, 2010) The question remains, therefore, whether

, 2010). The question remains, therefore, whether CP-868596 cell line intelligence

is supported by one or multiple systems, and if the latter is the case, which cognitive processes those systems can most broadly be described as supporting. Furthermore, even if multiple functionally distinct brain networks contribute to intelligence, it is unknown whether the capacities of those networks are independent or are related to the same set of diffuse biological factors that modulate general neural efficiency. It is unclear, therefore, whether the pattern of individual differences in intelligence reflects the functional organization of the brain. Here, we address the question of whether human intelligence is best conceived of as an emergent property of functionally distinct brain networks using factor analyses of brain imaging, behavioral,

and simulated data. First, we break MD cortex down into its constituent functional networks by factor analyzing regional activation levels during the performance of 12 challenging cognitive tasks. Then, we build a model, based on the extent to which the different functional networks are recruited during the performance of those 12 tasks, and determine how well that model accounts for cross-task correlations in performance in a large (n = 44,600) population sample. Factor solutions, generated from brain imaging Selleck FDA-approved Drug Library and behavioral data, are compared directly, to answer the question of whether the same set of cognitive entities is evident in the functional organization of the brain and in individual differences in performance. Simulations, based on the imaging data, are used to determine

the extent to which correlations between first-order behavioral components are predicted by cognitive tasks recruiting multiple functional brain networks, and the extent to which those correlations may be accounted for by a spatially diffuse general factor. Finally, we examine whether the behavioral components of intelligence show a degree of independence, as evidenced by dissociable Non-specific serine/threonine protein kinase correlations with the types of questionnaire variable that “g” has historically been associated with. Sixteen healthy young participants undertook the cognitive battery in the MRI scanner. The cognitive battery consisted of 12 tasks, which, based on well-established paradigms from the neuropsychology literature, measured a range of the types of planning, reasoning, attentional, and working memory skills that are considered akin to general intelligence (see Supplemental Experimental Procedures available online).

The following primers were used: ephrinA5 FW, AGAATCCAGAGACTGCTGA

The following primers were used: ephrinA5 FW, AGAATCCAGAGACTGCTGACATCT; ephrinA5 Rev1, TGAGGCCAAGTTTGTTTCCTTGAA; ephrinA5 Rev2, AGGACATACTGAAGTGGGAATCAG; rx-cre FW, GTTGGGAGAATGCTCCGTAA; rx-cre Rev, GTATCCCACAATTCCTTGCG; en1-cre FW, TAAAGATATCTCACGTACTGACGGTG; en1-cre Rev, TCTCTGACCAGAGTCATCCTTAGC. PCR product sizes were as follows: ephrinA5 wild-type, 450 bps; ephrinA5 floxed, 530 bps; ephrinA5 KO-first, 734 bps; rx:cre, 362 bps; en-1:cre, 300 bps. These experiments

were performed as previously described (Maiorano and Hindges, 2013). The probe for ephrinA5 corresponds to the sequence of exon2. For ephrinA2 and selleck ephrinA3, probes from the Allen Brain Atlas were used (http://www.brain-map.org).

We would like to thank Matthew Grubb, Robert Hindges, Sarah Guthrie, Phillip Gordon-Weeks (all KCL), and Franco Weth (KIT, Germany) for critically reading the manuscript. We would also like to thank the International Knockout Mouse Consortium (IKMC) and the European Conditional Mouse Mutagenesis (EUCOMM) project for providing KO-first ephrinA5 mutant mice, in particular Wolfgang Wurst, Joel Schick, and Susan Marschall; Pete Scambler (ICH, UCL) for the frt-deleter line; Albert Basson (Dental Institute, KCL) for en-1:cre and R26-stop-EYFP mice; Robert Hindges (KCL) learn more for rx:cre mice; and D. Feldheim (UCSC) for ephrinA2 and ephrinA5 full KO mice. We would also like to thank John Harris and Jan Soetaert from the Nikon Imaging Centre at KCL

