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PubMed1998

Identification of fucose alpha(1-2) galactose epitope-containing glycoproteins from rat hippocampus.

Fucosylation of terminal galactose residues of brain glycoproteins in the alpha(1-2) position has been shown to be crucial for neuronal plasticity, including phenomena such as long-term potentiation and long-term memory formation. We raised antibodies against the plasticity-relevant fucalpha(1-2)gal epitope and used them to determine the distribution of the epitope in adult rat hippocampus. To identify proteins bearing fucalpha(1-2)gal glycostructures antibodies against known synaptic fucoglycoproteins were used in combination with the fucalpha(1-2)gal antibodies. The NMDA receptor subunit NR1 and fractions of gp65 and cadherin were found to carry the epitope, while fucosylation of NCAM180 and NCAM140 obviously occurs via different linkages to the glycan chains.

Animals↗
PubMed2006

Neurobiology of pain.

The neurobiology of pain had a notable interest in research focused on the study of neuronal plasticity development, nociceptors, molecular identity, signaling mechanism, ionic channels involved in the generation, modulation and propagation of action potential in all type of excitable cells. All the findings open the possibility for developing new therapeutic treatment. Nociceptive/inflammatory pain and neuropathic pain represent two different kinds of persistent chronic pain. We have reviewed the different mechanism suggested for the maintenance of pain, like descending nociceptive mechanism and their changes after tissue damage, including suppression and facilitation of defence behavior during pain. The role of these changes in inducing NMDA and AMPA receptors gene expression, after prolonged inflammation is emphasized by several authors. Furthermore, a relation between a persistent pain and amygdale has been shown. Molecular biology is the new frontier in the study of neurobiology of pain. Since the entire genome has been studied, we will able to find new genes involved in specific condition such as pain, because an altered gene expression can regulate neuronal activity after inflammation or tissue damage.

Animals↗
PubMed2003

The correlation between tau protein in the brainstem and sleep apnea in SIDS victims.

BACKGROUND: Recently, it has been reported that neuronal plasticity in the brainstem arousal pathway is related to the sudden infant death syndrome (SIDS). Tau protein may contribute to axonal development and neural plasticity; therefore, the correlation between tau protein in the brainstem and sleep apnea in SIDS was investigated here. MATERIALS AND METHODS: Among 27,000 infants studied prospectively to characterize their sleep-wake behavior, 38 infants died under 6 months of age, including 26 cases of SIDS. The frequency and duration of sleep apnea were analyzed on all the infants, having been recorded during one night in a pediatric sleep laboratory some 3-12 weeks before death. The brainstem material was collected and immunohistochemistry of tau was carried out. The density of tau-positive elements was measured semiquantitatively. Correlation analyses were carried out between the density of tau-positive elements and the data of sleep apnea. RESULTS: In the 26 SIDS cases, tau-positive findings were observed in the sub-pia mater in two cases, in the colloid plexus in one case, in the ependyma and subependyma in five cases, in neurons in two cases and as a general diffusion in one case. In 12 control cases, tau-positive findings were observed in the sub-pia mater in one case and in neuronal elements in three cases. No correlation was found on analysis. CONCLUSIONS: There was no correlation between the finding of tau in the brainstem of SIDS victims and the incidence of sleep apnea.

Brain Stem↗
PubMed1992

A nitric oxide (NO) synthase inhibitor accelerates amygdala kindling.

In response to NMDA receptor activation, hippocampal, striatal and cerebellar neurons synthesize nitric oxide (NO), which in turn elevates cGMP levels via guanylate cyclase. NO is increasingly being considered as a transsynaptic retrograde messenger, involved in neuronal plasticity. The effect of an inhibitor of NO synthase, L-NG-nitroarginine (NOArg), was studied on amygdala kindling and on kindled seizures in rats. NOArg increased kindling rate, particularly in its initial period, but did not modify seizure severity in previously kindled rats, although we have no definitive explanation for this effect. However, an enhanced post-synaptic excitability could be attributed to the blockade of the negative feed-back exerted by NO on the NMDA receptor.

