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Different Brain Areas (different + brain_area)
Selected AbstractsTypical versus Atypical Absence Seizures: Network Mechanisms of the Spread of ParoxysmsEPILEPSIA, Issue 8 2007Jose L. Perez Velazquez Summary: Purpose: Typical absence seizures differ from atypical absence seizures in terms of semiology, EEG morphology, network circuitry, and cognitive outcome, yet have the same pharmacological profile. We have compared typical to atypical absence seizures, in terms of the recruitment of different brain areas. Our initial question was whether brain areas that do not display apparent paroxysmal discharges during typical absence seizures, are affected during the ictal event in terms of synchronized activity, by other, distant areas where seizure activity is evident. Because the spike-and-wave paroxysms in atypical absence seizures invade limbic areas, we then asked whether an alteration in inhibitory processes in hippocampi may be related to the spread seizure activity beyond thalamocortical networks, in atypical seizures. Methods: We used two models of absence seizures in rats: one of typical and the other of atypical absence seizures. We estimated phase synchronization, and evaluated inhibitory transmission using a paired-pulse paradigm. Results: In typical absence seizures, we observed an increase in synchronization between hippocampal recordings when spike-and-wave discharges occurred in the cortex and thalamus. This indicates that seizure activity in the thalamocortical circuitry enhances the propensity of limbic areas to synchronize, but is not sufficient to drive hippocampal circuitry into a full paroxysmal discharge. Lower paired-pulse depression was then found in hippocampus of rats that displayed atypical absence seizures. Conclusions: These observations suggest that circuitries in brain areas that do not display apparent seizure activity become synchronized as seizures occur within thalamocortical circuitry, and that a weakened hippocampal inhibition may predispose to develop synchronization into full paroxysms during atypical absence seizures. [source] Individual vulnerability to escalated aggressive behavior by a low dose of alcohol: decreased serotonin receptor mRNA in the prefrontal cortex of male miceGENES, BRAIN AND BEHAVIOR, Issue 1 2010S. Chiavegatto Low to moderate doses of alcohol consumption induce heightened aggressive behavior in some, but not all individuals. Individual vulnerability for this nonadaptive behavior may be determined by an interaction of genetic and environmental factors with the sensitivity of alcohol's effects on brain and behavior. We used a previously established protocol for alcohol oral self-administration and characterized alcohol-heightened aggressive (AHA) mice as compared with alcohol non-heightened (ANA) counterparts. A week later, we quantified mRNA steady state levels of several candidate genes in the serotonin [5-hydroxytryptamine (5-HT)] system in different brain areas. We report a regionally selective and significant reduction of all 5-HT receptor subtype transcripts, except for 5-HT3, in the prefrontal cortex of AHA mice. Comparable gene expression profile was previously observed in aggressive mice induced by social isolation or by an anabolic androgenic steroid. Additional change in the 5-HT1B receptor transcripts was seen in the amygdala and hypothalamus of AHA mice. In both these areas, 5-HT1B mRNA was elevated when compared with ANA mice. In the hypothalamus, AHA mice also showed increased transcripts for 5-HT2A receptor. In the midbrain, 5-HT synthetic enzyme, 5-HT transporter and 5-HT receptors mRNA levels were similar between groups. Our results emphasize a role for postsynaptic over presynaptic 5-HT receptors in mice which showed escalated aggression after the consumption of a moderate dose of alcohol. This gene expression profile of 5-HT neurotransmission components in the brain of mice may suggest a vulnerability trait for alcohol-heightened aggression. [source] Dopamine challenge tests as an indicator of psychological traitsHUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 2 2006P. Netter Abstract After discussing some introductory considerations about the value of challenge tests in general for discriminating personality dimensions which are considered extrapolations of psychopathological diseases, the present paper outlines the matter of responsivity to agonistic and antagonistic dopaminergic drugs or drugs of different mechanisms of action in the dopaminergic system, and elucidates that different hormones elicited by dopaminergic substances (prolactin, growth hormone) may indicate personality related differences in susceptibility of different brain areas. A further point was to demonstrate not only the well known relationship of dopaminergic hyperactivity with reward seeking