bluuebunny/crossref_metadata_2025_split huggingface dataset:
Two types of social buffering differentially mitigate conditioned fear responses
Authors: Kiyokawa Yasushi , Takeuchi Yukari , Mori Yuji 
Published: July 2010

AbstractIn a phenomenon known as ‘social buffering’ in various species, signals from a conspecific animal can mitigate stress responses. This buffering can be achieved either by ‘pair‐housing’ after a stressful event or by ‘pair‐exposure’ to an acute stressor with a conspecific animal. In this study, we compared the impacts of these two types of social buffering on auditory conditioned fear responses in male rats. When subjects were exposed to an auditory conditioned stimulus (CS) that had been paired with foot shocks on the previous day, they clearly exhibited behavioral (freezing), autonomic (aggravated stress‐induced hyperthermia) and neural (Fos expression) responses. Pair‐housing for 24 h with an unfamiliar rat following fear conditioning resulted in a suppressed autonomic, but not behavioral, response, with Fos expression in the lateral nucleus of the amygdala and ventrolateral periaqueductal gray. On the other hand, pair‐exposure to the CS with an unfamiliar rat eliminated the behavioral, but not the autonomic, response, with Fos expression in the basal nucleus of the amygdala and infralimbic region of the prefrontal cortex. Furthermore, subjects that had been pair‐housed and then pair‐exposed showed no behavioral, autonomic or neural responses, suggesting that the combination of the two procedures can completely block the fear conditioning sequence. These results demonstrate that two types of social buffering differentially relieve conditioned fear responses, by influencing different neural pathways in the amygdala.
Training‐induced changes in the expression of GABAA‐associated genes in the amygdala after the acquisition and extinction of Pavlovian fear
Authors: Heldt Scott A. , Ressler Kerry J. 
Published: July 2010

AbstractPrevious work suggests the γ‐aminobutyric acid (GABA)ergic system may be dynamically regulated during emotional learning. In the current study we examined training‐induced changes in the expression of GABAA‐related genes and the binding of GABA receptor radioligands in the amygdala after the acquisition and extinction of Pavlovian fear. Usingin situhybridization, we examined the expression pattern changes of mRNAs for GABAergic markers in the lateral, basolateral and central subdivisions of the amygdala in C57Bl/6J mice. These markers included GABA‐synthesizing enzymes (GAD67 and GAD65), major GABAAreceptor subunits (α1, α2, α3, α5, β2 and γ2) and the expression of mRNAs that are involved in a variety of GABA‐related intracellular processes, including GABA transporter‐1 (GAT1), GABAAreceptor‐associated protein and the GABAAclustering protein, gephyrin. With fear conditioning, we found decreased mRNA levels of α1, α5 and GAD67, as well as deceased benzodiazepine binding in the amygdala. Fear extinction induced an increase in mRNA levels of α2, β2, GAD67 and gephyrin, as well as a decrease in GAT1. Together, these findings indicate that the acquisition of fear induced a downregulation of mRNA markers related to a decrease in amygdala GABAergic function, whereas the acquisition of fear extinction produced an upregulation of GABAergic markers related to enhanced GABAergic transmission.
Conditioning of interictal behaviours, but not ictal behaviours, seizures or afterdischarge threshold, by kindling of the amygdala in rats
Authors: Wagner Jason P. , Corcoran Michael E. 
Published: July 2010

AbstractRats received 45 pairings of kindling or sham stimulation in distinctive contexts before a conditioned place preference/aversion test, to determine whether the stimulation and seizures were rewarding or punishing. After more pairings, rats received kindling stimulation in each context (switch test). Ictal measures in this test included afterdischarge duration, clonus duration, latency to clonus, class of convulsion and falls. After more pairings, afterdischarge threshold was measured in each context. On every fourth day of pairings, the rats' behaviour in the prestimulation interval was recorded, to measure conditioned anticipatory defensive behaviour. We partially replicated the finding of Barnes et al. (2001, Behav. Neurosci., 115, 1065–1072) that conditioned anticipatory responses and conditioned place aversion are associated with the kindling environment. However, there were no conditioned effects on any ictal measures, including afterdischarge threshold. Our results fail to support the hypothesis that conditioning is a universal mechanism for kindling.
Impaired nerve regeneration in reeler mice after peripheral nerve injury
Authors: Lorenzetto Erika , Panteri Roger , Marino Ramona , Keller Flavio , Buffelli Mario 
Published: July 2010