Amino Acid Oxidoreductases↗
PubMed2003

Potential use of estrogen-like drugs for the prevention of Alzheimer's disease.

Prior epidemiological studies have shown decreased incidence of Alzheimer's disease among women who were long-term users of hormone replacement therapy. In vitro studies have shown that estrogens possess antioxidant activity, protect cells from the cytotoxic effect of beta-amyloid peptides, and decrease the amyloidogenic processing of the amyloid precursor protein. Animal studies have shown that estrogens promote neuronal plasticity and lead to decreased levels of cerebral beta-amyloid peptide accumulation via decreased amyloidogenic processing of the amyloid precursor protein. Recently, a randomized double-blind placebo-controlled study of the effects of estrogen plus progestin treatment in women over 65 years of age found that this treatment was associated with increased incidence of probable dementia. It is not known whether this combination of hormones or the late age at which the therapy was administered was responsible for the adverse outcome.

Alzheimer Disease↗
PubMed2005

Long-lasting change in brain dynamics induced by methamphetamine: enhancement of protein kinase C-dependent astrocytic response and behavioral sensitization.

It is well known that long-term exposure to psychostimulants induces neuronal plasticity. Recently, accumulating evidence suggests that astrocytes may actively participate in synaptic plasticity. In this study, we found that in vitro treatment of cortical neuron/glia co-cultures with either methamphetamine (METH) or morphine (MRP) caused the activation of astrocytes via protein kinase C (PKC). Purified astrocytes were markedly activated by METH, whereas MRP had no such effect. METH, but not MRP, caused a long-lasting astrocytic activation in cortical neuron/glia co-cultures. Furthermore, MRP-induced behavioral sensitization to hyper-locomotion was reversed by 2 months of withdrawal following intermitted MRP administration, whereas behavioral sensitization to METH-induced hyper-locomotion was maintained even after 2 months of withdrawal. Consistent with this cell culture study, in vivo treatment with METH, which was associated with behavioral sensitization, caused a PKC-dependent astrocytic activation in the cingulate cortex and nucleus accumbens of mice. These findings provide direct evidence that METH induces a long-lasting astrocytic activation and behavioral sensitization through the stimulation of PKC in the rodent brain. In contrast, MRP produced a reversible activation of astrocytes via neuronal PKC and a reversibility of behavioral sensitization. This information can break through the definition of drugs of abuse and the misleading of concept that morphine produces a long-lasting neurotoxicity.

Amphetamine-Related Disorders↗
PubMed2004

Glycogen synthase kinase-3: a target for novel bipolar disorder treatments.

The enzyme glycogen synthase kinase-3 (GSK-3) is a direct target of lithium. While originally recognized as an important molecule in a limited number of cellular processes, with unclear significance for the treatment of bipolar disorder, recent evidence suggests it has critically important cellular functions in the adult brain. GSK-3 has an essential role in a number of signaling pathways and regulates the function of a diverse number of proteins, notably transcription factors and cytoskeletal elements. The most important functions of the enzyme in regard to bipolar disorder may be critical effects on cellular resilience and neuronal plasticity. There is tremendous interest in GSK-3 inhibitors as novel therapeutic agents, and selective, small-molecule compounds are rapidly being developed for a broad range of other maladies including diabetes, Alzheimer's disease, stroke, and inflammatory conditions. In this perspectives article, we provide an overview of the molecular targets of lithium, focusing on GSK-3-regulated signaling pathways and the important functions of GSK-3 that may have relevance for the treatment of bipolar disorder. We conclude with a discussion of the GSK-3 inhibitors furthest in development and the clinical trials that may emerge.

Antimanic Agents↗
PubMed1996

Early development in aquatic vertebrates in near weightlessness during the D-2 Mission STATEX project.

Aboard the German-Spacelab-Mission D-2 the project "Gravity Perception and Neuronal Plasticity (STATEX II)" was performed. STATEX is for STATolith EXperiment. Objects were growing tadpoles of the South African Toad (Xenopus laevis D.) and a juvenile cichlid fish (Oreochromis mossambicus). The results give a broader base for the understanding of how environmental stimuli (e.g. linear accelerations) affect the development and function of the gravity perceiving systems in these two vertebrates. These systems are accepted as models for the human vestibulum. Results of experiments in hyper-g (up to 5 g), simulated weightlessness (Fast-rotating-clinostat) and parabolic flights are compared and discussed.

