00, p <0.05). Expression of p53 and Bcl-2 protein did not differ between the groups, but Bax protein expression was significantly higher in the study group (85% vs 40%, p <0.05).

Conclusions: Transarterial chemoembolization induces tumor cell necrosis, degeneration and apoptosis, while also boosting interstitial fibrous tissue hyperplasia and lymphocyte infiltration. These histopathological findings could help explain the basis of the better clinical

outcome in patients with Wilms tumor who underwent preoperative transarterial chemoembolization.”
“Purpose: We assessed predictive factors for acute renal cortical scintigraphic lesion and ultimate scar formation in children with a first febrile urinary tract infection.

Materials and Methods: A total of 89 girls and 138 boys with a first febrile urinary tract infection were included in the study. We analyzed radiological (ultrasound, EPZ004777 molecular weight dimercapto-succinic acid scintigraphy, voiding cystourethrogram), clinical (age, gender, peak fever, therapeutic delay AG-120 time) and laboratory (complete blood count with differential count, absolute neutrophil count, blood urea nitrogen, creatinine, urinalysis, Gram’s stain, culture, C-reactive protein, erythrocyte sedimentation rate) variables. Dimercapto-succinic acid scintigraphy was performed within 5 days and at 6 months after diagnosis of urinary tract infection. Voiding cystourethrogram was performed after the acute

phase of the urinary tract infection. Predictive factors for acute scintigraphic lesion and ultimate scar formation were assessed using logistic regression analysis.

Results: Of 227 patients enrolled 140 had a refluxing and 87 a nonrefluxing urinary tract infection. On logistic regression analysis therapeutic delay time (p = 0.001) and presence of reflux (p = 0.011) were predictive of acute scintigraphic SSR128129E lesion and ultimate scar formation (p = 0.001 and p = 0.0001, respectively) in children with a first febrile urinary tract infection.

Conclusions: Since vesicoureteral reflux is the common risk factor for acute scintigraphic lesion and ultimate scar formation, voiding cystourethrogram

must be considered as an initial study in patients with acute febrile urinary tract infection.”
“Purpose: Although more common in adults, urolithiasis recently has been occurring with increasing frequency in children. Single institution reviews from 1950 to 1990 revealed that urolithiasis accounts for 1 in 7,600 to 1 in 1,000 pediatric hospitalizations. Stone prevalence and risk factors for hospitalization are less defined in children in North America compared to adults. To identify pediatric hospital admissions due to a diagnosis of urinary stones, we examined Pediatric Health Information System data from 41 freestanding pediatric hospitals.

Materials and Methods: We retrospectively studied patients younger than 18 years hospitalized between 2002 and 2007.

We explored the neural correlates of episodic memory in AD, MCI and healthy aging by correlating a measure of episodic memory with hippocampal volume and fractional anisotropy (FA) and mean diffusivity (MD) of the cingulum and fornix. Episodic

memory was associated with hippocampal volume and MD of the cingulum and fornix. In contrast, there were fewer significant associations between episodic memory and FA. These findings support a relationship between episodic memory and hippocampal circuitry, and suggest that MD is a more sensitive marker of decreased white matter integrity in the study of AD and MCI than FA. Furthermore, MD was significantly selleck inhibitor associated with hippocampal volume, indicating that white matter pathology is not completely independent of gray matter pathology. However, the pattern of diffusivity differences in AD and MCI implies a more complex pathology than simply Wallerian degeneration. (C) 2010 Elsevier Ireland Ltd. All rights reserved.”
“The most prominent mechanism proposed for death of dopaminergic neurons in Parkinson’s disease (PD) is elevated generation of reactive oxygen/nitrogen species (ROS/RNS). Recent studies suggest that ROS produced during PD pathogenesis may contribute to cytotoxicity in cell culture models of PD. We hypothesized that inhibition VE821 of ROS production would prevent PD symptoms in the LRRK2(R1441G) transgenic (tg)