AbstractReelin, an extracellular matrix protein, plays an important role in the regulation of neuronal migration and cortical lamination in the developing brain. Little is known, however, about the role of this protein in axonal regeneration. We have previously shown that Reelin is secreted by Schwann cells in the peripheral nerve compartment during postnatal development and that it is up‐regulated following nerve injury in adult mice. In this work, we generated mice deficient in Reelin (reeler) that express yellow fluorescent protein (YFP) in a subset of neurons and examined the axonal regeneration following nerve crush. We found that axonal regeneration was significantly altered compared with wild‐type mice. By contrast, retrograde tracing with Fluorogold dye after sciatic nerve crush was unaffected in these mutants, being comparable with normal axonal transport observed in wild‐type. These results indicate that the absence of Reelin impairs axonal regeneration following injury and support a role for this protein in the process of peripheral nerve regeneration.
Oxidative stress on EAAC1 is involved in MPTP‐induced glutathione depletion and motor dysfunction
Authors: Aoyama Koji , Matsumura Nobuko , Watabe Masahiko , Nakaki Toshio 
Published: July 2010

AbstractExcitatory amino acid carrier 1 (EAAC1) is a glutamate transporter expressed on mature neurons in the CNS, and is the primary route for uptake of the neuronal cysteine needed to produce glutathione (GSH). Parkinson's disease (PD) is a neurodegenerative disorder pathogenically related to oxidative stress and shows GSH depletion in the substantia nigra (SN). Herein, we report that 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated mice, an experimental model of PD, showed reduced motor activity, reduced GSH contents, EAAC1 translocation to the membrane and increased levels of nitrated EAAC1. These changes were reversed by pre‐administration of n‐acetylcysteine (NAC), a membrane‐permeable cysteine precursor. Pretreatment with 7‐nitroindazole, a specific neuronal nitric oxide synthase inhibitor, also prevented both GSH depletion and nitrotyrosine formation induced by MPTP. Pretreatment with hydrogen peroxide, l‐aspartic acid β‐hydroxamate or 1‐methyl‐4‐phenylpyridinium reduced the subsequent cysteine increase in midbrain slice cultures. Studies with chloromethylfluorescein diacetate, a GSH marker, demonstrated dopaminergic neurons in the SN to have increased GSH levels after NAC treatment. These findings suggest that oxidative stress induced by MPTP may reduce neuronal cysteine uptake, via EAAC1 dysfunction, leading to impaired GSH synthesis, and that NAC would exert a protective effect against MPTP neurotoxicity by maintaining GSH levels in dopaminergic neurons.
D1 dopamine receptor activation of NFAT‐mediated striatal gene expression
Authors: Groth Rachel D. , Weick Jason P. , Bradley Katherine C. , Luoma Jessie I. , Aravamudan Bharathi , Klug Jason R. , Thomas Mark J. , Mermelstein Paul G. 
Published: July 2010

AbstractExposure to drugs of abuse activates gene expression and protein synthesis that result in long‐lasting adaptations in striatal signaling. Therefore, identification of the transcription factors that couple drug exposure to gene expression is of particular importance. Members of the nuclear factor of activated T‐cells (NFATc) family of transcription factors have recently been implicated in shaping neuronal function throughout the rodent nervous system. Here we demonstrate that regulation of NFAT‐mediated gene expression may also be a factor in drug‐induced changes to striatal functioning. In cultured rat striatal neurons, stimulation of D1 dopamine receptors induces NFAT‐dependent transcription through activation of L‐type calcium channels. Additionally, the genes encoding inositol‐1,4,5‐trisphosphate receptor type 1 and glutamate receptor subunit 2 are regulated by striatal NFATc4 activity. Consistent with thesein‐vitrodata, repeated exposure to cocaine triggers striatal NFATc4 nuclear translocation and the up‐regulation of inositol‐1,4,5‐trisphosphate receptor type 1 and glutamate receptor subunit 2 gene expressionin vivo, suggesting that cocaine‐induced increases in gene expression may be partially mediated through activation of NFAT‐dependent transcription. Collectively, these findings reveal a novel molecular pathway that may contribute to the enduring modifications in striatal functioning that occur following the administration of drugs of abuse.
Dorsal cochlear nucleus responses to somatosensory stimulation are enhanced after noise‐induced hearing loss
Authors: Shore S. E. , Koehler S. , Oldakowski M. , Hughes L. F. , Syed S. 
Published: July 2010

