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Behavioral Paradigms (behavioral + paradigm)
Selected AbstractsApoptotic and behavioral sequelae of mild brain trauma in miceJOURNAL OF NEUROSCIENCE RESEARCH, Issue 4 2007David Tweedie Abstract Mild traumatic brain injury (mTBI) is a not uncommon event in adolescents and young adults. Although it does not result in clear morphological brain defects, it is associated with long-term cognitive, emotional, and behavioral problems. Herein, we characterized the biochemical and behavioral changes associated with experimental mTBI in mice that may act as either targets or surrogate markers for interventional therapy. Specifically, mTBI was induced by 30-g and 50-g weight drop, and at 8 and 72 hr thereafter markers of cellular apoptosis,caspase-3, Bax, apoptosis-inducing factor (AIF), and cytochrome-c (Cyt-c),were quantified by Western blot analysis in hippocampus ipsilateral to the impact. Levels of amyloid-, precursor protein (APP) were also measured, and specific behavioral tests,passive avoidance, open field, and forced swimming (Porsolt) paradigms,were undertaken to assess learning, emotionality, and emotional memory. In the absence of hemorrhage or infarcts, as assessed by triphenyltetrazolium chloride staining, procaspase-3 and Bax levels were markedly altered following mTBI at both times. No cleaved caspase-3 was detected, and levels of AIF and Cyt-c, but not APP, were significantly changed at 72 hr. Mice subjected to mTBI were indistinguishable from controls by neurological examination at 1 and 24 hr, and by passive avoidance/open field at 72 hr, but could be differentiated in the forced swimming paradigm. In general, this model mimics the diffuse effects of mTBI on brain function associated with the human condition and highlights specific apoptotic proteins and a behavioral paradigm as potential markers for prospective interventional strategies. © 2007 Wiley-Liss, Inc. [source] Differential expression of glycans in the hippocampus of rats trained on an inhibitory learning paradigmNEUROPATHOLOGY, Issue 6 2006Alejandra Hidalgo The glycan chains of glycoconjugates play important roles in cell,cell and cell,matrix interactions. In the CNS, previous studies on learning and memory suggest the importance of oligosaccharides attached to glycoconjugates in the modulation of synaptic connections. We studied the hippocampal glycan distribution of rats subject to an inhibitory avoidance task. The expression of glycans was examined by lectin-histochemistry using Vicia villosa lectin (VVL) for terminal ,/, N-acetylgalactosamine (,/, GalNAc); Galanthus nivalus lectin (GNL) for terminal mannose ,-1,3 (Man ,-1,3); Peanut agglutinin (PNA) for galactose ,-1,3N-acetylgalactosamine (Gal ,-1,3 GalNAc); Erythrina cristagalli lectin (ECL) for galactose ,-1,4 N-acetylglucosamine (Gal ,-1,4 GlcNAc); Sambucus nigra lectin (SNA) for sialic acid ,-2.6 galactose (SA ,-2,6 Gal); Maackia amurensis lectin II (MAL II) for sialic acid ,-2,3 (SA ,-2,3); Wheat germ agglutinin (WGA) for terminal N-acetylglucosamine with/without sialic acid (GlcNAc wo SA); succynilated WGA (sWGA) for terminal N-acetylglucosamine without sialic acid (terminal GlcNAc without SA); Griffonia simplicifolia lectin II (GSL II) for terminal ,/, N-acetylglucosamine (,/, GlcNAc terminal); and Lotus tetragonolobus lectin (LTL) ,,fucose. Two groups of 10 animals were examined: non-trained (Control) and Trained rats. ECL, sWGA and GSL II were negative for both groups in all the hippocampal subfields studied. For both groups, VVL was negative in CA4 and granular cells of the Dentate Gyrus (DG) and LTL was negative in the CA4 subfield. Expression of ,/, GalNAc, , -fucose and GlcNAc in other hippocampal subfields was positive, with no differences between groups. However, expression of Man ,-1,3 was significantly higher in the CA1, CA2, CA3, and CA4 subfields in the Trained group. On the other hand, expression of Gal ,-1,3 GalNAc was significantly low in CA4 and DG in the Trained group. In conclusion, the results here presented indicate that the exposure of rats to an associative behavioral paradigm related to declarative memory, involves some regulatory mechanism/s for the differential patterns of glycan expression. [source] Seizures in the Developing Brain Cause Adverse Long-term Effects on Spatial Learning and AnxietyEPILEPSIA, Issue 12 2004Umit Sayin Summary:,Purpose: Seizures in the developing brain cause less macroscopic structural damage than do seizures in adulthood, but accumulating evidence shows that seizures early in life can be associated with persistent behavioral and cognitive impairments. We previously showed that long-term spatial memory in the eight-arm radial-arm maze was impaired in rats that experienced a single episode of kainic acid (KA)-induced status epilepticus during early development (postnatal days (P) 1,14). Here we extend those findings by using a set of behavioral paradigms that are sensitive to additional aspects of learning and behavior. Methods: On P1, P7, P14, or P24, rats underwent status epilepticus induced by intraperitoneal injections of age-specific doses of KA. In adulthood (P90,P100), the