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Results for “Neuronal Plasticity”

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PubMed2001

Bidirectional regulation of mitochondrial gene expression during developmental neuroplasticity of visual cortex.

The first several months of life are a critical period for neuronal plasticity in the visual cortex, during which anatomical and physiological development depends upon visual experience. Rearing in darkness slows the time course of this critical period, such that at 5 weeks normal cats are more plastic than dark-reared cats, while at 20 weeks dark-reared cats are more plastic. This study reports the identification of a subset of mitochondrial genes that are regulated in this manner. Opponent patterns of bidirectional expression were found: several genes (ATPase 6, cytochrome b, NADH dehydrogenase subunits 4 and 2) showed elevation in normal cats at 5 weeks and in dark-reared cats at 20 weeks ("plasticity" genes); others (NADH dehydrogenase subunits 3 and 5) showed the opposite ("anti-plasticity" genes). These findings add a new dimension to the growing evidence that changes in mitochondrial gene expression are involved in the neuroplastic response.

Adenosine Triphosphatases↗

PubMed2001

Recent advances in pain research: implications for chronic headache.

Within the last 2 decades there has been an explosion in new information on mechanisms underlying pain. Unfortunately this information has not resulted in a similar improvement of our handling of patients with chronic pain including chronic musculoskeletal pain. Neuronal hyperexcitability, which apparently is a key phenomenon in many (if not all) types of chronic pain results in changes in the nervous system from the level of the peripheral nociceptor to the highest cortical centers in the brain. The neuronal plastic changes in chronic pain conditions makes the nociceptive system amenable for treatment with several traditional as well as nontraditional types of interventions. Two treatment areas that seem worth exploring within chronic pain including headache concerns preventive measures and endogenous pain modulation.

Animals↗

PubMedDate not supplied

The neural cell adhesion molecule (NCAM) in development and plasticity of the nervous system.

The neural cell adhesion molecule (NCAM) is a member of the immunoglobulin superfamily and is strongly expressed in the nervous system. NCAM is found in three major forms, of which two--NCAM-140 and NCAM-180--are transmembrane proteins, while the third--NCAM-120--is attached to the membrane via a glycosylphosphatidyl inositol anchor. In addition, soluble NCAM forms exist in brain, cerebrospinal fluid, and plasma. NCAM mediates cell adhesion through homophilic as well as through heterophilic interactions. Following NCAM binding, transmembrane signalling is believed to be activated, resulting in increased intracellular calcium. By mediating cell adhesion to other cells and to the extracellular matrix and by activating intracellular signaling pathways, NCAM influences cell migration, neurite extension, and fasciculation, and possibly formation of synapses in the brain. From studies on NCAM knock-out mice, NCAM have been shown to be crucial for the formation of the olfactory bulb and the mossy fiber system in the hippocampus. In addition, NCAM is important for neuronal plasticity in the adult brain associated with learning and regeneration.

Aging↗

PubMed2026

Genome-Wide Association Analysis of Hippocampal Neuroplasticity as an Indicator of Stress Responsiveness in Laying Hens (Gallus gallus domesticus).

Environmental stressors in commercial poultry systems can negatively affect bird welfare, although individuals vary considerably in their responses. Neuroplasticity within the hippocampus, measured through the density of doublecortin-positive (DCX+) neurons, provides a potential biomarker of stress experience in laying hens. However, the genetic basis underlying variation in this biomarker remains poorly understood. A total of 42 H&N and Hy-Line Brown hens housed in a multitier free range and enriched cage system, respectively, were genotyped using Genotyping by Sequencing, yielding over 200 000 SNP markers after initial filtering. Hippocampal tissue sections were immunostained for DCX to quantify the density of highly plastic neurons. A genome-wide association analysis identified 19 genomic regions across eight chromosomes within the top 1% of windows explaining the greatest proportion of genetic variance in the neuroplasticity phenotype. Within ±100 kb of these regions, 39 annotated genes were identified, several of which are involved in cellular regulation and genetic information processing pathways. Notably, PIK3R6, VPS37D, STX1A, BAZ1B, HGH1, MAF1, MAPK15, and PIT54 emerged as positional candidate genes potentially contributing to variation in stress responsiveness. These findings provide preliminary insight into the genetic architecture of hippocampal neuroplasticity in laying hens and highlight candidate genes that may contribute to individual differences in stress response, with potential implications for breeding strategies aimed at improving poultry welfare.