AbstractMultisensory neurons in the dorsal cochlear nucleus (DCN) achieve their bimodal response properties [Shore (2005) Eur. J. Neurosci., 21, 3334–3348] by integrating auditory input via VIIIth nerve fibers with somatosensory input via the axons of cochlear nucleus granule cells [Shore et al. (2000) J. Comp. Neurol., 419, 271–285; Zhou & Shore (2004)J. Neurosci. Res., 78, 901–907]. A unique feature of multisensory neurons is their propensity for receiving cross‐modal compensation following sensory deprivation. Thus, we investigated the possibility that reduction of VIIIth nerve input to the cochlear nucleus results in trigeminal system compensation for the loss of auditory inputs. Responses of DCN neurons to trigeminal and bimodal (trigeminal plus acoustic) stimulation were compared in normal and noise‐damaged guinea pigs. The guinea pigs with noise‐induced hearing loss had significantly lower thresholds, shorter latencies and durations, and increased amplitudes of response to trigeminal stimulation than normal animals. Noise‐damaged animals also showed a greater proportion of inhibitory and a smaller proportion of excitatory responses compared with normal. The number of cells exhibiting bimodal integration, as well as the degree of integration, was enhanced after noise damage. In accordance with the greater proportion of inhibitory responses, bimodal integration was entirely suppressive in the noise‐damaged animals with no indication of the bimodal enhancement observed in a sub‐set of normal DCN neurons. These results suggest that projections from the trigeminal system to the cochlear nucleus are increased and/or redistributed after hearing loss. Furthermore, the finding that only neurons activated by trigeminal stimulation showed increased spontaneous rates after cochlear damage suggests that somatosensory neurons may play a role in the pathogenesis of tinnitus.
Context‐specific sensitization of cocaine‐induced locomotor activity and associated neuronal ensembles in rat nucleus accumbens
Authors: Mattson Brandi J. , Koya Eisuke , Simmons Danielle E. , Mitchell Timothy B. , Berkow Alexander , Crombag Hans S. , Hope Bruce T. 
Published: July 2010

AbstractRepeated cocaine administration to rats outside their home cage induces behavioral sensitization that is strongly modulated by the drug administration environment. We hypothesized that stimuli in the drug administration environment activate specific sets of striatal neurons, called neuronal ensembles, for further cocaine‐enhanced activation, and that repeated activation of these neuronal ensembles underlies context‐specific sensitization. In the present study, we repeatedly administered cocaine or saline to rats on alternate days in two distinct environments outside the home cage, one paired with cocaine and the other with saline. On test day, cocaine challenge injections in the cocaine‐paired environment produced strongly enhanced levels of locomotor activity, while cocaine challenge injections in the saline‐paired environment did not. The corresponding record of past neuronal activation in nucleus accumbens and caudate‐putamen during repeated drug administration was assessed using FosB immunohistochemistry, while acute neuronal activation on test day was assessed usingc‐fos in situhybridization. Although only 2% of striatal neurons were FosB labeled, 87% of these FosB‐labeled neurons were co‐labeled withc‐foswhen cocaine was injected in the cocaine‐paired environment. The degree of co‐labeling was significantly less following cocaine or saline challenge injections in the saline‐paired environment. Furthermore, the total number ofc‐fos‐labeled neurons was greater with either cocaine or saline challenge injections in the cocaine‐paired environment than in the saline‐paired environment. These findings demonstrate that the drug administration environment partly determines which striatal neuronal ensembles are activated, and to what extent, following context‐specific sensitization to cocaine.
Novel neurons in ventral tegmental area fire selectively during the active phase of the diurnal cycle
Authors: Luo Alice H. , Georges François E. , Aston‐Jones Gary S. 
Published: July 2010