behavioral performance of these rats was compared with that of control rats that did not receive KA. A modified version of the radial-arm maze was used to assess short-term spatial memory; the Morris water maze was used to evaluate long-term spatial memory and retrieval; and the elevated plus maze was used to determine anxiety. Results: Compared with controls, rats with KA seizures at each tested age had impaired short-term spatial memory in the radial-arm maze (longer latency to criterion and more reference errors), deficient long-term spatial learning and retrieval in the water maze (longer escape latencies and memory for platform location), and a greater degree of anxiety in the elevated plus maze (greater time spent in open arms). Conclusions: These findings provide additional support for the concept that seizures early in life may be followed by life-long impairment of certain cognitive and behavioral functions. These results may have clinical implications, favoring early and aggressive control of seizures during development. [source] Hypolocomotion, anxiety and serotonin syndrome-like behavior contribute to the complex phenotype of serotonin transporter knockout miceGENES, BRAIN AND BEHAVIOR, Issue 4 2007A. V. Kalueff Although mice with a targeted disruption of the serotonin transporter (SERT) have been studied extensively using various tests, their complex behavioral phenotype is not yet fully understood. Here we assess in detail the behavior of adult female SERT wild type (+/+), heterozygous (+/,) and knockout (,/,) mice on an isogenic C57BL/6J background subjected to a battery of behavioral paradigms. Overall, there were no differences in the ability to find food or a novel object, nest-building, self-grooming and its sequencing, and horizontal rod balancing, indicating unimpaired sensory functions, motor co-ordination and behavioral sequencing. In contrast, there were striking reductions in exploration and activity in novelty-based tests (novel object, sticky label and open field tests), accompanied by pronounced thigmotaxis, suggesting that combined hypolocomotion and anxiety (rather than purely anxiety) influence the SERT ,/, behavioral phenotype. Social interaction behaviors were also markedly reduced. In addition, SERT ,/, mice tended to move close to the ground, frequently displayed spontaneous Straub tail, tics, tremor and backward gait , a phenotype generally consistent with ,serotonin syndrome'-like behavior. In line with replicated evidence of much enhanced serotonin availability in SERT ,/, mice, this serotonin syndrome-like state may represent a third factor contributing to their behavioral profile. An understanding of the emerging complexity of SERT ,/, mouse behavior is crucial for a detailed dissection of their phenotype and for developing further neurobehavioral models using these mice. [source] Dopamine and Oxytocin Interactions Underlying Behaviors: Potential Contributions to Behavioral DisordersCNS: NEUROSCIENCE AND THERAPEUTICS, Issue 3 2010Tracey A. Baskerville Dopamine is an important neuromodulator that exerts widespread effects on the central nervous system (CNS) function. Disruption in dopaminergic neurotransmission can have profound effects on mood and behavior and as such is known to be implicated in various neuropsychiatric behavioral disorders including autism and depression. The subsequent effects on other neurocircuitries due to dysregulated dopamine function have yet to be fully explored. Due to the marked social deficits observed in psychiatric patients, the neuropeptide, oxytocin is emerging as one particular neural substrate that may be influenced by the altered dopamine levels subserving neuropathologic-related behavioral diseases. Oxytocin has a substantial role in social attachment, affiliation and sexual behavior. More recently, it has emerged that disturbances in peripheral and central oxytocin levels have been detected in some patients with dopamine-dependent disorders. Thus, oxytocin is proposed to be a key neural substrate that interacts with central dopamine systems. In addition to psychosocial improvement, oxytocin has recently been implicated in mediating mesolimbic dopamine pathways during drug addiction and withdrawal. This bi-directional role of dopamine has also been implicated during some components of sexual behavior. This review will discuss evidence for the existence dopamine/oxytocin positive interaction in social behavioral paradigms and associated disorders such as sexual dysfunction, autism, addiction, anorexia/bulimia, and depression. Preliminary findings suggest that whilst further rigorous testing has to be conducted to establish a dopamine/oxytocin link in human disorders, animal models seem to indicate the existence of broad and integrated brain circuits where dopamine and oxytocin interactions at least in part mediate socio-affiliative behaviors. A profound disruption to these pathways is likely to underpin associated behavioral disorders. Central oxytocin pathways may serve as a potential therapeutic target to improve mood and socio-affiliative behaviors in patients with profound social deficits and/or drug addiction. [source] | |||||||||||||