Animals↗
PubMed1994

Trial-spacing effects in Hermissenda suggest contributions of associative and nonassociative cellular mechanisms.

In behaving Hermissenda, a preparatory conditioned response developed across repeated pairings of light (conditioned stimulus; CS) and rotation (unconditioned stimulus; US) with intertrial intervals (ITIs) of 60 and 120 s, but not 30 s. Likewise, contiguous in vitro stimulation of the visual and vestibular receptors, an analog of behavioral conditioning, resulted in an increase in the input resistance (i.e., excitability, a correlate of conditioning) of the B photoreceptors of the Hermissenda's eye, but only with ITIs greater than 60 s. Calcium signaling in the B cell, critical to the induction of this neuronal plasticity, was attenuated with shorter ITIs owing to (a) a reduction of the light-induced generator potential and hence voltage-dependent Ca2+ influx during the light CS, (b) a depression of the Ca2+ current that persisted throughout shorter ITIs, and (c) a steady-state inactivation of the Ca2+ current as a result of a sustained depolarization persisting from the previous trial. These results are consistent with a 2-process theory of associative learning in which a primary process (Ca2+ influx) may be opposed by a secondary process (depression of the Ca2+ current) during short ITIs.

Animals↗
PubMed1996

c-Fos expression as a tool to search for the neurobiological base of the sexual behaviour of males.

Elevated expression of c-fos mRNA and/or its protein (c-Fos) has been repeatedly observed following activation of brain cells with various stimuli. As a consequence it has been proposed that elevated c-fos expression may serve as a marker of neuronal activation reflecting a predisposal to long-term changes in cell functioning (neuronal plasticity). In studies on copulatory behaviour of male animals, elevated Fos immunoreactivity (related most probably to c-Fos) has been used by many researchers as a tool to reveal functional neuroanatomy of the behaviour. They found that brain regions such as medial preoptic area (MPOA), bed nucleus of stria terminalis (BNST), medial amygdala (MeAm) and central tegmental field (CTF) are always activated in a copulation-dependent manner in various species (rats and hamsters were the most often studied in this regard). This paper reviews the data gathered in this field, and discusses them in the context of a role of elevated Fos expression in acquisition vs. performance of the sexual behaviour.

Animals↗
PubMed1999

Lesion-induced changes of electrophysiological properties in astrocytes of the rat dentate gyrus.

Reorganization of the adult dentate gyrus following unilateral entorhinal cortex lesion (ECL) is a well-established model for studying mechanisms of trauma-induced neuronal plasticity. The lesion induces deafferentiation of the outer molecular layer, which is accompanied by a strong astroglial reaction. This glial response is thought to contribute to subsequent repair processes, but the underlying mechanisms are poorly understood. In this study we addressed the question whether denervation leads to modifications in the electrophysiological properties of astrocytes, assuming that such changes might be involved in the remodeling of neural circuitry. Patch-clamp recordings were obtained from astrocytes in the dentate gyrus of adult rats that underwent ECL and compared to corresponding data from control animals. We observed a significant reduction of inward rectifier K(+) current densities, a positive shift of resting potentials, and an increase in input resistance in astrocytes of the denervated molecular layer. Current densities were reduced between 6 and 19 days postlesion (dpl), reaching a minimum at 10 dpl. Voltage-gated outward K(+) currents were not affected by the lesion. Inward rectifier K(+) currents increase with maturation in astrocytes. Thus, our results provide evidence that, following ECL, mature astrocytes dedifferentiated and readapted an immature current pattern. Presumably, these changes lead to stronger and prolonged depolarization of glial cells and neurons in response to activity-dependent K(+) release, which in turn might enhance the synthesis of neurotrophic factors and contribute to a permissive environment for neuronal reorganization.

