different patterns of induction of FGF-2, FGF-1 and BDNF mRNAs during kindling epileptogenesis in the rat.

Neurotrophic factors (NTF) play important roles in the developing and in the adult brain. NTF involvement in neuronal plasticity is suggested by the modulation of NTF expression patterns in different physiological and pathological situations and by the effects they produce in the adult brain (e.g. axonal sprouting induction and neuroprotection). We used the RNAase protection assay to investigate the expression patterns of some NTFs during amygdala kindling, an animal model of epilepsy in which 'pathological' neuronal plasticity appears to occur. After a single kindling stimulation, fibroblast growth factor-2 (FGF-2) mRNA levels were increased in the hippocampus, the cortex and the hypothalamus, whereas they were not significantly altered in the thalamus and the striatum. A single stimulation did not alter fibroblast growth factor-1 (FGF-1) and brain-derived neurotrophic factor (BDNF) gene expression. Fully kindled animals, left unstimulated for a week, did not exhibit any alteration in the mRNA levels for any of the NTFs examined. However, in contrast with the effect of a single stimulation, amygdala stimulation of kindled animals (evoking a generalized tonic-clonic seizure) produced a great increase in hippocampal and cortical BDNF mRNA levels, but FGF-1 mRNA levels were not altered, and FGF-2 mRNA levels were significantly increased only in the cortex. These results suggest that different NTFs can be recruited at different stages of kindling epileptogenesis and, accordingly, may play different parts in the adaptive changes taking place in this experimental paradigm.

Amygdala↗

PubMed2005

Activity-dependent neurotrophic factor-9 and NAP promote neurite outgrowth in rat hippocampal and cortical cultures.

Activity-dependent neurotrophic factor (ADNF) is a novel, femtomolar-acting, glial-derived polypeptide (14 kDa) known to protect neurons from a variety of toxic insults. The active site for ADNF function is localized to a 9-amino-acid stretch (SALLRSIPA; ADNF-9). A few years later, a novel ADNF-9-like active peptide (NAPVSIPQ or NAP) was identified and shown to be expressed in the CNS and exhibit an activity profile similar to ADNF-9. Such studies suggest that ADNF-9 and NAP might function like other known neurotrophins and play a role in neural development and maintenance. The purpose of the present studies was to determine if ADNF-9 or NAP affects neurite outgrowth and synaptogenesis in rat hippocampal and cortical cultures. Using MAP2-FITC immunofluorescent labeling, we found that ADNF-9 and NAP promoted neurite outgrowth in a concentration-dependent manner, with maximal activity observed at femtomolar concentrations. Both peptides stimulated robust outgrowth in hippocampal cells (approximately 150% of control; p < 0.01) with a modest effect on cortical cells (approximately 20% of control; p < 0.05) similar to other known growth factors. However, the outgrowth-promoting effect was abolished in the absence of serum, suggesting that soluble factors might be necessary for the neurotrophic activity. Finally, we found that ADNF-9 and NAP increased synaptophysin expression in both rat hippocampal and cortical cultures. These results suggest that ADNF-9 and NAP might contribute to neuronal plasticity associated with development and repair after injury.

Animals↗

PubMed1993

The induction of LTP increases BDNF and NGF mRNA but decreases NT-3 mRNA in the dentate gyrus.

We have investigated the expression of the mRNAs for brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), neurotrophin-3 (NT-3) and neurotrophin-4 (NT-4) in the hippocampus before and after induction of long term potentiation (LTP) of synaptic transmission in the dentate gyrus through stimulation of the perforant path (PP). A unilateral PP stimulation produced a bilateral increase in the mRNA for both BDNF and NGF in granular neurones of the dentate gyrus but not in other neurones in the hippocampus. The mRNA for neurotrophin-3 (NT-3) was bilaterally decreased by LTP but that of NT-4 remained at the basal level. These results suggest that individual neurotrophic factors may play different roles in neuronal plasticity.

Animals↗

PubMed1984

Physiological plasticity of single neurons in auditory cortex of the cat during acquisition of the pupillary conditioned response: II. Secondary field (AII).