Animals↗

PubMed1998

The absence of a major Ca2+ signaling pathway in GABAergic neurons of the hippocampus.

The Ca2+/calmodulin-dependent protein phosphatase 2B or calcineurin (CN) participates in several Ca2+-dependent signal transduction cascades and, thus, contributes to the short and long term regulation of neuronal excitability. By using a specific antibody to CN, we demonstrate its absence from hippocampal interneurons and illustrate a physiological consequence of such CN deficiency. Consistent with the lack of CN in interneurons as detected by immunocytochemistry, the CN inhibitors FK-506 or okadaic acid significantly prolonged N-methyl-D-aspartate channel openings recorded in the cell-attached mode in hippocampal principal cells but not those recorded in interneurons. Interneurons were also devoid of Ca2+/calmodulin-dependent protein kinase IIalpha, yet many of their nuclei contained the cyclic AMP-responsive element binding protein. On the basis of the CN and Ca2+/calmodulin-dependent protein kinase IIalpha deficiency of interneurons, entirely different biochemical mechanisms are expected to govern Ca2+-dependent neuronal plasticity in interneurons versus principal cells.

Animals↗

PubMed2005

Stimulation of endocannabinoid formation in brain slice cultures through activation of group I metabotropic glutamate receptors.

Activation of group I metabotropic glutamate (mGlu) receptors drives the endocannabinoid system to cause both short- and long-term changes of synaptic strength in the striatum, hippocampus, and other brain areas. Although there is strong electrophysiological evidence for a role of endocannabinoid release in mGlu receptor-dependent plasticity, the identity of the endocannabinoid transmitter mediating this phenomenon remains undefined. In this study, we show that activation of group I mGlu receptors triggers the biosynthesis of the endocannabinoid 2-arachidonoylglycerol (2-AG), but not anandamide, in primary cultures of corticostriatal and hippocampal slices prepared from early postnatal rat brain. Pharmacological studies suggest that 2-AG biosynthesis is initiated by activation of mGlu5 receptors, is catalyzed by phospholipase C (PLC) and 1,2-diacylglycerol lipase (DGL) activities, and is dependent on intracellular Ca2+ ions. Realtime polymerase chain reaction and immunostaining analyses indicate that DGL-beta is the predominant DGL isoform expressed in corticostriatal and hippocampal slices and that this enzyme is highly expressed in striatal neurons, where it is colocalized with PLC-beta1. The results suggest that 2-AG is a primary endocannabinoid mediator of mGlu receptor-dependent neuronal plasticity.

Amino Acid Sequence↗

PubMed1997

Neuropsychiatric complications after temporal lobe limbic system surgery.

Although control of seizure activity is the main goal of temporal lobectomies for complex partial epilepsy, the results of surgery must be viewed within the larger context of possible ramifications of limbic system disruption. The neuropsychiatric complications may be significant and influence the patient's perceived qualify of life, thus detracting from the benefits of seizure control. It is apparent from the previous studies that the modalities affected are influenced by the laterality of the resection, with left-sided lobectomies more often affecting verbal memory and learning, whereas right-sided resections may cause visual/spatial memory and cognitive declines. Preoperative neuropsychologic testing may help to predict these possible complications. General psychosocial function, memory, and cognition all seem to be less affected when complete seizure control is attained, with nearly 80% experiencing no significant change in neuropsychologic testing and the gain and losses being equal in magnitude. Also, younger patients and those with a shorter history of seizure activity may fare better after surgery because of a greater capacity for neuronal plasticity to subserve these functions. These findings support the contention that early diagnosis and surgical treatment may help to minimize potential neuropsychiatric complications in conjunction with improved postoperative seizure control.

Age Factors↗

PubMedDate not supplied

A role for sleep in brain plasticity.

The idea that sleep might be involved in brain plasticity has been investigated for many years through a large number of animal and human studies, but evidence remains fragmentary. Large amounts of sleep in early life suggest that sleep may play a role in brain maturation. In particular, the influence of sleep in developing the visual system has been highlighted. The current data suggest that both Rapid Eye Movement (REM) and non-REM sleep states would be important for brain development. Such findings stress the need for optimal paediatric sleep management. In the adult brain, the role of sleep in learning and memory is emphasized by studies at behavioural, systems, cellular and molecular levels. First, sleep amounts are reported to increase following a learning task and sleep deprivation impairs task acquisition and consolidation. At the systems level, neurophysiological studies suggest possible mechanisms for the consolidation of memory traces. These imply both thalamocortical and hippocampo-neocortical networks. Similarly, neuroimaging techniques demonstrated the experience-dependent changes in cerebral activity during sleep. Finally, recent works show the modulation during sleep of cerebral protein synthesis and expression of genes involved in neuronal plasticity.

