52 research outputs found
Action planning and the timescale of evidence accumulation
Perceptual decisions are based on the temporal integration of sensory evidence for different states of the outside world. The timescale of this integration process varies widely across behavioral contexts and individuals, and it is diagnostic for the underlying neural mechanisms. In many situations, the decision-maker knows the required mapping between perceptual evidence and motor response (henceforth termed “sensory-motor contingency”) before decision formation. Here, the integrated evidence can be directly translated into a motor plan and, indeed, neural signatures of the integration process are evident as build-up activity in premotor brain regions. In other situations, however, the sensory-motor contingencies are unknown at the time of decision formation. We used behavioral psychophysics and computational modeling to test if knowledge about sensory-motor contingencies affects the timescale of perceptual evidence integration. We asked human observers to perform the same motion discrimination task, with or without trial-to-trial variations of the mapping between perceptual choice and motor response. When the mapping varied, it was either instructed before or after the stimulus presentation. We quantified the timescale of evidence integration under these different sensory-motor mapping conditions by means of two approaches. First, we analyzed subjects’ discrimination threshold as a function of stimulus duration. Second, we fitted a dynamical decision-making model to subjects’ choice behavior. The results from both approaches indicated that observers (i) integrated motion information for several hundred ms, (ii) used a shorter than optimal integration timescale, and (iii) used the same integration timescale under all sensory-motor mappings. We conclude that the mechanisms limiting the timescale of perceptual decisions are largely independent from long-term learning (under fixed mapping) or rapid acquisition (under variable mapping) of sensory-motor contingencies. This conclusion has implications for neurophysiological and neuroimaging studies of perceptual decision-making
Synthesis, antimicrobial and antituberculosis activities of <i>N</i>-bridged heterocycles
828-833The reactions of
3-[(((α-phenyl/methyl)benzylidene)amino)oxy]methyl/ethyl-4-amino-5-mercapto-4(H)-1,2,4-triazoles
1a-d, with various aliphatic/aromatic acids 2a-d-5a-d, oxalic
acid 6a-d, cyanogen bromide 7a-d, carbon disulphide 8a-d, hydrazine
hydrate (99%) 9a-d, monochloroacetic acid 10a-d, phenacyl bromide
11a-d, benzoin 12a-d, dimidone 13a-d and
chalcone 14a-d are described. The
characterisation of the compounds have been done on the basis of elemental
analysis and spectral (IR, 1H NMR and mass) data. All the newly
synthesised compounds have been screened for antimicrobial activity against B.
cirroflagellosus, E. coli, A. niger and R. bataticola.
Most of the compounds have also been screened for antituberculosis activity
against M. tuberculosis, H37Rv strain. Results of antimicrobial
screening revealed that majority of the newly synthesised N-bridged
heterocycles exhibit better antimicrobial activity than the standards
cotrimoxazole and fluconazole. A few of the compounds exhibit significant
antituberculosis activity in comparison with rifampin, the standard used
Stress-induced spine loss in the medial amygdala is mediated by tissue-plasminogen activator. Neuroscience. 2007
Abstract-The amygdala, which exerts a regulatory influence on the stress response, is itself affected by stress. It has been reported that the serine protease tissue-plasminogen activator (tPA), a key mediator of spine plasticity, is required for stress-induced facilitation of anxiety-like behavior. Importantly, tPA is also involved in stress-induced activation of molecular signals that have the potential to contribute to neuronal remodeling in the medial amygdala (MeA). However, little is known about the precise nature of, and specific role played by tPA in, stress-induced structural plasticity in the MeA. Hence, we compared the impact of chronic restraint stress on spine density of medium spiny stellate neurons in MeA in wild-type mice with mice in which the tPA gene is disrupted (tPA ؊/؊ ). In wild-type mice, chronic stress caused significant reduction in MeA spine density, which was in contrast to enhanced spine density in the neighboring basolateral amygdala (BLA). Strikingly, tPA ؊/؊ mice exhibited significant attenuation of stress-induced spine retraction in the MeA, but BLA spinogenesis was not affected. Therefore, tPA-dependence of stress-induced modulation in spine density was restricted to the MeA. Further, MeA neurons in tPA ؊/؊ mice, even when challenged with repeated stress, were able to maintain levels of spine density that were comparable to that of wild-type mice without stress. Our findings provide novel evidence for a permissive role for tPA in amygdalar spine plasticity elicited by behavioral stress
Biotransformation of Δ3-carene by <i style="mso-bidi-font-style:normal">Penicillium nigricans</i>
217-222A fungus was isolated from forest soil by
selective enrichment method with Δ3-carene as a sole source of carbon and
identified as Penicillium nigricans. The
isolate was capable of transforming Δ3-carene into neutral [dihydrocarvone,
carvone, carveol, (+)-trans-p-mentha-5,8-dien-2-ol and
(+)-trans-p-mentha-5,8-dien-2-one] and acidic (perillic acid and
2-hydroxy-p-menth-8-ene-7-oic-acid) metabolic compounds. These compounds were
identified based on infrared (IR), proton nuclear magnetic resonance (1H
NMR) and mass spectrum (MS) studies. Three pathways have been proposed for the
transformation of Δ3-carene into the neutral and acid metabolic compounds based
on the study of oxygen consumption by Δ3-carene grown fungal cells. As the
different metabolic intermediates of Δ3-carene are much used in the perfume
industry, the Δ3-carene, which is abundantly available, can be used as a
starting material in the perfume industry by microbial techniques, using this
fungal strain
Palladium(II) containing hydrotalcite as an efficient heterogeneous catalyst for Heck reaction
Palladium(II) containing hydrotalcite (Pd-HT) has been found to be an efficient and reusable catalyst in Heck reaction between aryl halides (X = Br, I) and olefins to give carbon-carbon coupled products in good to moderate yields
Stress-induced spine loss in the medial amygdala is mediated by tissue-plasminogen activator
The amygdala, which exerts a regulatory influence on the stress response, is itself affected by stress. It has been reported that the serine protease tissue-plasminogen activator (tPA), a key mediator of spine plasticity, is required for stress-induced facilitation of anxiety-like behavior. Importantly, tPA is also involved in stress-induced activation of molecular signals that have the potential to contribute to neuronal remodeling in the medial amygdala (MeA). However, little is known about the precise nature of, and specific role played by tPA in, stress-induced structural plasticity in the MeA. Hence, we compared the impact of chronic restraint stress on spine density of medium spiny stellate neurons in MeA in wild-type mice with mice in which the tPA gene is disrupted (tPA<sup>−/−</sup>). In wild-type mice, chronic stress caused significant reduction in MeA spine density, which was in contrast to enhanced spine density in the neighboring basolateral amygdala (BLA). Strikingly, tPA<sup>−/−</sup>). mice exhibited significant attenuation of stress-induced spine retraction in the MeA, but BLA spinogenesis was not affected. Therefore, tPA-dependence of stress-induced modulation in spine density was restricted to the MeA. Further, MeA neurons in tPA<sup>−/−</sup>). mice, even when challenged with repeated stress, were able to maintain levels of spine density that were comparable to that of wild-type mice without stress. Our findings provide novel evidence for a permissive role for tPA in amygdalar spine plasticity elicited by behavioral stress
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