mouse model of PD. These mice

overexpress a mutant form of leucine-iich repeat kinase 2 (LRRK2) and are reported to develop PD-like symptoms at approximately 10 months of age. Despite similar expression of the transgene, our colony did not recapitulate the same type of motor dysfunction L-NAME HCl originally reported. However, tests of motor coordination (pole test, Rotor-Rod) revealed a significant defect in LRRK2(R1441G) mice by 16 months of age. LRRK2(R1441G) tg mice, or wild type littermates, were given diapocynin (200 mg/kg, a proposed NADPH oxidase inhibitor) three times per week by oral gavage starting at 12 weeks of age. Decreased performance on the pole test and Rotor-Rod in the LRRK2(R1441G) mice was prevented with diapocynin treatment. No loss in open field movement or rearing was found. As expected, tyrosine hydroxylase staining was similar in both the substantia nigra and striatum in all treatment groups. Together these data demonstrate that diapocynin is a viable agent for protection of neurobehavioral function. (C) 2013 Elsevier Ireland Ltd. All rights reserved.”
“N-acylethanolamines (NAEs) constitute a class of bioactive lipid molecules present in animal and plant tissues. Among the NAEs, N-arachidonoylethanolamine (anandamide), N-palmitoylethanolamine, and N-oleoylethanolamine attract much attention due to cannabimimetic activity as an endocannabinoid, anti-inflammatory and analgesic activities, and anorexic activity, respectively.

“
“Purpose:

The chronic pelvic pain syndrome is characterized by pelvic pain, voiding symptoms and varying degrees of inflammation within expressed prostatic secretions. We evaluated the chemokines monocyte chemoattractant protein 1 (CCL2) and macrophage inflammatory protein-1 alpha (CCL3) in expressed prostatic secretions to identify marker increases associated with inflammatory (IIIA) and noninflammatory (IIIB) chronic pelvic pain syndrome. In addition, chemokine levels were correlated with clinical pain as determined by the National Institutes of Health chronic prostatitis symptom index.

Materials and Methods: Expressed prostatic secretions were collected by digital rectal examination, and evaluated by enzyme linked immunosorbent assays for monocyte chemoattractant protein 1 and macrophage inflammatory protein-la in 154 patients including controls (13), those with benign prostatic hyperplasia (54), chronic pelvic pain syndrome Defactinib nmr IIIA (37) and IIIB (50). Monocyte chemoattractant protein 1 and macrophage inflammatory protein-la levels were compared between IIIA, IIIB and the control subgroups, and correlated

against the chronic prostatitis symptom index and pain subscore using a Spearman test.

Results: Mean levels of monocyte chemoattractant protein 1 in the control, inflammatory benign prostatic hyperplasia, noninflammatory benign prostatic hyperplasia, inflammatory Selleckchem VX 809 chronic pelvic pain syndrome and noninflammatory chronic pelvic pain syndrome were 599.4, 886.0, 1,636.5, 3,261.2 and 2,272.7 pg/ml, respectively. Mean levels of macrophage inflammatory protein-1 alpha in the control, inflammatory benign prostatic hyperplasia, noninflammatory benign prostatic hyperplasia, IIIA chronic pelvic pain syndrome and IIIB chronic pelvic pain syndrome were 140.1, 299.4, 238.7, 1,057.8 and 978.4 pg/ml, respectively. For each cytokine both

chronic pelvic pain syndrome subtypes had statistically higher levels than the control group and patients with benign prostatic hyperplasia (p = 0.0002). Tryptophan synthase Receiver operating curves using monocyte chemoattractant protein 1 levels greater than 704 pg/ml and macrophage inflammatory protein-la greater than 146 pg/ml identified patients with chronic pelvic pain syndrome with an accuracy of 90% from control patients. Macrophage inflammatory protein-la levels (p = 0.0007) correlated with the pain subscore of the chronic prostatitis symptom index while monocyte chemoattractant protein 1 (p = 0.71) did not.

Conclusions: Monocyte chemoattractant protein I and macrophage inflammatory protein-la within the prostatic fluid in both chronic pelvic pain syndrome subtypes provide candidate future biomarkers for chronic pelvic pain syndrome. In addition, macrophage inflammatory protein-la increase in expressed prostatic secretions provides a new marker for clinical pain in chronic pelvic pain syndrome patients.