Animals↗

PubMed2001

Differential regulation of transcripts for dystrophin Isoforms, dystroglycan, and alpha3AChR subunit in mouse sympathetic ganglia following postganglionic nerve crush.

Previous data suggest that in mouse superior cervical ganglion (SCG) the dystrophin-dystroglycan complex may be involved in the axotomy-induced intraganglionic synapse remodeling. Here we analyzed the levels of mRNAs encoding dystrophins, dystroglycan (Dg), and the alpha3 subunit of the nicotinic acetylcholine receptor (alpha3AChR) in mouse SCG at various postaxotomy intervals. We found that axotomy downregulates the levels of transcripts for molecules related to synaptic transmission (alpha3AChR) and those presumably involved in postsynaptic apparatus organization (dystrophin isoforms) and upregulates the transcript encoding Dg, which, by binding dystrophin, bridges the actin cytoskeleton and several extracellular matrix proteins and may thus be involved in postaxotomy neuronal recovery. The observed transcriptional modulation of the components of dystrophin-dystroglycan complexes indicates their involvement in injury-induced neuronal plasticity and suggests a role in other forms of plasticity such as those required in learning and memory, functions often impaired in Duchenne muscular dystrophy patients.

Animals↗

PubMed2006

Sexual experience in female rodents: cellular mechanisms and functional consequences.

The neurobiology of female sexual behavior has largely focused on mechanisms of hormone action on nerve cells and how these effects translate into the display of copulatory motor patterns. Of equal importance, though less studied, are some of the consequences of engaging in sexual behavior, including the rewarding properties of sexual interactions and how sexual experience alters copulatory efficiency. This review summarizes the effects of sexual experience on reward processes and copulation in female Syrian hamsters. Neural correlates of these sexual interactions include long-term cellular changes in dopamine transmission and postsynaptic signaling pathways related to neuronal plasticity (e.g., dendritic spine formation). Taken together, these studies suggest that sexual experience enhances the reinforcing properties of sexual behavior, which has the coincident outcome of increasing copulatory efficiency in a way that can increase reproductive success.

Animals↗

PubMed2005

Altered production and proteolytic processing of brevican by transforming growth factor beta in cultured astrocytes.

Brevican, a proteoglycan of the lectican family, inhibits neurite outgrowth and may also stabilize synapses. Little is known about its expression or function in vitro. This study seeks to determine whether a brevican-containing matrix is present in neural cultures, and if so, how the production of brevican may be modulated. To accomplish this, the content of brevican and its proteolytic fragments were measured in primary cultures of neurons, astrocytes and microglia after treatment with cytokines. These experiments revealed that astrocytes and neurons express several isoforms of brevican, whereas microglia do not produce this proteoglycan. Cleavage fragments of brevican were found primarily in neuronal and astrocyte culture medium. ADAMTS4 (a disintegrin and metalloproteinase with thrombospondin motifs), a protease that selectively cleaves lecticans, was detected in cultures of neurons, astrocytes and microglia. When astrocytes were challenged with various cytokines, it was found that treatment with transforming growth factor beta (TGFbeta) resulted in a marked increase in intact brevican in the culture medium that was accompanied by a trend for a decrease in ADAMTS-generated fragments of brevican and apparent ADAMTS activity. Thus, TGFbeta may play a role in neuronal plasticity through its regulation of brevican and the activity of the ADAMTSs.

ADAM Proteins↗

PubMed1998

The NO/cGMP pathway and the development of neural networks in postembryonic lobsters.