The discharges of 22 single neurons were recorded in the secondary auditory cortical field (AII) during acquisition of the pupillary dilation conditioned defensive response in chronically prepared cats. All 22 neurons developed discharge plasticity in background activity, and 21/22 cells developed plasticity in their responses to the acoustic conditioned stimulus (CS). Nonassociative factors were ruled out by the use of a sensitization phase (CS and US [unconditioned stimulus] unpaired) preceding the conditioning phase and by ensuring stimulus constancy at the periphery by neuromuscular paralysis. Changes in background neuronal activity were related to measures of behavioral learning or to changes in the level of arousal. Specifically, decreases in background activity (17/22 cells) developed at the time that subjects began to display conditioned responses. Increases in background activity (5/22) developed in animals that became more tonically aroused during conditioning. However, both increases (11/22) and decreases (10/22) in evoked activity developed independently of the rate of pupillary learning, tonic arousal level, or changes in background activity. These findings indicate that changes in background activity are closely related to behavioral processes of learning and arousal whereas stimulus-evoked discharge plasticity develops solely as a consequence of stimulus pairing. A comparative analysis of the effects of conditioning on secondary and primary (AI) auditory cortex indicates that both regions develop neuronal discharge plasticity early in the conditioning phase and that increases in background activity in primary auditory cortex are also associated with elevated levels of tonic arousal. In addition, the overall incidence of single neurons developing learning-related discharge plasticity is significantly greater in AII than in AI. The relevance of these findings is discussed in terms of parallel processing in sensory systems and multiple sensory cortical fields.

Animals↗

PubMed2003

Tyrosinated alpha-tubulin changes following epileptogenic and non-epileptogenic lesions in rat brain cortex.

The expression of the tyrosinated isoform of alpha-tubulin was monitored in rat frontal cortex, in order to investigate the neuronal plasticity changes occurring either in a mirror focus or in a deafferented area. A mirror focus was triggered by epidural implantation of a cobalt gelatin disk in the contralateral left somatosensory area (group one). A deafferented area was obtained by surgical removal of the left frontal cortex (group two). All animals including controls underwent EcoG recordings immediately before killing (45, 60, 90 days post surgery). The right frontal cortex was removed from all the animals and processed with Western blot method. EcoG recordings revealed a paroxysmal activity in epileptic rats, whereas in rats with frontal deafferentation and controls, EcoG activity was normal. A significant increase in tyrosinated alpha-tubulin expression was detected both in the mirror focus (group one) and the "non-epileptic" deafferented frontal cortex (group two) in comparison with controls (group three). The transcallosal deafferentation, which is involved in both epileptogenic and non-epileptogenic lesions, is supposed to play a role in the mechanism responsible for the plasticity responses recorded in the cortical areas studied.

Action Potentials↗

PubMed2000

Site-specific phosphorylation of neurofilament-L is mediated by calcium/calmodulin-dependent protein kinase II in the apical dendrites during long-term potentiation.

Neurofilament-L (NF-L), one subunit of the neuronal intermediate filaments, is a major element of neuronal cytoskeletons. The dynamics of NF-L are regulated by phosphorylation of its head domain. The phosphorylation sites of the NF-L head domain by protein kinase A, protein kinase C, and Rho-associated kinase have been previously identified, and those by calcium/calmodulin-dependent protein kinase II (CaMKII) were identified in this study. A series of site- and phosphorylation state-specific antibodies against NF-L was prepared to investigate NF-L phosphorylation in neuronal systems. Long-term potentiation (LTP) is a cellular model of neuronal plasticity that is thought to involve the phosphorylation of various proteins. NF-L is considered a possible substrate for phosphorylation. During LTP stimulation of mouse hippocampal slices, the series of antibodies demonstrated the increase in the phosphorylation level of Ser(57) in NF-L and the visualization of the localized distribution of Ser(57) phosphorylation in a subpopulation of apical dendrites of the pyramidal neurons. Furthermore, Ser(57) phosphorylation during LTP is suggested to be mediated by CaMKII. Here we show that NF-L is phosphorylated by CaMKII in a subpopulation of apical dendrites during LTP, indicating that Ser(57) is a novel phosphorylation site of NF-L in vivo related to the neuronal signal transduction.

Amino Acid Sequence↗

PubMed2000

Ultrastructural identification of storage compartments and localization of activity-dependent secretion of neurotrophin 6 in hippocampal neurons.