and motivational factors associated with extraversion and novelty seeking, but also the relationship of dopaminergic hypofunction with the personality dimension of depression which had already been reported in studies on animals and psychiatric patients. A final point was to demonstrate that besides size of hormone responses additional parameters like time of response onset and initial prolactin increase can be used as biochemical indicators for identifying certain personality types, like highly depressive neurotic persons characterized by lower and later dopamine responses as compared to low depressives, and extraverted sensation-seeking types responding by an initial prolactin peak as opposed to low sensation seekers. Copyright © 2006 John Wiley & Sons, Ltd. [source] Soluble oligomers from a non-disease related protein mimic A,-induced tau hyperphosphorylation and neurodegenerationJOURNAL OF NEUROCHEMISTRY, Issue 2 2007Marcelo N. N. Vieira Abstract Protein aggregation and amyloid accumulation in different tissues are associated with cellular dysfunction and toxicity in important human pathologies, including Alzheimer's disease and various forms of systemic amyloidosis. Soluble oligomers formed at the early stages of protein aggregation have been increasingly recognized as the main toxic species in amyloid diseases. To gain insight into the mechanisms of toxicity instigated by soluble protein oligomers, we have investigated the aggregation of hen egg white lysozyme (HEWL), a normally harmless protein. HEWL initially aggregates into ,-sheet rich, roughly spherical oligomers which appear to convert with time into protofibrils and mature amyloid fibrils. HEWL oligomers are potently neurotoxic to rat cortical neurons in culture, while mature amyloid fibrils are little or non-toxic. Interestingly, when added to cortical neuronal cultures HEWL oligomers induce tau hyperphosphorylation at epitopes that are characteristically phosphorylated in neurons exposed to soluble oligomers of the amyloid-, peptide. Furthermore, injection of HEWL oligomers in the cerebral cortices of adult rats induces extensive neurodegeneration in different brain areas. These results show that soluble oligomers from a non-disease related protein can mimic specific neuronal pathologies thought to be induced by soluble amyloid-, peptide oligomers in Alzheimer's disease and support the notion that amyloid oligomers from different proteins may share common structural determinants that would explain their generic cytotoxicities. [source] Increased turnover of Na-K ATPase molecules in rat brain after rapid eye movement sleep deprivationJOURNAL OF NEUROSCIENCE RESEARCH, Issue 6 2003Sudipta Majumdar Abstract It has been shown that rapid eye movement (REM) sleep deprivation increases Na-K ATPase activity. Based on kinetic study, it was proposed that increased activity was due to enhanced turnover of enzyme molecules. To test this, anti-,1 Na-K ATPase monoclonal antibody (mAb 9A7) was used to label Na-K ATPase molecules. These labeled enzymes were quantified on neuronal membrane by two methods: histochemically on neurons in tissue sections from different brain areas, and by Western blot analysis in control and REM sleep-deprived rat brains. The specific enzyme activity was also estimated and found to be increased, as in previous studies. The results confirmed our hypothesis that after REM sleep deprivation, increased Na-K ATPase activity was at least partly due to increased turnover of Na-K ATPase molecules in the rat brain. © 2003 Wiley-Liss, Inc. [source] Effects of some synthetic kynurenines on brain amino acids and nitric oxide after pentylenetetrazole administration to ratsJOURNAL OF PINEAL RESEARCH, Issue 4 2004Leila Bikjdaouene Abstract:, We have previously proven that some synthetic kynurenines behave as antagonists of the N-methyl- d -aspartate receptor inhibiting neuronal subtype of nitric oxide synthase activity. We now investigate the anticonvulsant activity of four of these kynurenines in pentylenetetrazole (PTZ)-treated rats. The rats were treated with each kynurenine (10,160 mg/kg, s.c.) 30 min before PTZ administration (100 mg/kg, s.c.). Then, latency, duration and intensity of the first seizure and the percent animal survival were noted. PTZ-induced death was counteracted by high doses of kynurenines. Latency of the first seizure was significantly increased and its intensity reduced at the same doses, whereas the duration of the first seizure significantly decreased with doses of 20 mg/kg in most of the kynurenines tested. Three hours after PTZ administration, the surviving animals were sacrificed and the levels of brain amino acids and nitrite were measured. PTZ administration increased glutamate, glutamine, serine and taurine levels in different brain areas. High doses of kynurenines generally counteracted the effects