The nitric oxide/cyclic 3',5'-guanosine monophosphate (NO/cGMP) signaling pathway has been implicated in certain forms of developmental and adult neuronal plasticity. Here we use whole-mount immunocytochemistry to identify components of this pathway in the nervous system of postembryonic lobsters as they develop through metamorphosis. We find that the synthetic enzyme for NO (nitric oxide synthase, or NOS) and the receptor for this transmitter (NO-sensitive soluble guanylate cyclase) are broadly distributed in the central nervous system (CNS) at hatching. In the brain, NOS immunoreactivity is intensified during glomerular development in the olfactory and accessory lobes. Whereas only a few neurons express NOS in the CNS, many more neurons synthesize cGMP in the presence of NO. NO-sensitive guanylate cyclase activity is a stable feature of some cells, while in others it is regulated during development. In the stomatogastric nervous system, a subset of neurons become responsive to NO at metamorphosis, a time when larval networks are reorganized into adult motor circuits. cGMP accumulation was occasionally detected in the nucleus of many cells in the CNS, which suggests that cGMP may have a role in transcription. Based on these findings, we conclude that the NO/cGMP signaling pathway may participate in the development of the lobster nervous system. Furthermore, NO may serve as a modulatory neurotransmitter for diverse neurons throughout the CNS.

1-Methyl-3-isobutylxanthine↗

PubMed1997

Antibody to day-old chick brain glycoprotein produces amnesia in adult rats.

Polyclonal antibody R-1, raised against a chick synaptic membrane glycoprotein fraction whose synthesis is enhanced following training on a passive avoidance task, produces amnesia when injected into chick forebrain 5.5 h posttraining. The amnestic IgG fraction specifically recognizes a low sialylated isoform of NCAM (Mileusnic Rose, Lancashire, & Bullock, 1995). We have now investigated the effects of this antibody on memory formation in adult rats. R-1, preimmune serum, or saline was injected intracerebroventricularly 5.5 h posttraining through bilaterally implanted cannulae. Rats injected with R-1 and tested 48 h later showed a significant amnesia for avoidance compared with the controls. Amnesia was not apparent at 24 h posttraining. R-1 injections were without effect on spontaneous locomotor or exploratory activity in a holeboard test. The results contribute to the argument that the role of cell adhesion molecules in neuronal plasticity is not limited to the developing nervous system, but they play a more general role in the experience-dependent synaptic remodeling underlying long-term memory.

Amnesia↗

PubMed2002

Understanding and controlling the enteric nervous system.

The enteric nervous system or the 'Little Brain' of the gut controls gastrointestinal motility and secretion, and is involved in visceral sensation. In this chapter, new developments in understanding the function of the enteric nervous system are described. In particular, the interaction of this system with the interstitial cells of Cajal, the pacemaker cells of the gut, is highlighted. The importance of the interaction between the enteric nervous system and the immune system is discussed, especially in relation to functional bowel disorders and post-operative ileus. Evidence is also provided that neurones can change their function and phenotype, a phenomenon called neuronal plasticity, which contributes to the pathogenesis of visceral hypersensitivity. Finally, new developments in stem cell transplantation are described. All these new insights should lead to a better understanding of the enteric nervous system and hopefully to better ways of controlling it.

Coiled Bodies↗

PubMed2001

Effects of exercise on gene-expression profile in the rat hippocampus.

Exercise has beneficial effects on brain function, including the promotion of plasticity and the enhancement of learning and memory performance. Previously we found that exercise increases the expression of certain neurotrophic factors including brain derived neurotrophic factor in the rat hippocampus. To further explore the molecular mechanisms underlying these changes, we used high-density oligonucleotide microarrays containing probe sets representing approximately 5000 genes to analyze the level of gene transcripts in the hippocampus of rats voluntary running for 3 weeks in comparison with sedentary animals. An improved statistical approach for the analysis of DNA microarray data, Cyber-T, was utilized in data analysis. Here we show that exercise leads to changes in the level of a large number of gene transcripts, many of which are known to be associated with neuronal activity, synaptic structure, and neuronal plasticity. Our data indicate that exercise elicits a differential gene expression pattern with significant changes in genes of relevance for brain function.

Aging↗

PubMed2000

Brain plasticity: to what extent do aged animals retain the capacity to coordinate gene activity in response to acute challenges.