for expert advice in establishing time-lapse experiments. This work was supported by a Wellcome Trust programme grant (D. Willshaw [Principle Investigator], I. Thompson [KCL], S. Eglen [Cambridge], and U.D.), a Wellcome Trust project grant to U.D., and a BBSRC no grant to U.D. “
“(Neuron 84, 416–431; October 22, 2014) As a result of a Production error, JeongSeop Rhee was not correctly listed as a co-senior author and was erroneously affiliated with the Department of Pathology and Immunology, Baylor College of Medicine, Houston, TX 77030, USA. JeongSeop Rhee’s current affiliation is with the Department of Molecular Neurobiology, Max Planck Institute of Experimental Medicine, 37075 Göttingen, Germany. This affiliation has been corrected online, and the journal regrets the error. “
“Recent articles published in Nature point out how sex bias, primarily concerning male-exclusivity, in biological research result in misleading and ambiguous science. 1, 2, 3 and 4 For example, the majority of animal studies published in academic journals used only males, while only very limited studies were investigated in females or both sexes. The consequences of such male-favored sex bias in biomedical studies had lead to a huge cost in the biomedical industry including drug development.

motifs X; motifs are neuroethologically relevant sequences of son

motifs.X; motifs are neuroethologically relevant sequences of song notes, Hahnloser et al., DNA Methyltransferas inhibitor 2002), with 1,132 genes common to both. In sharp contrast, 0 probes in the VSP had significant GS.singing.V or GS.motifs.V scores (Table S2). We observed small differences in probe expression values in the singing versus nonsinging birds: in area X, only 177 probes (∼0.9% of the total) showed > 100%

up- or downregulation, 65 probes > 200%, 3 probes > 1000%. In the VSP, only 17 probes showed > 100% up- or downregulation (∼0.08%), 6 probes > 200%, and 0 probes > 1000%. We also measured correlations to individual acoustic features such as Wiener entropy (a measure of width and uniformity of the power spectrum (Tchernichovski et al., 2000; GS.entropy) that are typically used to assess song (Figures 2B and S3, Table S2). GS.age was computed for

each bird as a negative control. Importantly, GS results did not influence network construction in any way. During preprocessing, all samples were hierarchically clustered to visualize interarray correlations ABT-199 solubility dmso and remove outliers (Supplemental Experimental Procedures). The area X versus VSP samples segregated into two distinct clusters, as would be expected if tissue source influences gene expression (Figure S1A). Within area X, the singing versus nonsinging birds segregated into two distinct subclusters (Figure S1B), indicating that singing is a profound regulator of gene expression in area X. Singing birds sang throughout the 2 hr recording period (Figures 2A and S2). There was a significant correlation between the number of motifs sung and Wiener entropy, replicating our prior finding of heightened vocal variability after 2 hr of singing (Figure 2B; Miller et al., 2010). To identify ensembles of genes that were tightly

coregulated (modules) during singing, we performed WGCNA (Experimental Procedures) of the area X samples and quantitatively related the resulting modules to traits. Coexpression networks were built based exclusively on expression levels, via unsupervised hierarchical clustering on a biologically significant not distance metric (topological overlap, TO; Experimental Procedures), and relationships between GS and network structure were only examined post hoc. Modules were defined as branches of the dendrogram obtained from clustering and labeled by colors beneath the dendrogram (Figure 3A; probes outside properly defined modules were considered background and colored gray). To study module composition we defined the first principal component of each module as the module eigengene (ME), which can be considered a weighted average of the probe expression profiles that make up the module. Correlating MEs to traits, e.g., number of motifs sung, is an efficient way to relate expression variability within modules to trait variability.

The resistant Z bailii sub-population

The resistant Z. bailii sub-population Bortezomib clinical trial cultured in 6 mM sorbic acid showed a considerably reduced uptake of 14C-acetic acid, the plateau level of uptake being ~ 4-fold lower than in the bulk Z. bailii population. These data confirm that the resistant sub-population of Z. bailii took up a lower dose of weak-acid, thus potentially accounting for the high level of resistance. Uptake, and cytoplasmic accumulation, of weak acids in yeast is primarily controlled by the differential between the media pH and intracellular pH. Since the media pH was constant at pH 4.0 in

all experiments, it is probable that the lower uptake of acetic acid in the resistant sub-population (Fig. 5) was due to a consistently lower intracellular pH in sub-populations grown in any weak acid. Intracellular

