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Kasia Radwanska, Grace Schenatto-Pereira, Magdalena Ziółkowska, Kacper Łukasiewicz, K Peter Giese
Understanding the molecular and cellular process specifically regulated during fear memory consolidation and extinction is a critical step toward development of new strategies in the treatment of human fear disorders. Here we used inhibitory component of AP-1 transcription factor, JunB, in order to map brain regions where JunB-dependent transcription is regulated during consolidation and extinction of contextual fear memory. We found that contextual fear memory consolidation induced JunB expression in the medial nucleus and intercalated cells of the amygdala while extinction training induced JunB in the CA1 and CA3 areas of the dorsal hippocampus...
November 2015: Neurobiology of Learning and Memory
Roopashri Holehonnur, Jonathan A Luong, Dushyant Chaturvedi, Anthony Ho, Srihari K Lella, Matthew P Hosek, Jonathan E Ploski
BACKGROUND: In recent years, there has been an increased interest in using recombinant adeno-associated viruses (AAV) to make localized genetic manipulations within the rodent brain. Differing serotypes of AAV possess divergent capsid protein sequences and these variations greatly influence each serotype's ability to transduce particular cell types and brain regions. We therefore aimed to determine the AAV serotype that is optimal for targeting neurons within the Basal and Lateral Amygdala (BLA) since the transduction efficiency of AAV has not been previously examined within the BLA...
2014: BMC Neuroscience
A Spalloni, N Origlia, C Sgobio, A Trabalza, M Nutini, N Berretta, G Bernardi, L Domenici, M Ammassari-Teule, P Longone
Although amyotrophic lateral sclerosis (ALS) has long been considered as a lower motor neuron (MN) disease, degeneration of upper MNs arising from a combination of mechanisms including insufficient growth factor signaling and enhanced extracellular glutamate levels is now well documented. The observation that these mechanisms are altered in presymptomatic superoxide dismutase (SOD1) mice, an ALS mouse model, suggests that defective primary motor cortex (M1) synaptic activity might precede the onset of motor disturbances...
April 2011: Cerebral Cortex
Shingo Miyata, Yasutake Mori, Masaya Tohyama
Protein arginine N-methyltransferase 3 (PRMT3) is a cytoplasmic enzyme that utilizes S-adenosyl-L-methionine (AdoMet) to methylate specific proteins, most of which contain GAR (glycine-arginine rich) motifs. PRMT3 has been shown to play a role in the proper maturation of the 80S ribosome by binding to and catalyzing the methylation of rpS2, a component of the 40S ribosomal subunit. However, the other roles of PRMT3 are fairly unclear, particularly in the brain, which is abundant in methylated proteins. In this study, we perturbed PRMT3 expression in cultured rat hippocampal neurons by transiently introducing siRNA oligonucleotides that were designed to hybridize with PRMT3 mRNA and then we examined the morphological and functional effects of neuronal PRMT3 depletion...
September 17, 2010: Brain Research
Linda Wilbrecht, Anthony Holtmaat, Nick Wright, Kevin Fox, Karel Svoboda
The stabilization of new spines in the barrel cortex is enhanced after whisker trimming, but its relationship to experience-dependent plasticity is unclear. Here we show that in wild-type mice, whisker potentiation and spine stabilization are most pronounced for layer 5 neurons at the border between spared and deprived barrel columns. In homozygote alphaCaMKII-T286A mice, which lack experience-dependent potentiation of responses to spared whiskers, there is no increase in new spine stabilization at the border between barrel columns after whisker trimming...
April 7, 2010: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
B F Singer, J A Loweth, R L Neve, P Vezina
Calcium/calmodulin-dependent protein kinase II (CaMKII) activity is necessary for the long-lasting expression of locomotor sensitization and enhanced drug-taking observed in rats previously exposed to psychostimulants. Exposure to these drugs also transiently increases alphaCaMKII levels in the nucleus accumbens (NAcc), an effect that, when mimicked by transient viral-mediated overexpression of alphaCaMKII in NAcc shell neurons, leads to long-lasting enhancement in locomotor responding to amphetamine and NAcc alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA)...
April 2010: European Journal of Neuroscience
Júlia D Moreira, Luisa Knorr, Marcelo Ganzella, Ana Paula Thomazi, Carolina G de Souza, Débora G de Souza, Carolina F Pitta, Tadeu Mello e Souza, Susana Wofchuk, Elaine Elisabetsky, Lúcia Vinadé, Marcos L S Perry, Diogo O Souza
Essential omega-3 polyunsaturated fatty acids (omega3) are crucial to brain development and function, being relevant for behavioral performance. In the present study we examined the influence of dietary omega3 in the development of the glutamatergic system and on behavior parameters in rats. Female rats received isocaloric diets, either with omega3 (omega3 group) or a omega3 deficient diet (D group). In ontogeny experiments of their litters, hippocampal immunocontent of ionotropic NMDA and AMPA glutamatergic receptors subunits (NR2 AB and GluR1, respectively) and the alpha isoform of the calcium-calmodulin protein kinase type II (alphaCaMKII) were evaluated...