AbstractThe ventral tegmental area (VTA) contains dopamine (DA) and γ‐aminobutyric acid (GABA) neurons involved in motivation and behavioral state. These phenomena are also influenced by circadian factors. The goal of our studies was to examine the impulse activity of neurochemically identified VTA neurons during dark (active) vs light (rest) phases of the circadian cycle. Using extracellular single‐unit recordings with juxtacellular labeling in anesthetized rats, we found multiple neuronal subpopulations including ‘novel neurons’ that selectively fired during the dark phase. These novel neurons were electrophysiologically categorized into two groups, ‘novel wide‐spike’ and ‘novel thin‐spike’ neurons. Characterization of novel wide‐spike neurons found they were consistently non‐dopaminergic and non‐GABAergic [tyrosine hydroxylase (TH)(–), glutamic acid decarboxylase (GAD)(–)]. However, they were inhibited by the D2 agonist quinpirole, an effect that could be reversed by the D2 antagonist eticlopride. Physiologically, they were fast firing (mean = 18.9 ± 1.2 spikes/s), low bursting neurons (median = 6.2 ± 3.0% of spikes in bursts) with spike durations ≥ 2.0 ms, but slightly shorter than TH(+) neurons. They were also consistently non‐responsive to footpad stimulation. The novel thin‐spike neurons were neurochemically heterogeneous, and were located more ventrally than thin‐spike neurons found during the light phase. These findings reveal previously unknown populations of VTA neurons whose activities are sensitive to diurnal phase, and whose functions may be in the temporal regulation of arousal and motivational processes.
Developmental exposure to polychlorinated biphenyls PCB153 or PCB126 impairs learning ability in young but not in adult rats
Authors: Piedrafita Blanca , Erceg Slaven , Cauli Omar , Monfort Pilar , Felipo Vicente 
Published: July 2010

AbstractPolychlorinated biphenyls (PCBs) are persistent organic pollutants present in the food chain and in human blood and milk. Exposure to PCBs during pregnancy and lactation leads to cognitive impairment in children. The underlying mechanisms remain unclear. Some PCBs are endocrine disrupters. The aim of this work was to assess whether exposure of rats to PCB126 (dioxin‐like) or PCB153 (non‐dioxin‐like) during pregnancy and lactation affects the ability of the pups to learn a Y maze conditional discrimination task and/or the function of the glutamate–nitric oxide (NO)–cGMP pathway in brain in vivo when the rats are young (3 months) or adult (7–8 months). After finishing the learning experiments, the function of the pathway was analysed in the same rats by in vivo brain microdialysis. The results obtained show that perinatal exposure to PCB153 or PCB126: (1) impairs learning ability in young but not in adult rats, (2) impairs the glutamate–NO–cGMP pathway function in cerebellum in vivo in young but not in adult rats and (3) affect these parameters in males and females similarly. PCB126 is around 10 000‐fold more potent than PCB153. In control rats the function of the glutamate–NO–cGMP pathway and learning ability are lower in adult than in young rats. These age‐related differences are not present in rats exposed to PCBs. The impairment of the glutamate–NO–cGMP pathway function induced at young age by developmental exposure to the PCBs could be one of the mechanisms contributing to the cognitive impairment found in children whose mothers ingested PCB‐contaminated food during pregnancy and lactation.
Motor cortical control of internal pallidal activity through glutamatergic and GABAergic inputs in awake monkeys
Authors: Tachibana Yoshihisa , Kita Hitoshi , Chiken Satomi , Takada Masahiko , Nambu Atsushi 
Published: July 2010

AbstractThe internal segment of the globus pallidus (GPi) receives motor‐related cortical signals mainly through the striatum, the external segment of the globus pallidus (GPe) and the subthalamic nucleus (STN). The GPi sends its outputs outside the basal ganglia and plays a key role in motor control. Extracellular unit recordings were performed in awake monkeys to explore how glutamatergic STN inputs and GABAergic striatal and GPe inputs control spontaneous activity and how these inputs contribute to motor cortex stimulation‐induced responses of GPi neurons. The typical responses of GPi neurons to cortical stimulation consisted of an early excitation, an inhibition and a late excitation. Local applications of the NMDA receptor antagonist 3‐(2‐carboxypiperazin‐4‐yl)‐propyl‐1‐phosphonic acid and/or the AMPA/kainate receptor antagonist 1,2,3,4‐tetrahydro‐6‐nitro‐2,3‐dioxo‐benzo[f]quinoxaline‐7‐sulphonamide in the vicinity of recorded GPi neurons reduced the firing rate, and abolished or attenuated both early and late excitations following cortical stimulation. Local application of the GABAA receptor antagonist gabazine increased the firing rate, induced oscillatory firings and diminished the cortically induced inhibition. Muscimol or gabazine injection into the STN or GPe also altered the firing rate, and attenuated the late excitation of GPi neurons. The gabazine injection into the STN occasionally induced dyskinesia with significantly decreased GPi activity. These data suggest that the early and late excitations are glutamatergic and induced by the cortico‐STN‐GPi and cortico‐striato‐GPe‐STN‐GPi pathways, respectively. The inhibition is GABAergic and induced by the cortico‐striato‐GPi pathway. In addition, these inputs are the main factors governing the spontaneous activity of GPi neurons.
Binocular rivalry reveals a dissociation between the subjective experience and induced gamma oscillations
Authors: Fairhall Scott L. , Hamm Jeff P. , Kirk Ian J. 
Published: July 2010