pH in cells within the Z. bailii population was therefore determined by flow cytometry on CFDASE-treated cells, stained in the growth media to avoid anomalies caused by cell washing. Results confirmed that the mean intracellular pH of bulk populations of exponentially-growing Z. bailii and S. cerevisiae were similar ( Fig. 6). In contrast, the mean intracellular pH values of the resistant sub-populations of Z. bailii were consistently lower by 0.4–0.8 pH units, Paclitaxel cost depending on the weak acid (sorbic acid p = 0.00271; benzoic acid p = 0.00436; acetic acid p = 0.00857). These data on the lower internal pH of sub-populations grown in weak acid are consistent with the observed Astemizole reduction in weak-acid uptake ( Fig. 5) and are discussed below. The data presented in this paper confirm the high resistance of all 38 tested strains of Z. bailii to weak-acid preservatives. Further tests showed that a representative strain of Z. bailii was resistant to a wide variety of lipophilic and hydrophilic weak acids. On average ~ 3-fold more weak-acid was required to inhibit growth of Z bailii than S. cerevisiae. No enhanced resistance was found to alcohols, aldehydes or esters. Previous reports of Z. bailii resistance to alkanols ( Fujita et al., 2008, Goswell, 1986 and Thomas

and Davenport, 1985) remain valid, but comparable resistance is also found in S. cerevisiae and therefore those data do not address the issue of relative resistance between Z. bailii and other yeasts. Resistance in Z. bailii was shown to a wide variety of weak acids. Degradation of acids is unlikely to be a significant factor in resistance, due to the diversity of acid structures (including adamantane carboxylic acid), the lack of growth rate restoration in sub-populations, cross-resistance between dissimilar acids, and earlier studies showing that acid metabolism was insufficient to determine resistance ( Warth, 1977). In Z. bailii, extreme weak-acid resistance was most probably due to the presence of low numbers of resistant cells in the Z. bailii bulk populations.

Such a pathway through the parameter space of network connectivit

Such a pathway through the parameter space of network connectivity could be utilized during development, with the integrator network beginning in a more topographically organized form and moving to a more distributed connectivity pattern in the mature state, where the functional signatures of topography seem to be weaker (as discussed in Miri et al., 2011). In addition, our approach can be extended to allow greater heterogeneity in synaptic parameters or to model

circuits with nonmonotonic tuning curves (D.F., unpublished data). We have considered a single shape of synaptic activation function for all excitatory neurons, and a separate single shape for all inhibitory neurons, regardless of threshold. Relaxing this constraint might identify circuit architectures in which there are gradients Paclitaxel in vitro in synaptic activation parameters as a function of neuronal threshold. Our work makes several predictions about the mechanisms of integration in the oculomotor integrator

and possibly other short-term memory circuits. First, in contrast to the previous spiking model of the oculomotor integrator based upon purely saturating synapses (Seung et al., 2000; Figure S4D), which modeled a single unilateral population and was generated before the inactivation experiments had been performed, our sensitivity analysis suggests that both inhibition and excitation are likely to be mediated by approximately linear or sigmoidal synaptic activation functions. Second, our quantitative fits to the drift rates following

inactivation suggest that the Lenvatinib research buy observed long integration time constants may not be solely due to network mechanisms, and instead suggest the presence of an intrinsic cellular or synaptic process with a time constant of order 1 s. Third, we suggest that integration depends critically upon the presence of a threshold mechanism. This could either take the form of a synaptic (or dendritic) threshold, as suggested by Aksay et al. (2007), or result from the circuit’s recurrent connectivity depending critically upon neurons with high eye-position thresholds, particularly for inhibition. Potential “synaptic” mechanisms consistent with a sigmoidal dependence upon presynaptic firing rate and an ∼1 s time constant are presynaptic facilitation (Wang Rutecarpine et al., 2006) or, postsynaptically, localized dendritic plateau potentials (Major et al., 2008 and Wei et al., 2001). The long time constants associated with these mechanisms could provide robustness against disruptions of circuit connectivity (Camperi and Wang, 1998, Goldman et al., 2003, Koulakov et al., 2002 and Mongillo et al., 2008). The high thresholds could be useful in filtering out low firing rates (Chichilnisky and Rieke, 2005), which are noisier in the oculomotor integrator than higher firing rates (Aksay et al., 2003).