Animals↗
PubMed2002

Molecular abnormalities in the major psychiatric illnesses: Classification and Regression Tree (CRT) analysis of post-mortem prefrontal markers.

Post-mortem specimens from the Stanley Foundation Neuropathology Consortium, which contains matched samples from patients with schizophrenia, bipolar disorder, non-psychotic depression and normal controls (n = 15 per group), have been distributed to many research groups around the world. This paper provides a summary of abnormal markers found in prefrontal cortical areas from this collection between 1997 and 2001. With parametric analyses of variance of 102 separate data sets, 14 markers were abnormal in at least one disease. The markers pertained to a variety of neural systems and processes including neuronal plasticity, neurotransmission, signal transduction, inhibitory interneuron function and glial cells. The data sets were also examined using the non-parametric Classification and Regression Tree (CRT) technique for the four diagnostic groups and in pair-wise combinations. In contrast to the results obtained with analyses of variance, the CRT method identified a smaller set of nine markers that contributed maximally to the diagnostic classifications. Three of the nine markers observed with CRT overlapped with the ANOVA results. Six of the nine markers observed with the CRT technique pertained to aspects of glutamatergic, GABA-ergic, and dopaminergic neurotransmission.

Adult↗
PubMed2007

Brain nitric oxide synthases and mitochondrial function.

Nitric oxide is a small signaling molecule, which may act as a neurotransmitter and neuromodulator, exerting a regulatory effect on neuronal function. It can diffuse from its site of synthesis to different intra and extracellular compartments, being therefore present in the pre-synaptic, synaptic and post-synaptic spaces. Recently, a NOS located in the mitochondria (mtNOS) has been observed in different brain regions, responsible for the production of NO in these organelles and identified as nNOS. A regulatory effect of NO on mitochondrial function was described in brain mitochondria, where NO acts mainly by inhibiting cytochrome oxidase activity. Hippocampal mitochondrial dysfunction and decreased mtNOS activity and expression were reported in association with ultrastructural damage in an experimental model of hepatic encephalopathy. Enriched environment exposure preserved the aged animals from spatial cognition impairment; also environment and training modulated neuronal plasticity in pre-pubertal rats through NO-dependent mechanisms. In addition, brain cortical mitochondrial respiration and mtNOS activity and expression were analyzed as function of age. Mitochondrial NO production showed a decreasing tendency as a function of age. These results are in accordance with the protein expression analyzed by Western Blot of mitochondrial fractions which was 6.5 times higher in 1 month aged rats as compared with 14 old animals. Concomitant with these results, a clear increasing oxygen uptake tendency in state 3 respiration was observed, meanwhile only a slight increase was observed in state 4. All these results seems to be clearly related with the reversible and concentration-dependent attenuation of the respiratory chain by NO.

Aging↗
PubMed1999

Control of spine formation by electrical activity in the adult rat cerebellum.

Dendritic spines are a key structure in neuronal plasticity. Enhanced activity is commonly associated with an increase in spine size and density. Purkinje cell dendrites are characterized by a proximal and a distal compartment on which climbing fibers and parallel fibers, respectively, impinge. The proximal region has a very low spine density, whereas the distal region has a high density. Previous experiments showed that after climbing fiber deletion, Purkinje cells become hyperactive, and a large number of spines develop on the proximal dendrites. Here we show that the same hyperspiny transformation occurs in the proximal dendrites of adult Purkinje cells by depressing electrical activity with tetrodotoxin. Thus, spines in different dendritic compartments are created or maintained independently from the level of Purkinje cell-firing rate and when the afferent activity is blocked. This conclusion supports the view that spinogenesis is the expression of an intrinsic program and the two regions of the dendritic tree respond differently to activity block because of differences in the inputs that they receive. On tetrodotoxin treatment, climbing fibers become atrophic and may sprout thin collateral ramifications directed mainly toward the granular layer. All changes are reversible on tetrodotoxin removal. Therefore, Purkinje cells provide a model where spines in different compartments of the same neuron are differently regulated by the activity of their local afferents. In addition, electrical activity is also essential to maintain the full climbing fiber innervation.