AbstractBinocular rivalry occurs when separate incompatible images are presented, one to each eye. The subjective experience of viewing these stimuli is not of a fused image, rather the perceiver experiences either one or the other percept alternating across time. Manipulation of rivalry transfer, through an abrupt focal contrast change, causes the emerging percept to radiate across the declining image. This spreading percept transition has been likened to a wave of neural excitation propagating across the excitable medium of the visual cortex [H.R. Wilson et al. (2001) Nature, 412, 907–910; S.H. Lee et al. (2005) Nat. Neurosci., 8, 22–23]. Electrophysiologically, scalp‐recorded gamma oscillations (30–70 Hz) have been reported to persist for several hundred milliseconds in response to changes in the subjective experience induced by alterations in incoming sensory information (moving‐bar stimuli). Here, we used electroencephalographic recordings in the human and binocular rivalry transition to assess the role of scalp‐recorded gamma in purely subjective changes in the visual experience. Despite the protraction of perceptual binding over a 900 ms period, no deviation in the pattern of induced gamma was observed from that reported during the perceptual closure of static images. These results suggest that localized scalp‐recorded gamma oscillations are dissociable from the subjective visual experience.
Dendritic nicotinic receptors modulate backpropagating action potentials and long‐term plasticity of interneurons
Authors: Rózsa Balázs , Katona Gergely , Kaszás Attila , Szipöcs Róbert , Sylvester Vizi E. 
Published: July 2010

AbstractStratum radiatum interneurons, unlike pyramidal cells, are rich in nicotinic acetylcholine receptors (nAChRs); however, the role of these receptors in plasticity has remained elusive. As opposed to previous physiological studies, we found that functional α7‐subunit‐containing nAChRs (α7‐nAChRs) are abundant on interneuron dendrites of rats. Moreover, dendritic Ca2+transients induced by activation of α7‐nAChRs increase as a function of distance from soma. The activation of these extrasynaptic α7‐nAChRs by cholinergic agonists either facilitated or depressed backpropagating action potentials, depending on the timing of α7‐nAChR activation. We have previously shown that dendritic α7‐nAChRs are involved in the regulation of synaptic transmission, suggesting that α7‐nAChRs may play an important role in the regulation of the spike timing‐dependent plasticity. Here we provide evidence that long‐term potentiation is indeed boosted by stimulation of dendritic α7‐nAChRs. Our results suggest a new mechanism for a cholinergic switch in memory encoding and retrieval.
Parkin occurs in a stable, non‐covalent, ∼110‐kDa complex in brain
Authors: Van Humbeeck Cindy , Waelkens Etienne , Corti Olga , Brice Alexis , Vandenberghe Wim 
Published: July 2010

AbstractMutations in the gene for parkin, a 52‐kDa E3 ubiquitin ligase, are a major cause of hereditary Parkinson's disease (PD). In vitro studies have identified a large number of parkin‐interacting proteins. Whether parkin exists as a monomer or as part of a stable protein complex in vivo is uncertain. Here we demonstrate that endogenous parkin occurs in a stable, non‐covalent, ∼110‐kDa complex in native extracts from mouse brain, heart and skeletal muscle, while monomeric parkin is undetectable. Partial denaturation experiments indicate that this complex is at least a tetramer. Reported parkin‐binding partners do not show detectable association with the parkin complex on native gels. Upon overexpression in COS1, SH‐SY5Y or CHO cells, parkin accumulates predominantly as a monomer, suggesting that the interactors required for complex formation are available in limiting amounts in these cells. Importantly, PD‐linked parkin mutations significantly impair parkin complex formation. These data demonstrate that parkin oligomerizes into a stable, non‐covalent, heteromeric complex in vivo, and suggest that parkin may have as yet unidentified stable binding partners.