A modulatory role of neurotrophins (NTs) in activity-dependent neuronal plasticity by pre- and postsynaptic mechanisms is now well established. In this context, it is important to identify the storage compartments and to localize the precise site(s) and mechanism of NT secretion in order to deduce the spatial and temporal availability of NTs. We approached these questions at the ultrastructural level, exploiting the unique property of NT6 to bind tightly to heparan sulfate proteoglycans at the neuronal surface (R. Götz et al., 1994, Nature 372, 266-269), permitting the localization of secretion sites excluding diffusion artifacts. The myc tagging of NT6 permitted glutaraldehyde fixation and hence good preservation of the membrane structure, permitting immunogold labeling of NT6myc at the neuronal surface. NT6myc is preferentially secreted from neurites compared to neuronal cell bodies. In agreement with light-microscopic observations, the ultrastructural localization of NT6myc by postembedding procedures showed a predominant localization in ER-like membrane-confined compartments, partially associated with microtubules.

Amino Acid Sequence↗

PubMed2003

Changes in spinal GDNF, BDNF, and NT-3 expression after transient spinal cord ischemia in the rat.

Previous studies have demonstrated that the expression of several growth factors including glial cell-derived neurotrophic factor (GDNF), brain-derived growth factor (BDNF), and neurotrophin-3 (NT-3) play an important role in defining neuronal survival after brain ischemia. In the present study, using a well-defined model of transient spinal ischemia in rat, we characterized the changes in spinal GDNF, BDNF, and NT-3 expression as defined by enzyme-linked immunosorbent assay (ELISA) and immunofluorescence coupled with deconvolution microscopy. In control animals, baseline levels of GDNF, BDNF, and NT-3 (74 +/- 22, 3,600 +/- 270, 593 +/- 176 pg/g tissue, respectively) were measured. In the ischemic group, 6 min of spinal ischemia resulted in a biphasic response with increases in tissue GDNF and BDNF concentrations at the 2-hr and 72-hr points after ischemia. No significant differences in NT-3 concentration were detected. Deconvolution analysis revealed that the initial increase in tissue GDNF concentration corresponded to a neuronal upregulation whereas the late peak seen at 72 hr corresponded with increased astrocyte-derived GDNF synthesis. Increased expression of BDNF was seen in neurons, astrocytes, and oligodendrocytes. These data suggest that the early increase in neuronal GDNF/BDNF expression likely modulates neuronal resistance/recovery during the initial period of postischemic reflow. Increased astrocyte-derived BDNF/GDNF expression corresponds with transient activation of astrocytes and may play an active role in neuronal plasticity after non-injurious intervals of spinal ischemia.

Animals↗

PubMed1995

Intracerebroventricular kainic acid administration in adult rat alters hippocampal calbindin and non-phosphorylated neurofilament expression.

Calbindin and non-phosphorylated neurofilament proteins were assessed in hippocampus following a unilateral intracerebroventricular kainic acid injection at 4, 26, and 60 days post-lesion, using immunocytochemical expression. The density of calbindin-positive non-pyramidal neurons throughout the hippocampus showed no significant alteration at 4 days post-lesion, a significant decrease at 26 days post-lesion, and a partial recovery at 60 days post-lesion. In addition, calbindin immunoreactivity was dramatically reduced at 26 days post-lesion in the CA1 pyramidal and dentate granule cell layers and the mossy fibers, bilaterally. Although not significant statistically, most of these reductions showed signs of reversal at 60 days post-lesion except the CA1 pyramidal cell layer where the dramatic reductions persisted. Neurofilaments were also altered throughout the post-lesion period, particularly in abnormal expression of non-phosphorylated neurofilament proteins in mossy fibers. The apparent return of calbindin immunoreactivity in non-pyramidal neurons by 60 days post-lesion suggests that recovery from the lesion may involve remaining neuronal elements which either become reactivated with time or have the capability to express normal levels of calbindin with re-innervation. On the other hand, prolonged calbindin reductions in superficial CA1 pyramidal cells suggest sustained down-regulation of calbindin expression owing to persistent reductions in the activity of these neurons. The temporal correlation of the expression of non-phosphorylated neurofilaments in mossy fibers with their sprouting response following target loss suggests a potential role for non-phosphorylated neurofilaments in neuronal plasticity involving axonal sprouting. Alternatively, it may also suggest that injury-induced neurofilament modifications are either conducive or permissive for axonal sprouting.

Animals↗