Animals↗
PubMed2003

Repair of amyloid beta(25-35)-induced memory impairment and synaptic loss by a Kampo formula, Zokumei-to.

Although Zokumei-to (ZMT), a Kampo formula, has been used for postapopletic sequelae such as paralysis and logopathy, only few studies of this drug have been carried out. We hypothesized that ZMT may affect neuronal plasticity and investigated whether or not this drug is capable of improving learning impairment and synaptic loss observed in patients with Alzheimer's disease (AD). Amyloid beta(25-35) [Abeta(25-35)] (4.7 nmol) was intracerebroventricularly injected into ddY mice (male, 6 weeks old). Fourteen days after the injection, mice were given ZMT extract (500 mg/kg/day) per os for 15 days. In a memory acquisition test, the Abeta(25-35)-injected mice required more time to master this task than did mice in the saline- or reverse peptide Abeta(35-25)-treated groups. ZMT-treated mice shortened escape latencies during trial days 3-5, but not significantly. Three days after the last drug treatment, a retention test was performed. Following ZMT, the number of crossings over a platform was significantly decreased in Abeta(25-35)-injected mice compared with those in the control groups. However, ZMT-treated mice showed complete recovery of this number. Although Abeta(25-35) injection decreased synaptophysin expression in the cerebral cortex and the hippocampus, ZMT treatment significantly increased the level of expression of synaptophysin up to the control level. Donepezil hydrochloride (DNP, 0.5 mg/kg/day, p.o.) clinically used for AD had no effect on memory retention and synaptophysin levels. Abeta(25-35)-induced neuronal loss was not observed in any region of the brain. The present results suggest that memory impairment and synaptic loss in AD patients may be improved by treatment with ZMT, even after such impairment has already progressed.

Alzheimer Disease↗
PubMed1995

PCR differential display identifies a rat brain mRNA that is transcriptionally regulated by cocaine and amphetamine.

Neuronal plasticity associated with both short- and long-term administration of psychomotor stimulants involves alterations in specific patterns of gene expression. In order to screen for brain region specific mRNAs which are transcriptionally regulated by acute cocaine and amphetamine, PCR differential display was employed. This approach identified a previously uncharacterized mRNA whose relative levels in the striatum are induced four- to fivefold by acute psychomotor stimulant administration. Isolation and characterization of corresponding cDNA clones resulted in complete nucleotide sequence analysis, including prediction of the encoded protein product. Alternate polyA site utilization in the predicted 3' noncoding region results in the appearance of an RNA doublet, approximately 700 and 900 bases in length, following Northern analysis. A presumed alternate splicing event further generates diversity within the transcripts, and results in the presence or absence of an in-frame 39 base insert within the putative protein coding region. As a result, the predicted translation products are either 129 or 116 amino acids in length. A common hydrophobic leader sequence at the amino terminus is present within each predicted polypeptide, suggesting that the protein product is targeted for entry into the secretory pathway. Basal expression of the RNA doublet is limited to neuroendocrine tissues, further implying that the protein product plays a functional role in both neuronal and endocrine tissues.

Amino Acid Sequence↗
PubMed1996

Sympathetic sprouting reverses decreases in membrane-associated activity of protein kinase C following septohippocampal denervation of the rat hippocampus.

Hippocampal sympathetic ingrowth (HSI), a form of neuronal plasticity, is induced by medial septal lesions and consists of the sprouting of peripheral sympathetic fibers, arising from the superior cervical ganglion, into the dentate gyrus and CA3 region of the hippocampus. HSI has been previously shown to alter learned and spontaneous behaviors, phosphatidyl inositide hydrolysis, and the antagonist binding kinetics of both muscarinic cholinergic receptors and phorbol ester receptors. We now report that sympathetic sprouting reverses decreases in membrane-associated activity of protein kinase C (PKC) following septohippocampal denervation of the rat hippocampus. Further, no changes were found in alpha, beta or gamma PKC isoenzymes among experimental groups, suggesting that the group A PKC isoforms do not mediate the observed changes in activity and phorbol ester binding.

Analysis of Variance↗