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Neuronal spontaneous activity was not changed with NBM stimulation or lesion. Leading to more sublinear response summation and decreased condition-test ratio, NBM lesion decreased ON response magnitude and facilitation, increased AW surround inhibition in paired whisker deflection, increased excitatory and decreased inhibitory receptive fields, weakened information processing during whisking, and resulted in AD-like declined PAL performance. These findings provide further understandings to develop translational approaches in precision therapeutics to target highly specific regions such as NBM or SC, and pathways like cholinergic system involved in tactile and memory deficits in AD. The globus pallidus (GP) plays an important role in the flow of information between input and output structures of the basal ganglia (BG) circuit. In addition to participating in motor control, the GP may also be involved in cognitive and emotional functions related to the symptoms of patients with Parkinson's disease (PD). Since the GP receives dopaminergic innervation from the substantia nigra pars compacta (SNc), it is important to determine whether a local dopamine (DA) deficit in the GP is related not only to motor but also to the cognitive and emotional alterations of PD. The aim of this study was to examine the effects of lesions in the GP (induced by 6-OHDA) on anxiety, depression and ambulation in rats. Such lesions are known to reduce dopaminergic innervation in this brain structure. Additionally, the effect on DA receptors in the GP was tested by local administration of the dopamine agonist PD168,077, antagonist haloperidol and psychostimulant amphetamine. Experimental anxiety was evaluated with the elevated plus maze (EPM), burying behavior test (BBT) and social interaction test, while depressive-like behavior was assessed with the sucrose preference test. Rats with unilateral and bilateral lesions showed a higher level of anxiety than intact animals in both the EPM and BBT, an effect also obtained after intrapallidal injection of haloperidol. The administration of methamphetamine or PD-168.077 caused the opposite effect. The dopaminergic lesions in the GP did not affect sucrose preference, social interaction or ambulation. These results show that dopamine in the GP, acting through D2 or D4 receptors, may be involved in the manifestation of anxiety, a non-motor symptom of PD that often appears before motor symptoms. The aim of this study was to explore the neurobiological background of individual susceptibility and resistance to the development of posttraumatic stress disorder (PTSD)-like behaviours. Rats were divided into susceptible, PTSD(+), and resistant, PTSD(-), groups based on freezing duration during exposure to aversive context and the time spent in the central area in open field test one week after threefold stress experience (modified single prolonged stress). PTSD(-) rats showed increased concentrations of corticosterone in plasma and changes in GAD67 expression decreased in the infralimbic cortex (IL) and increased in the lateral amygdala (LA), dentate gyrus (DG), and CA1 area of the hippocampus. Moreover, in this group, we found an increase in the number of CRF-positive nuclei in the parvocellular neurons of the paraventricular hypothalamic nucleus (pPVN). Selleckchem BIBF 1120 The PTSD(+) group, compared to PTSD(-) rats, had decreased concentrations of corticosterone in plasma and reduced CRF expression in the pPVN, higher CRF expression in the CA1, increased expression of CRF-positive nuclei and GR receptors in the CA3 area of the hippocampus, and increased expression of GR receptors in the DG and the central amygdala (CeA). Biochemical analysis showed higher concentrations of noradrenaline, glutamic acid in the dorsal hippocampus and amygdala and lower levels of dopamine and its metabolites in the amygdala of the PTSD(+) group than in the PTSD(-) group. The study revealed different behavioural and biochemical profiles of PTSD(+) and PTSD(-) rats and suggested that individual differences in hypothalamic-pituitary-adrenal (HPA) axis activity may determine hippocampal- and amygdala-dependent memory and fear processing. People who have developed a good sense of smell could experience much more happiness and pleasure, which would trigger a discussion that olfactory disorder might correlate with the pathogenesis of major depressive disorder (MDD). Similar experiments conducted on rats have confirmed that nerve damage of olfactory pathway can induce a series of depression-like changes, including behavior, neurobiochemistry, and neuroimmunity. These changes will recover progressively with anti-depression treatment. While in similar studies on human beings, olfactory dysfunction has been found in people suffering from depression. link2 This review briefly discusses the correlation between olfactory deficits and clinical traits of depression in different dimensions, such as the severity, duration and cognitive impairment of depression. Improving olfactory function may be expected to be a potential antidepressant therapy. Cocaine-cue extinction training combined with brief interventions of environmental enrichment (EE) was shown previously to facilitate extinction and attenuate reacquisition of cocaine self-administration in rats. It is unknown whether or not the usefulness of this approach would be undermined if extinction training took place in a novel rather than familiar context. Drawing on previous studies involving pharmacological interventions, we hypothesized that the facilitative effects of EE for cocaine relapse prevention would be independent of the context used for extinction training. Rats trained to self-administer cocaine underwent cocaine-cue extinction training in either the familiar self-administration context or a novel context, with or without EE. Rats then were tested for reacquisition of cocaine self-administration in the familiar context. Target brain regions were lysed and probed for memory-related changes in receptors for glutamate