of PTZ on excitatory amino acids, but they also reduced inhibitory aminoacids. However, the most consistent effect of kynurenines was the dose-dependent reduction of brain nitrite levels induced by PTZ. These results reveal a new family of anticonvulsant drugs that affect mainly to nitric oxide production in the brain. [source] Neuropeptide S Receptor Gene Expression in Alcohol Withdrawal and Protracted Abstinence in Postdependent RatsALCOHOLISM, Issue 1 2010Barbara Ruggeri Background:, Alcoholism is a chronic disease characterized by frequent intoxications followed by withdrawal episodes and relapse to alcohol use. Neuroplastic changes associated with these intoxication and withdrawal cycles are thought to play a key role in disease progression. Recently, it has been shown that neuropeptide S (NPS), a newly deorphanized neuropeptide receptor system, facilitates relapse to alcohol seeking in laboratory animals. Given that a history of ethanol intoxication may increase vulnerability to alcohol addiction, we sought to determine whether NPS receptor (NPSR) gene expression is altered during withdrawal. Methods:, Rats were subjected to 1 week of intoxication by oral alcohol administration. NPSR gene expression was analyzed by in situ hybridization in rats 12 hours and 7 days after the last alcohol administration. To investigate the functional significance of NPSR system adaptation following protracted withdrawal 7 days after intoxication, we tested the anxiolytic-like properties of NPS in nondependent and postdependent rats using the shock probe defensive burying test (DB). Results:, At both time points, increased NPSR gene expression was observed in several brain areas, including the endopiriform nucleus, the motor cortex, and the medial amygdaloid nucleus. Moderate increases in gene expression were also found in the lateral hypothalamus, paraventricular nucleus, basolateral and central amygdala. Differences from control animals were more pronounced after 7 days of abstinence. The upregulation of the NPSR system at this time point was confirmed by functional data indicating that intracerebroventricular (ICV) NPS administration (0.0, 0.3, and 0.1 nmol/rat) elicits more pronounced anxiolytic effects in postdependent animals than in controls subjected to the electric shock probe DB test. Conclusions:, Neuropeptide S receptor mRNA expression is increased in different brain areas of postdependent rats; as shown in the DB test, this expression change is functionally relevant. [source] Nonspatial intermodal selective attention is mediated by sensory brain areas: Evidence from event-related potentialsPSYCHOPHYSIOLOGY, Issue 5 2001Durk Talsma The present study focuses on the question of whether inter- and intramodal forms of attention are reflected in activation of the same or different brain areas. ERPs were recorded while subjects were presented a random sequence of visual and auditory stimuli. They were instructed to attend to nonspatial attributes of either auditory or visual stimuli and to detect occasional target stimuli within the attended channel. An occipital selection negativity was found for intramodal attention to visual stimuli. Visual intermodal attention was also manifested in a similar negativity. A symmetrical dipole pair in the medial inferior occipital areas could account for the intramodal effects. Dipole pairs for the intermodal attention effect had a slightly more posterior location compared to the dipole pair for the intramodal effect. Auditory intermodal attention was manifested in an early enhanced negativity overlapping with the N1 and P2 components, which was localized using a symmetrical dipole pair in the lateral auditory cortex. The onset of the intramodal attention effect was somewhat later (around 200 ms), and was reflected in a frontal processing negativity. The present results indicate that intra- and intermodal forms of attention were indeed similar for visual stimuli. Auditory data suggest the involvement of multiple brain areas. [source] Protective Effect of Sesamol against 3-Nitropropionic Acid-Induced Cognitive Dysfunction and Altered Glutathione Redox Balance in RatsBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 1 2010Puneet Kumar It is a well-known antioxidant, currently being tried against several neurological disorders. The present study was designed to evaluate the potential of sesamol treatment against 3-nitropropionic acid (3-NP)-induced cognitive impairment and oxidative damage in striatal, cortex and hippocampal regions of the rat. The memory performance was assessed by Morris water maze and elevated plus maze paradigms. The oxidative damage was assessed by estimating the total glutathione, reduced glutathione, oxidized glutathione levels and glutathione redox ratio. Glutathione- S -transferase and lactate dehydrogenase enzymes were also measured in different brain areas. 