In this scenario, the

effect of a small amount of Ca2+ in

In this scenario, the

effect of a small amount of Ca2+ influx can be swiftly amplified giving rise to an increase in neurotransmitter release independent of APs as previously documented in hippocampal synapses (Sharma and Vijayaraghavan, 2003 and Xu et al., 2009). BAY 73-4506 in vivo To test if Reelin alters cytosolic Ca2+ levels through RyRs, we preincubated neurons in the ryanodine receptor blockers, dantrolene (10 μM) or ryanodine (10 μM). Preincubation in either dantrolene or ryanodine abolished the effect of Reelin (Figures 3K and 3L, respectively). Together these data suggest that Ca2+-induced Ca2+ release is necessary for the Reelin-dependent increase in spontaneous neurotransmitter release. In the next set of experiments, we attempted to visualize the EPZ-6438 research buy Reelin-mediated Ca2+ signal predicted by the results of the experiments manipulating Ca2+ signaling within presynaptic boutons described above. For this purpose, we infected neurons with a red-shifted pH-sensitive fluorescent protein, mOrange, fused to the luminal end of syb2 (syb2-mOrange) to identify presynaptic terminals (Raingo et al., 2012 and Ramirez et al., 2012). Cells were incubated with the Ca2+ indicator Fluo-4 AM (Ca2+ KD ∼335 nM) or the higher affinity indicator Calcium

Green 1 (Ca2+ KD ∼190 nM). After washing out extracellular dye, cells were imaged for 2 min in the presence of blockers to silence

APs (TTX), ionotropic AMPA receptors (NBQX), and NMDA receptors (AP-5). In presynaptic terminals colabeled with syb2-mOrange, application of Reelin, as opposed to vehicle perfusion, caused a small but significant increase in intracellular Ca2+ that was observable across nearly all boutons (Figure 3M). The Reelin-induced rise in presynaptic Ca2+ was particularly robust when monitored with Calcium Green 1 whereas the lower affinity dye Fluo-4 was not as effective in detecting the Reelin-induced Ca2+ signal (Figures 3N and 3O). The more pronounced shift in the distribution of Ca2+ increases observed with Calcium Green 1 suggests that Reelin application results in a modest increase in presynaptic Ca2+ that in turn increases baseline spontaneous SV release rates (Lou et al., 2005 and Sun et al., 2007). Our results so far suggest Sclareol that Reelin acting via its canonical receptors ApoER2 and VLDLR causes a modest but significant increase in presynaptic Ca2+ that in turn augments resting neurotransmitter release rate without significantly altering the properties of evoked neurotransmitter release. At synaptic terminals, SNARE protein interactions are largely responsible for vesicle fusion and neurotransmitter release. The canonical synaptic SNARE complex composed of syb2 on the SV and syntaxin 1 and SNAP-25, both on the target plasma membrane, mediates rapid exocytosis.

, 2008) with minor modifications Prior to bleaching, neurons wer

, 2008) with minor modifications. Prior to bleaching, neurons were imaged every 30 s for 2 min at 15% laser power. For photobleaching, ROI was exposed to 75% laser power every 1.6 s for 40 frames. Recovery was monitored every 60 s

over 20 min at 15% laser power. To test for translation dependence, we pretreated cultures with 50 μM anisomycin for 30 min before the photobleaching BMN 673 sequence. FRAP quantification and statistical tests are detailed in Supplemental Experimental Procedures. Dissociated DRG cultures were transfected with Dendra2 reporter constructs fused to Importin β1 3′ UTR axonal and cell body variants using Amaxa nucleofection. Dendra2 was photoconverted using a 405 nm laser at 5% energy power and 40× oil objective for 30 s. Images were captured every 4 min under the AT13387 in vitro same conditions using 488 nm (0.1% energy) and 559 nm (4%

energy) lasers. The proximal region was photoconverted using a 405 laser at 0.5% energy power for 2 min every 4 min. Dendra2 quantification and statistical tests are detailed in Supplemental Experimental Procedures. L4/L5 DRGs were dissected from crush-lesioned or control animals at the indicated time points. Total RNA pooled from three animals was extracted using Trizol (TRI, Sigma-Aldrich). Total RNA (200 ng) was amplified, labeled, and hybridized on Illumina arrays (MouseRef-8 version 2.0 Expression BeadChip Kit). Data analysis was performed in the R environment using Bioconductor packages (http://www.bioconductor.org). Briefly, log2-transformed data was normalized using quantile normalization and differential expression analysis was performed using the LIMMA package as previously described PAK6 (Coppola, 2011). Total RNA was extracted from total DRGs pooled from three adult animals per replicate, using the Trizol reagent (TRI, Sigma-Aldrich) according to manufacturer’s instructions. Replicates consisting of at least 10 μg of total RNA each were processed for RNA expression analysis (RNA-Seq) on an Illumina Genome Analyzer IIx at the