In this study, we showed that the exogenous expression of TLS in TLS-KO neurons did not rescue the abnormal spine phenotypes. The

degree of colocalization between exogenous TLS and Nd1-L mRNA was significantly decreased in both the neuronal dendrites and the spines of TLS-KO neurons. Our results indicate that formation of TLS-Nd1-L mRNA complex clusters, presumable mRNA pools for the local protein synthesis in the spines, was impaired in TLS-deficient neurons. NeuroReport 20:57-61 (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.”
“This study was carried out based on the assumption that brain-derived neurotrophic factor (BDNF) may counterbalance the action of morphine in the brain. Morphine analgesic tolerance after daily administrations for six days was blocked by intracerebroventricular

injection of anti-BDNF IgG on day 5, but Selleck RepSox not by administrations on days 1-4. Chronic morphine treatment significantly increased the expression of exon I and IV BDNF transcripts, indicating differential regulation of BDNF gene expression. Daily administration of the CREB-binding protein inhibitor curcumin abolished the upregulation of BDNF transcription and morphine analgesic tolerance. These results suggest that curcumin might be a promising adjuvant to reduce morphine analgesic tolerance, and that epigenetic control could be a new strategy useful for the control of this problem. NeuroReport 20:63-68 (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williams tetracosactide & Wilkins.”
“The AMG510 supplier reliability

of the immune response to pathogenic challenge depends critically on the size and diversity of the T cell repertoire. We study naive T cell repertoire diversity maintenance by a stochastic model that incorporates the concept of competition between T cells for survival stimuli emanating from self-antigen presenting cells (APCs). in the mean field approximation we show that clonotype extinction is certain and compute mean extinction times. We introduce the concept of mean niche overlap and show that clones with a mean niche overlap greater than one have a short repertoire lifespan. This selection differential induces minimal recognition commonality between T cell receptors (TCRs) resulting in a diverse T cell repertoire. (C) 2008 Elsevier Ltd. All rights reserved.”
“Although manganese (Mn) has been shown to increase prolactin (PRL) by decreasing dopamine (DA) in the hypothalamus, the mechanism of Mn-induced regulation of the hypothalamic-hypophyseal-pituitary axis is unclear. We assessed the effects of inhaled Mn on hypothalamic DA and pituitary PRL production and evaluated the role of pituitary-specific transacting factor 1 (Pit-1), a transacting factor of PRL gene, in Mn-induced changes in PRL secretion in the rat brain. Male rats exposed to Mn for 4 or 13 weeks (1.

Apoptosis ratio was analyzed

by flow cytometry. Bcl-2 and Bax and the coding mRNA were examined. It was found that the apoptosis ratio in NE group (29.4 +/- 1.8%) was significantly greater (P < 0.05) than that of the control group (10.1 +/- 1.7%). The effect of NE was attenuated by CGRP (18.7 +/- 2.1%), which was reversed by CGRP(8-37) (24.9 +/- 2.9%). NE treatment resulted in reductions in the ratio of Bcl-2/Bax (by 33%) and their mRNA (by 53%). CGRP restored the level of Bcl-2/Bax, which was abolished by CGRP(8-37). Current study suggests that norepinephrine inhibits synthesis of Bcl-2 and increases Bax and apoptosis of cardiomyocytes. CGRP restores the ratio of Bcl-2/Bax and attenuates Epigenetics inhibitor Givinostat in vitro the apoptosis induced by NE, via specific CGRP receptor. (C) 2013 Elsevier Ireland Ltd. All rights reserved.”
“Plasmalogens, 1-O-alk-1′-enyl 2-acyl glycerol phospholipids and glycolipids, seem to have evolved first in anaerobic bacteria, but they did not persist when facultative and aerobic species appeared after the concentration of oxygen increased in the early earth’s history. Later, when aerobic animal cells appeared with their mitochondria and other intracellular organelles, plasmalogen biosynthesis requiring molecular oxygen, reappeared. The possible reasons for the disappearance and reappearance

of plasmalogens in the evolution of life on earth are discussed. The sensitivity of plasmalogens