3-NP significantly impaired memory performance as assessed in Morris water maze and elevated plus maze, which was significantly attenuated by sesamol (5, 10 and 20 mg/kg) pre-treatment. On the other hand, 3-NP significantly induced oxidative stress and depleted total glutathione, reduced glutathione, glutathione- S -transferase, lactate dehydrogenase enzyme levels and redox ratio in the striatum, cortex and hippocampal regions as compared to the vehicle-treated group. Sesamol pre-treatment restored oxidative defence possibly by its free radical scavenging activity as compared to the 3NP-treated group. The present study suggests that sesamol could be used as an effective agent in the management of Huntington's disease. [source] The endocannabinoid system in brain reward processesBRITISH JOURNAL OF PHARMACOLOGY, Issue 2 2008M Solinas Food, drugs and brain stimulation can serve as strong rewarding stimuli and are all believed to activate common brain circuits that evolved in mammals to favour fitness and survival. For decades, endogenous dopaminergic and opioid systems have been considered the most important systems in mediating brain reward processes. Recent evidence suggests that the endogenous cannabinoid (endocannabinoid) system also has an important role in signalling of rewarding events. First, CB1 receptors are found in brain areas involved in reward processes, such as the dopaminergic mesolimbic system. Second, activation of CB1 receptors by plant-derived, synthetic or endogenous CB1 receptor agonists stimulates dopaminergic neurotransmission, produces rewarding effects and increases rewarding effects of abused drugs and food. Third, pharmacological or genetic blockade of CB1 receptors prevents activation of dopaminergic neurotransmission by several addictive drugs and reduces rewarding effects of food and these drugs. Fourth, brain levels of the endocannabinoids anandamide and 2-arachidonoylglycerol are altered by activation of reward processes. However, the intrinsic activity of the endocannabinoid system does not appear to play a facilitatory role in brain stimulation reward and some evidence suggests it may even oppose it. The influence of the endocannabinoid system on brain reward processes may depend on the degree of activation of the different brain areas involved and might represent a mechanism for fine-tuning dopaminergic activity. Although involvement of the various components of the endocannabinoid system may differ depending on the type of rewarding event investigated, this system appears to play a major role in modulating reward processes. British Journal of Pharmacology (2008) 154, 369,383; doi:10.1038/bjp.2008.130; published online 14 April 2008 [source] Trait impulsivity in female patients with borderline personality disorder and matched controlsACTA NEUROPSYCHIATRICA, Issue 3 2010Jørgen Assar Mortensen Mortensen JA, Rasmussen IA, Håberg A. Trait impulsivity in female patients with borderline personality disorder and matched controls. Objective: Impulsivity has been shown to load on two separate factors, rash impulsivity and sensitivity to reward (SR) in several factor analytic studies. The aims of the current study were to explore the nature of impulsivity in women with borderline personality disorder (BPD) and matched controls, and the underlying neuronal correlates for rash impulsivity and SR. Methods: Fifteen females diagnosed with BPD and 15 matched controls were recruited. All completed the impulsiveness-venturesomeness scale (I7), the sensitivity to punishment (SP) - sensitivity to reward (SR) questionnaire, and performed a Go-NoGo block-design functional magnetic resonance imaging (fMRI) paradigm at 3T. Correlation analyses were done with I7, SP and SR scores with the level of activation in different brain areas in the whole group. An independent group t -test was used to explore any differences between the BPD group and the matched controls. Results: I7 scores correlated negatively with activity in the left orbitofrontal cortex, amygdala and precuneus, and bilaterally in the cingulate cortices during response inhibition for the entire sample. SP yielded negative correlations in the right superior frontal gyrus and parahippocampal gyrus. No activity related to response inhibition correlated to SR. The Go-NoGo task gave similar brain activity in BPD and matched controls, but behaviourally the BPD group had significantly more commission errors in the NoGo blocks. The BPD group had increased I7 and SP scores indicating rash impulsiveness combined with heightened SP. Conclusion: These results imply that successful impulse inhibition involves interaction between the impulsive and the emotional systems. Furthermore, impulsivity in BPD is described as rash impulsivity, coexisting with increased SP. 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