and BDNF by western blotting. Contrary to our hypothesis, the facilitative effects of EE for cocaine relapse prevention were dependent on the context used for extinction training. While EE facilitated extinction regardless of context used, it inhibited cocaine relapse only after extinction training in the familiar context. EE was associated with increased GluA2 in nucleus accumbens, TrkB in dorsal hippocampus and activated TrkB in ventromedial prefrontal cortex. Of these, the changes in dorsal hippocampus and ventromedial prefrontal cortex mirrored outcomes of the cocaine relapse tests in that these changes were specific to rats receiving EE plus extinction training in the familiar context. These findings support a role for hippocampal-prefrontal BDNF-TrkB signaling in extinction-based relapse prevention strategies involving EE. Previous neuroimaging studies have reported differences in regional brain activation between males and females during stop signal task performance, suggesting the presence of sex-linked differences in brain network organization of inhibitory ability. Despite a growing literature on sex differences during stop signal task performance, a consensus still has not been reached due to variations in task design and analysis methods. Due to these disparate findings we used up to date stop signal task methods to compare behavioral performance and associated brain activation between males and females using an event-related functional magnetic resonance imaging design. We observed that males were faster in inhibiting their responses, but females exhibited marked increased in stopping network activation, in addition to increased activation of the anterior insula and left amygdala. These findings suggest that males and females process stop signals differently. Speaking involves information-universal and information specific systems, and it remains unknown about the influence of two systems in spoken word production. We manipulated time pressure (with and without) as an information-universal factor and the semantic relatedness between target names and distractor words (semantically related and unrelated) as an information-specific factor in the picture-word interference (PWI) task, while electrophysiological signals were measured concurrently. Naming latencies showed a significant semantic interference effect in the condition without time pressure but none in the condition with time pressure. Spatio-temporal segmentation analysis indicated that time pressure only prolonged the duration of Map 4 ranging from about 250 to 350 ms post picture presentation, and meanwhile shortened the duration of Map 5 starting around 350 to 520 ms. Within the framework of serial models, the two time periods were presumably associated with lexical selection and phonological encoding in spoken word production. Cluster-based permutation analysis revealed that semantic relatedness modulated ERPs around 320-360 ms after picture onset in the condition without time pressure, while 530-570 ms in the condition with time pressure. Our findings reveal that time pressure prolongs lexical selection and shortens phonological encoding. Furthermore, time pressure dynamically modulates whether semantically related distractors exceed a competition threshold to interfere with target word selection. V.Present study has been carried out to assess whether early alterations of the behavioural structure may be detected in mice affected by Duchenne muscular dystrophy (DMD). To this purpose, both quantitative and T-pattern analysis (TPA) were used to analyse the behaviour of two groups of male, two months old mice, 18 MDX and 18 normal as control, tested in an open-field apparatus. T-pattern analysis is a multivariate technique able to reveal hidden structural features of behaviour and, in particular, its temporal characteristics. As to quantitative analyses, mean durations evidenced a significant increase of Walking, Modified Climbing and Rearing and a significant reduction of Immobile-Sniffing, Paw Licking and Immobility in MDX animals. A similar outcome was present in mean occurrences where the only difference was a significant result in Climbing rather than Immobile Sniffing. In addition, mean occurrences, evaluated for all the behavioural components, showed a significant increase for MDX mice. As to TPA, control mice performed 78 different T-patterns occurring 9500 times, whereas in MDX group 47 different T-patterns occurring 7082 times. Overall, MDX mice showed T-patterns of significantly shorter length. Finally, percent distribution of T-patterns encompassing each component of the behavioural repertoire showed significant differences between Control and MDX groups in all the behavioural components, except Climbing. Results suggest that the combined use of quantitative and temporal pattern analyses offers a useful approach to deeply investigate from a behavioural point of view pre-symptomatic stages of DMD in humans and related animal models as well. Regulated fear and extinction memory is essential for balanced behavioral response. Limbic brain regions are susceptible to hypobaric hypoxia (HH) and are putative target for fear extinction deficit and dysregulation. The present study aimed to examine the effect of HH and Ginkgo biloba extract (GBE) on fear and extinction memory with the underlying mechanism. Adult male Sprague-Dawley rats were evaluated for fear extinction and anxious behavior following GBE administration during HH exposure. Blood and tissue (PFC, hippocampus and amygdala) samples were collected for biochemical, morphological and molecular studies. link3 Results revealed deficit in contextual and cued fear extinction following 3 days of HH exposure. Increased corticosterone, glutamate with decreased GABA level was found with marked pyknosis, decrease in apical dendritic length and number of functional spines. Decline in mRNA expression level of synaptic plasticity genes and immunoreactivity of BDNF, synaptophysin, PSD95, spinophilin was observed following HH exposure.

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