to reactive oxygen species may have caused their disappearance when respiration Idelalisib concentration first evolved. Special features of plasmalogen structure and the resulting lipid packing may account for their reappearance. (C) 2010 Elsevier Ltd. All rights reserved.”
“Increased expression of thioredoxin-interacting protein (TXNIP) has recently been proved to be a crucial event for irremediable endoplasmic reticulum (ER) stress resulting in the programmed cell death (apoptosis) of pancreatic beta-cells. The present study demonstrated that treatment with 1-10 mu g/ml tunicamycin, a potent revulsant of ER stress, drastically induced TXNIP expression accompanied by the generation of cleaved caspase-3 as an indicator of apoptosis in SK-N-SH human neuroblastoma cells. This result substantiated that TXNIP is also involved in neurodegeneration triggered by ER stress. Moreover, we evaluated the effects of nobiletin, a citrus polymethoxyflavonoid, on tunicamycin-induced apoptosis and TXNIP expression in SK-N-SH cells, because we reported previously that this flavonoid might be able to reduce TXNIP expression. Co-treatment of SK-N-SH cells with 100 mu M nobiletin and 1 mu g/ml tunicamycin for 24 h strongly suppressed apoptosis and increased TXNIP expression induced by 1 mu g/ml tunicamycin treatment alone.

1AKO mice did not differ from wild-type mice in startle plasticity.

Serotonin(1A) receptor deletion does not enhance vulnerability to the effects of MS on startle plasticity. The life-long increase in startle reactivity and PPI deficit induced

by MS are strain-dependent. Further, the use of startle reactivity and plasticity may have added value in translational studies relating to early life stress.”
“Enterovirus 71 (EV-71) infections are usually associated with mild hand, foot, and mouth disease in young children but have been reported to cause GW3965 severe neurological complications with high mortality rates. To date, four EV-71 receptors have been identified, but inhibition of these receptors by antagonists did not completely abolish EV-71 infection, implying that there is an as yet undiscovered receptor(s). Since

EV-71 has a wide range of tissue tropisms, we hypothesize that EV-71 infections may be facilitated by using receptors that are widely expressed in all cell types, such as heparan sulfate. In this study, heparin, polysulfated dextran sulfate, and suramin were found to significantly prevent EV-71 infection. Heparin inhibited infection by all the EV-71 strains tested, including those with a single-passage history. Neutralization of the cell surface anionic charge by polycationic poly-D-lysine and blockage of heparan sulfate by an anti-heparan sulfate peptide also inhibited EV-71 infection. Interference with heparan sulfate biosynthesis either by sodium chlorate treatment or through transient knockdown Selinexor cell line of N-deacetylase/N-sulfotransferase-1 and exostosin-1 expression reduced EV-71 infection in RD cells. Enzymatic removal of cell surface heparan sulfate by heparinase I/II/III inhibited EV-71 infection. Furthermore, the level of EV-71 attachment to CHO cell lines that are variably deficient in cell surface glycosaminoglycans

was significantly lower than that to wild-type CHO cells. Direct enough binding of EV-71 particles to heparin-Sepharose columns under physiological salt conditions was demonstrated. We conclude that EV-71 infection requires initial binding to heparan sulfate as an attachment receptor.”
“It is known that dopaminergic cell loss leads to increased endogenous cannabinoid levels and CB1 receptor density.

The aim of this study was to evaluate the influence of dopaminergic cell loss, induced by injection of 6-hydroxydopamine, on the effects exerted by cannabinoid agonists on neuron activity in the subthalamic nucleus (STN) of anesthetized rats.

We have previously shown that Delta(9)-tetrahydrocannabinol (Delta(9)-THC) and anandamide induce both stimulation and inhibition of STN neuron activity and that endocannabinoids mediate tonic control of STN activity. Here, we show that in intact rats, the cannabinoid agonist WIN 55,212-2 stimulated all recorded STN neurons.