May 2010: Neurochemistry International
Jessica A Loweth, Bryan F Singer, Lorinda K Baker, Georgia Wilke, Hidetoshi Inamine, Nancy Bubula, John K Alexander, William A Carlezon, Rachael L Neve, Paul Vezina
Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is known to contribute to the expression of psychostimulant sensitization by regulating dopamine (DA) overflow from DA neuron terminals in the nucleus accumbens (NAcc). The present experiments explored the contribution of CaMKII in NAcc neurons postsynaptic to these terminals where it is known to participate in a number of signaling pathways that regulate responding to psychostimulant drugs. Exposure to amphetamine transiently increased alphaCaMKII levels in the shell but not the core of the NAcc...
January 20, 2010: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Hamid R Maei, Kirill Zaslavsky, Afra H Wang, Adelaide P Yiu, Cátia M Teixeira, Sheena A Josselyn, Paul W Frankland
In the water maze, mice are trained to navigate to an escape platform located below the water's surface, and spatial learning is most commonly evaluated in a probe test in which the platform is removed from the pool. While contemporary tracking software provides precise positional information of mice for the duration of the probe test, existing performance measures (e.g., percent quadrant time, platform crossings) fail to exploit fully the richness of this positional data. Using the concept of entropy (H), here we develop a new measure that considers both how focused the search is and the degree to which searching is centered on the former platform location...
2009: Frontiers in Integrative Neuroscience
S Lynn Bostrom, Justin Dore, Leslie C Griffith
The vast majority of serine/threonine protein kinases have a strong preference for ATP over GTP as a phosphate donor. CK2 (Casein kinase 2) is an exception to this rule and in this study we investigate whether calcium/calmodulin-dependent protein kinase II (CaMKII) has the same extended nucleotide range. Using the Drosophila enzyme, we have shown that CaMKII uses Mg(2+)GTP with a higher K(m) and V(max) compared to Mg(2+)ATP. Substitution of Mn(2+) for Mg(2+) resulted in a much lower K(m) for GTP, while nearly abolishing the ability of CaMKII to use ATP...
December 25, 2009: Biochemical and Biophysical Research Communications
Mauro Racaniello, Alessio Cardinale, Cristiana Mollinari, Margherita D'Antuono, Giovanna De Chiara, Virginia Tancredi, Daniela Merlo
Protein phosphorylation is the main signaling system known to trigger synaptic changes underlying long-term potentiation (LTP). The timing of these phosphorylations plays an essential role to maintain the potentiated state of synapses. However, in mice a simultaneous analysis of phosphorylated proteins during early-LTP (E-LTP) has not been thoroughly carried out. Here we described phosphorylation changes of alphaCaMKII, ERK1/2, PKB/Akt and CREB at different times after E-LTP induced at Schaffer collateral/commissural fiber-CA1 synapses by 1 s 100 Hz tetanic stimulation in mouse hippocampal slices...
February 2010: Neurochemical Research
Abdirahman M Jama, Jon Fenton, Saralili D Robertson, Katalin Török
Ca(2+)/calmodulin-dependent protein kinase II (alphaCaMKII) is thought to exert its role in memory formation by autonomous Ca(2+)-independent persistent activity conferred by Thr(286) autophosphorylation, allowing the enzyme to remain active even when intracellular [Ca(2+)] has returned to resting levels. Ca(2+) sequestration-induced inhibition, caused by a burst of Thr(305/306) autophosphorylation via calmodulin (CaM) dissociation from the Thr(305/306) sites, is in conflict with this view. The processes of CaM binding, autophosphorylation, and inactivation are dissected to resolve this conflict...
October 9, 2009: Journal of Biological Chemistry
Jason M Uslaner, Sophie Parmentier-Batteur, Rosemarie B Flick, Nathaniel O Surles, June S H Lam, Caitlyn H McNaughton, Marlene A Jacobson, Pete H Hutson
In the search for strategies to treat schizophrenia, attention has focused on enhancing NMDA receptor function. In vitro experiments show that metabotropic glutamate 5 receptor (mGluR5) activation enhances NMDA receptor activity, and in vivo experiments indicate that mGluR5 positive allosteric modulators (PAMs) are effective in preclinical assays measuring antipsychotic potential and cognition. Here we characterized the dose-effect function of CDPPB (3-cyano-N-(1,3-diphenyl-1H-pyrazol-5-yl)benzamide), an mGluR5 PAM, on novel object recognition memory in unimpaired Wistar Hannover rats (0, 10 or 30 mg/kg CDPPB) and animals with an MK-801-induced deficit (0, 3, 10, or 30 mg/kg CDPPB)...