High-Throughput Sequencing Unit in the Weizmann Institute of Science. RNA-Seq data was analyzed using DESeq (Anders and Huber, 2010). CatWalk training was carried out as previously described (Deumens et al., 2007). Motivation was achieved by a combination of food restriction during the initial training and placing of palatable reward at runway ends. Data were collected and analyzed with CatWalk software version 9.0 at days 0, 2, 4, 6, 8, 10, 14, 18, 22, and 26 postinjury. The analyzed indices are shown as a ratio between the ipsilateral (right) hind paw and contralateral (left) hind paw and are expressed as mean ± SEM. Quantification and statistical tests are detailed in Supplemental Experimental Procedures. We thank Erin Schuman for the myristylated GFP reporter, Freda Miller for the Tα1 tubulin promoter, and Fan Wang for the Advilin-Cre mice.

They found that mEPSC amplitudes were unchanged at 6 and 18 hr po

They found that mEPSC amplitudes were unchanged at 6 and 18 hr postlesion but then increased at

24 and 48 hr, closely matching the time course of activity rate homeostasis. Because spine size is correlated with synaptic strength, and changes in a predictable manner when circuits are weakened or strengthened in response to MD in vivo (Hofer et al., 2009), Keck et al. (2013) hypothesized that in vivo scaling of synaptic strengths should have a structural correlate in altered dendritic spine size. Remarkably, they indeed found that spine size on L5 pyramidal neurons increased 24 hr after the retinal lesion and was maintained at 48 hr, thus following the same time course as the changes in Ponatinib chemical structure mEPSC amplitude and cortical activity in vivo. Altogether, these data and those obtained by Hengen et al. (2013) are consistent with the hypothesis that synaptic scaling could underlie homeostatic adjustments in neocortical firing rates in vivo. The studies by Hengen et al. (2013) and Keck et al. (2013) provide much anticipated evidence supporting that neuronal activity levels are homeostatically regulated in the neocortex in vivo. While both studies report an initial drop in activity levels in response to sensory deprivation, followed by a subsequent rebound, the time courses of the

two observations are dramatically different. Interestingly, the rapid sensory deprivation induced drop in overall activity levels observed by Keck et al. (2013) recovered to control levels within 24 hr, which is when Hengen et al. (2013)

obtained their first measurements Ipatasertib nmr also showing baseline firing rates in excitatory neurons. Discrepancies between the two studies are evident only at 48 hr, when Hengen et al. (2013) see significant depression of firing rates in excitatory neurons, whereas Keck et al. (2013) observe baseline activity Cediranib (AZD2171) levels. Most likely, differences are due to the widely diverse experimental conditions in the two studies—including deprivation protocols (monocular lid suture versus binocular retinal lesion), species (rat versus mouse), and ages (juvenile versus adult; Figure 1). Future experiments utilizing similar paradigms, while independently varying the individual parameters, will shed light on the mechanisms and origins of these differences. Several testable predictions arise from these studies and lead to exciting new avenues of research. While these studies support that synaptic scaling could be responsible for homeostatic regulation of firing rates in the neocortex, they do not exclude that alternative mechanisms of synaptic plasticity, such as plasticity of intrinsic excitability, anti-Hebbian mechanisms, or Hebbian modifications of excitatory or inhibitory synapses, are also at play. One prediction is that a homeostatic set point should operate bidirectionally; and consequently, enhanced firing rates due to sensory overstimulation should be homeostatically downregulated.

In this light it is plausible that Cajal’s depiction of the nucle

In this light it is plausible that Cajal’s depiction of the nuclear organization and settling position of neurons in the developing brain represents a supraspinal complement to Romanes’s focused analysis of motor pool organization. If so, neuronal settling position could turn out to be a critical determinant

of connectivity and circuit assembly throughout the vertebrate CNS. We are indebted to George Romanes for many enlightening discussions on spinal cord anatomy and function, and for his gracious mTOR inhibitor hospitality. We also thank Gwen and Muriel Romanes for kindly providing the photograph shown in Figure 2, Kendall Doerr for an objective view on neural architecture, and Trevor Drew for advice on motor cortical maps. T.M.J. is supported by grants from NINDS and ProjectALS and is an HHMI Investigator. “
“The sensorimotor control system has exceptional abilities to perform skillful action. For example as an opposing ice hockey player skates in on the net and shoots, within a split second the goalie reaches out, catches the puck, and prevents the goal. However, there are several issues that make this a difficult computational problem for the

brain to solve. The first is uncertainty: although the goalie sees the puck coming toward the goal, he cannot be certain when and where the player will aim or where the puck will actually go. Second, once the goalie estimates the puck’s likely trajectory, Selleck Cabozantinib he must determine which of the over 200 joints and 600 muscles he will use in order to move his body Tryptophan synthase or stick to block the puck—this is the problem of redundancy.