The ability of the rodent brain to support plasticity-related phenomena declines with increasing age. A decreased coordination of genes implicated in brain plasticity may be one factor contributing to this decline. Synaptic rearrangement that occurs after seizure activity is regarded as a model of brain plasticity. In a rat model of seizure-related brain plasticity, we found that the induction of immediate-early genes, as exemplified by c-fos and tissue plasminogen activator (TPA) is not impaired in the aged rat brain. However, the aged rat brain responded more slowly to chemically induced seizure and the levels of c-fos and TPA mRNAs induction are decreased in the cortex and in the hippocampus of 30-month-old rats, as compared to the levels expressed by 3-month-old rats. In addition, at the peak induction the TPA transcripts were restricted to certain cortical layers of the older rats. Surprisingly, in applying the same experimental paradigm to late genes we found that there was a shift toward earlier times in the maximum expression of growth-related molecule, the microtubule-associated protein 1B (MAP1B) mRNA, which was very evident in 18-month-old rats. Aberrant immunolabeling of MAP1B occurred in cortical layer VI of the aged rats where, unlike in young rats, there was heavy staining of neuronal somata. These results suggest that (i) one consequence of aging, besides decreases in the levels of mRNA, is a progressive loss of coordination in gene activity following the administration of a stimulus; (ii) since c-fos, TPA and MAP1B have been implicated in neuronal plasticity, these findings could explain, in part, the limited plasticity of the aging brain.

Aging↗

PubMed1993

Perinatal morphine treatment inhibits pruning effect and regeneration of serotoninergic pathways following neonatal 5,7-HT lesions.

Lesion of the serotoninergic system in neonate rats is an ideal model for assessing the activity of chemical substances capable of affecting neuronal plasticity and regeneration (Jonsson et al., Dev Brain Res 16: 171-180, 1984). Treatment of newborn rats within 6 hr from birth with the selective neurotoxin 5,7-dihydroxytryptamine causes degeneration of the most distal serotoninergic axons. In our experimental conditions we have observed that after such neurotoxic treatment there is spinal cord denervation, which is particularly remarkable in the lumbar segment. This degenerative event is followed by gradual regeneration of the lesioned axons, with good reinnervation of the entire cord within 8 weeks. The degeneration-regeneration process is correlated with a transient hyperinnervation of the pons-medulla and hypothalamus by the short collaterals (pruning effect), as evidenced by increased serotonin content. Perinatal morphine exposure markedly impairs serotonin regeneration in the spinal cord. In addition, opiate treated rats are more susceptible to lesions, as shown by the neurotoxin induced denervation of the cortex, pons-medulla, and hypothalamus, which does not occur in lesioned controls. Therefore, our observations suggest that perinatal exposure to morphine affects the plasticity and regeneration of the developing serotoninergic system by increasing its susceptibility to neurotoxic lesions and reducing its regenerative capacity.

5,7-Dihydroxytryptamine↗

PubMed2006

Mechanism of action of atypical antipsychotic drugs and the neurobiology of schizophrenia.

Atypical antipsychotics have greatly enhanced the treatment of schizophrenia. The mechanisms underlying the effectiveness and adverse effects of these drugs are, to date, not sufficiently explained. This article summarises the hypothetical mechanisms of action of atypical antipsychotics with respect to the neurobiology of schizophrenia.When considering treatment models for schizophrenia, the role of dopamine receptor blockade and modulation remains dominant. The optimal occupancy of dopamine D(2) receptors seems to be crucial to balancing efficacy and adverse effects - transient D(2) receptor antagonism (such as that attained with, for example, quetiapine and clozapine) is sufficient to obtain an antipsychotic effect, while permanent D(2) receptor antagonism (as is caused by conventional antipsychotics) increases the risk of adverse effects such as extrapyramidal symptoms. Partial D(2) receptor agonism (induced by aripiprazole) offers the possibility of maintaining optimal blockade and function of D(2) receptors. Balancing presynaptic and postsynaptic D(2) receptor antagonism (e.g. induced by amisulpride) is another mechanism that can, through increased release of endogenous dopamine in the striatum, protect against excessive blockade of D(2) receptors. Serotonergic modulation is associated with a beneficial increase in striatal dopamine release. Effects on the negative and cognitive symptoms of schizophrenia relate to dopamine release in the prefrontal cortex; this can be modulated by combined D(2) and serotonin 5-HT(2A) receptor antagonism (e.g. by olanzapine and risperidone), partial D(2) receptor antagonism or the preferential blockade of inhibitory dopamine autoreceptors. In the context of the neurodevelopmental disconnection hypothesis of schizophrenia, atypical antipsychotics (in contrast to conventional antipsychotics) induce neuronal plasticity and synaptic remodelling, not only in the striatum but also in other brain areas such as the prefrontal cortex and hippocampus. This mechanism may normalise glutamatergic dysfunction and structural abnormalities and affect the core pathophysiological substrates for schizophrenia.

Animals↗