Such correlative light electron microscopy (CLEM) experiments thus rely on using markers that are both fluorescent and electron dense. Unfortunately, there are very few markers that possess both these properties. Markers for

light microscopy such as green fluorescent protein are generally not directly visible in the electron microscopy and vice versa for gold particles. Hence, there has been an intensive search for markers that are directly visible both in the light microscope and in the electron microscope. Here we discuss some of the strategies and pitfalls that are associated with the use of CLEM markers, which might serve as a “”warning”" that new probes should be extensively tested before use. We focus on the use of CLEM markers for the study of intracellular transport and specifically endocytosis.”
“Paired-pulse

stimulation, the application of two stimuli Nepicastat ic50 in close succession, is a useful tool to investigate cortical excitability. Suppression of the second response after short interstimulus intervals characterizes paired-pulse behavior. Although paired-pulse www.selleckchem.com/products/Cisplatin.html suppression is often studied as a marker of cortical excitability in humans, little is known about the influence of stimulation intensity on paired-pulse suppression. To systematically explore the effect of stimulus intensity on paired-pulse suppression of median nerve somatosensory evoked potentials (MNSEPs), we recorded single-pulse Tyrosine-protein kinase BLK or paired-pulse MNSEPs in healthy volunteers using stimulation intensities ranging from the sensory threshold to 1.2 times the motor threshold using interstimulus intervals of 10, 30, and 100

ms. Of the various somatosensory evoked potential components, only the N20-P25 component showed an effect of intensity, where higher intensities resulted in stronger paired-pulse suppression. However, when only intermediate intensities were considered, paired-pulse suppression was not or only weakly influenced. Our data suggest that stimulation intensity in contrast to single pulse-evoked MNSEPs has only a weak influence on the paired-pulse suppression of early MNSEPs. Paired-pulse suppression is believed to arise from inhibition generated by intracortical networks. The lack of intensity dependence within the range tested can be considered as a step toward creating invariance against fluctuations of stimulus intensity. Thus, intracortical computations as apparent in paired-pulse behavior might be characterized by different properties compared with feed-forward processing.”
“During a study of the fecal microbiomes from two healthy piglets using high-throughput sequencing (HTS), we identified a viral genome containing an open reading frame encoding a predicted polyprotein of 2,133 amino acids. This novel viral genome displayed the typical organization of picornaviruses, containing three structural proteins (VP0, VP3, and VP1), followed by seven nonstructural proteins (2A, 2B, 2C, 3A, 3B, 3C(Pro), and 3D(Pol)).

G(i) inactivator (pertussis toxin) lowered TPVR but not in all SHR. Delta TPVR induced by alpha 1-adrenoceptor agonist (phenylephrine) was reduced by 8CPT-cAMP and milrinone in both strains. They also clearly reduced the response to endogenous noradrenaline release (tyramine) in SHR but had little effect in WKY. When pertussis toxin reduced baseline, it also eliminated the

tyramine TPVR response. Propranolol did not change the effect of milrinone on the phenylephrine or tyramine response. Strain-related differences in aorta, femoral arteries or skeletal muscle PDE activity (total/PDE3/PDE4) were absent. Conclusions: cAMP signaling down-stream of cAMP was functional in SHR, and opposed alpha 1-adrenoceptor vasoconstriction in both strains. G(i) activity greatly influenced the MX69 order TPVR baseline and adrenergic TPVR responses, and its activity appeared increased in SHR. Therapeutics aiming to increase signaling through this pathway may turn out to be valuable in the treatment of hypertension. Copyright (C) 2008 S. Karger AG, Basel”
“Autism is a neurodevelopmental disorder

characterized by disorders in social interaction and emotional reciprocity which can be explained by impairments of the ability to understand the mental states of others (“”theory of mind”") and recognition of facial expressions. These impairments may be related to the difficulties with face recognition characteristic of this disorder. Face perception find more plays a critical role in the development of social interaction and understanding of the internal emotional state of others. It depends on initial oculomotor exploration. The aim of DOK2 this study was to quantify ocular behaviour in 11 adults with autism and 23 healthy subjects (15-35 years) while exploring neutral faces and faces expressing an emotion using an eye tracking method. The strategy used to explore faces was also studied. All subjects spent significantly