Third, both his sensory feedback, such as the puck’s visual location, and his motor outputs are corrupted by noise. This noise in combination with the variable environment, such as the unevenness of the ice surface, leads to variability in both perception and action. Fourth, both the sensory feedback processing and motor outputs are subject to delays, with visual perception of the puck location, for example, already around 100 ms out of date. The fifth issue is nonstationarity—the system’s physical properties do not remain constant. Throughout a game the goalie must correct for weaker muscles as he fatigues, and changes in the ice surface. Finally, the entire neuromuscular system is nonlinear: for example the output of the muscle (force) is dependent on the descending activation command in a complexly nonlinear manner based on the muscle state. We will discuss each of these issues and then describe five computational mechanisms that the sensorimotor control system uses to solve the complex problem of motor control, which it does with so much skill. Our primary focus will be at the computational and behavioral level because, at present, rather little is known about how these computations are implemented. Our hope is that the neurophysiological community will see ways in which different neural areas and circuits might be mapped onto these computations.

Seventy two hours after initiation of infection, the treatment gr

berghei. Seventy two hours after initiation of infection, the treatment group was orally given the extract of Neopetrosia exigua with the dosages of 50, 100, 200, and 400 mg/kg, the reference group with 10 mg/kg of chloroquine, and control

group with 0.2 ml of distilled water every day for 6 days. On the seventh day, the blood was taken through the tail to prepare thin blood smear by using Giemsa stain. Observation was conducted up to 30 days after the initiation of Libraries infection to determine the survival of infected mice and the effect of the extract. Residual malaria infection model was used for 30 mice of ICR strain that had been randomly taken into every stable, which consisted of 5 mice. The treatment group was given the extract of Neopetrosia exigua in an oral way with the dosages of 50, 100, 200, and 400 mg/kg, reference group with 10 mg/kg of chloroquine, and control group with 0.2 ml of distilled water for 3 days (D0–D2). On the third day, the mice were Selumetinib mw infected with suspense that contained 1 × 106 of P. berghei. On the seventh day, blood was taken through the tail to prepared blood smear by using Giemsa stain. Data are expressed as mean ± S.E.M. this website and analyzed using one way analysis of variance (ANOVA) followed

by Dunnett test for comparing pairs of data. The significant level was set at p < 0.05. The study showed that antimalarial activity of Neopetrosia exigua had a good activity against the growth of P. berghei. Dichloromethane dehalogenase Assay with chemosuppression test method showed that extracts with doses of 400 mg/kg and 200 mg/kg could suppress the growth of P. berghei by 80.69% and 60.62% compared to 98.32% inhibition of P. berghei growth using chloroquine with a dose of 10 mg/kg ( Table 1). Ethanolic extract of N. exigua dose of 400, 200 and 100 mg/kg group was significantly different than dose of 50 mg/kg and vehicle (*). Oral administration of Neopetrosia exigua extract with a dose of 400 mg/kg could not increase body weight of the mice, compared the mice given with 10 mg/kg of chloroquine.

On the other hand, chloroquine with doses of 200, 100, and 50 mg/kg could decrease body weight as shown in Table 2. Antimalarial test using prophylactive method showed that Neopetrosia exigua extract with doses of 400 and 200 mg/kg could inhibit the growth of P. berghei by 71.76% and 52.43%, respectively, while chloroquine group could provide P. berghei growth inhibition of 97.63%. Antimalarial test for curative effect showed that Neopetrosia exigua extract with oral doses of 400 and 200 mg/kg in mice could survive up to 14.64 ± 1.72 and 12.72 ± 0.98 respectively, compared to a survival of 30.00 ± 0.00 with chloroquine. Up to the first hour of infection, all mice were still in normal condition. Three hours after the infection, the mice began to show a declining motor activity, such as the sign of silence and confusion, and deteriorating physical conditions, such as hair loss and damage.