October 2009: Neuropharmacology
Li-Hong Long, Rui-Li Liu, Fang Wang, Jue Liu, Zhuang-Li Hu, Na Xie, You Jin, Hui Fu, Jian-Guo Chen
1. Age-related impairments in hippocampus-dependent spatial learning and memory are not associated with a loss of neurons, but may be related to synaptic changes. In the present study, we analysed the behavioural performance of adult, middle-aged and old Wistar rats using the Morris water maze, as well as the structure of synapses and the expression of autophosphorylated Ca(2+)/calmodulin-dependent protein kinase II at threonine 286 (pThr286-alphaCaMKII), a key post-synaptic protein in the CA1 stratum radiatum, in the same rats...
July 2009: Clinical and Experimental Pharmacology & Physiology
Naveed Aslam, Yoshi Kubota, David Wells, Harel Z Shouval
Memory can last a lifetime, yet synaptic contacts that contribute to the storage of memory are composed of proteins that have much shorter lifetimes. A physiological model of memory formation, long-term potentiation (LTP), has a late protein-synthesis-dependent phase (L-LTP) that can last for many hours in slices or even for days in vivo. Could the activity-dependent synthesis of new proteins account for the persistence of L-LTP and memory? Here, we examine the proposal that a self-sustaining regulation of translation can form a bistable switch that can persistently regulate the on-site synthesis of plasticity-related proteins...
2009: Molecular Systems Biology
Evgeny A Sametsky, John F Disterhoft, Masuo Ohno
It has been well documented that alpha-calcium/calmodulin-dependent protein kinase II (alphaCaMKII) is central to synaptic plasticity such as long-term potentiation, an activity-dependent strengthening of synapses that is thought to underlie certain types of learning and memory. However, the mechanisms by which alphaCaMKII may regulate neuronal excitability remain unclear. Here, we report that alphaCaMKII knock-in mice with a targeted T286A point mutation that prevents its autophosphorylation (alphaCaMKII(T286A)) showed increased excitability of CA1 pyramidal neurons compared with wild-type controls, as measured by a decrease in the slow component of post-burst afterhyperpolarization (sAHP) following high-frequency stimulation of Schaffer collateral afferent fibers...
July 2009: Neurobiology of Learning and Memory
M Cecilia Martínez, Sebastian P Fernandez, Leonardo M Loscalzo, Cristina Wasowski, Alejandro C Paladini, Mariel Marder, Jorge H Medina, Haydée Viola
The aim of this work was to evaluate if the intraperitoneal administration of the natural compound hesperidin, in a sedative dose, and neo-hesperidin, a hesperidin structural analog that exerts minor sedative effect, were able to induce changes in intracellular signaling cascades in different areas of the brain. The systemic administration of hesperidin produced a marked reduction in the phosphorylation state of extracellular signal-regulated kinases 1/2 (ERK 1/2), but not of Ca(+2)/calmodulin-dependent protein kinase II alpha subunit (alphaCaMKII), in the cerebral cortex, cerebellum and hippocampus...
April 2009: Pharmacology, Biochemistry, and Behavior
Carla Cunha, Andrea Angelucci, Angela D'Antoni, Mate D Dobrossy, Stephen B Dunnett, Nicoletta Berardi, Riccardo Brambilla
In this study we analyzed the effect on behavior of a chronic exposure to brain-derived neurotrophic factor (BDNF), by analysing a mouse line overexpressing BDNF under the alphaCaMKII promoter, which drives the transgene expression exclusively to principal neurons of the forebrain. BDNF transgenic mice and their WT littermates were examined with a battery of behavioral tests, in order to evaluate motor coordination, learning, short and long-term memory formation. Our results demonstrate that chronic BDNF overexpression in the central nervous system (CNS) causes learning deficits and short-term memory impairments, both in spatial and instrumental learning tasks...
March 2009: Neurobiology of Disease
Ryoichi Kimura, Alcino J Silva, Masuo Ohno
Accumulating evidence indicates the key role of alpha-calcium/calmodulin-dependent protein kinase II (alphaCaMKII) in synaptic plasticity and learning, but it remains unclear how this kinase participates in the processing of memory extinction. Here, we investigated the mechanism by which alphaCaMKII may mediate extinction by using heterozygous knock-in mice with a targeted T286A mutation that prevents the autophosphorylation of this kinase (alphaCaMKII(T286A+/-)). Remarkably, partial reduction of alphaCaMKII function due to the T286A(+/-) mutation prevented the development of extinction without interfering with initial hippocampus-dependent memory formation as assessed by contextual fear conditioning and the Morris water maze...
November 2008: Learning & Memory
Rachel Aronoff, Carl Petersen
Viral vectors injected into the mouse brain offer the possibility for localized genetic modifications in a highly controlled manner. Lentivector injection into mouse neocortex transduces cells within a diameter of approximately 200mum, which closely matches the lateral scale of a column in barrel cortex. The depth and volume of the injection determines which cortical layer is transduced. Furthermore, transduced gene expression from the lentivector can be limited to predominantly pyramidal neurons by using a 1...
2007: Frontiers in Integrative Neuroscience
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