more time on the eye region than on the rest of the face. However, subjects with autism spent less time on the eye region than healthy subjects. The latter used a strategy based on their own eye dominance when exploring faces. All healthy subjects significantly began their exploration of a face by looking at the eye in the contralateral visual field to their dominant eye. This strategy seemed to be impaired in patients with autism. To conclude, these results contrast with earlier reports regarding the lack of interest in the eye region in patients with autism, and demonstrate for the first time that perception of the face is dependent on eye dominance. (c) 2008 Elsevier Ltd. All rights reserved.”
“This study investigated the effects of 7-ketocholesterol on interleukin (IL)-6 expression in vascular smooth muscle cells (VSMC). Among the 7 IL examined, only IL-6 transcript was increased by 7-ketocholesterol treatment in human aorta smooth muscle cells.

In contrast, the motoneurons supplying the multiply-innervated muscle fibers of the extraocular muscles, the motoneurons

of the levator palpebrae muscle in the central caudal nucleus, and especially the preganglionic neurons supplying the ciliary ganglion received a strong orexin input. We interpret these results as evidence that orexin-A does modulate pupil size, lid position, and possibly convergence NCT-501 nmr and eye alignment via the motoneurons of multiply-innervated muscle fibres. However orexin-A does not directly modulate premotor pathways for saccades or the singly-innervated muscle fibre motoneurons. (C) 2009 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Purpose: Although the importance of myocardin in smooth muscle development is well established, many tissue specific intricacies of smooth muscle differentiation remain to be determined. We characterized

myocardin expression in the developing and adult bladder to identify potential tissue specific differences that may have a role in detrusor smooth muscle development.

Materials and Methods: Reverse transcriptase and quantitative polymerase chain reaction were done to determine myocardin expression in the mouse and human bladder vs various other tissues. Sequence analysis was done to confirm the genomic location of the various polymerase chain reaction products.

Results: Exonic profiling of the mouse myocardin gene identified a series of unique myocardin splice variants derived from a novel 305 bp exon between exons 2 and 3 of the previously identified myocardin gene. Each variant showed LCL161 a differential Vildagliptin pattern of expression in the mouse and primary protein sequences suggested a unique function for each myocardin variant identified. Identical myocardin splice variants were also observed in the human bladder as well as a unique human specific exon 12 myocardin splice variant that was not observed in the mouse.

Conclusions:

Identifying a series of unique myocardin splice variants that are differentially expressed in the bladder, and other muscle and nonmuscle tissues provides a potential molecular platform for mediating many unique tissue specific functions associated with the myocardin transcriptional program.”
“L-type calcium channels play an essential role in synaptic activity-dependent gene expression and are implicated in long-term alterations in synaptic efficacy underlying learning and memory in the hippocampus. The two principal pore-forming subunits of L-type Ca(2+) channels expressed in neurons are the Ca(v)1.2 (alpha(1C)) or Ca(v)1.3 (alpha(1D)) subtypes. Experimental evidence suggests that calcium entry through Ca(v)1.2 and Ca(v)1.3 Ca(2+) channels occurs in close proximity to key signalling molecules responsible for triggering signalling pathways leading to transcriptional responses.

To understand these phenomena,

we examined the effects of the P90A and A92E changes in the HIV-1 CA protein on the stability of capsid complexes assembled in vitro and on capsid disassembly in the cytosol of virus-exposed target cells. The A92E change impaired CA-CA interactions in vitro and decreased the amount of particulate capsids in the cytosol of HeLa target cells. Reducing the binding of CypA to the A92E mutant capsid, either by Cs treatment or by an additional P90A change in the CA protein, increased the amount of particulate capsids and viral infectivity in HeLa cells. In contrast, reduction of the binding of CypA to HIV-1 capsids in Jurkat T lymphocytes resulted in a decrease in the amount of particulate capsids

and infectivity. Thus, depending on the capsid and the target cell, CypA-CA binding either stabilized or destabilized the capsid, indicating that CypA modulates HIV-1 SC79 molecular weight capsid disassembly. In both cell types examined, decreased stability of the capsid was associated with a decrease Omipalisib cost in the efficiency of HIV-1 infection.”
“The indirubins long have been used in Chinese medicine for treatment of myelocytic leukemia. Among the many more recently described biological activities of the indirubins, attention has been directed toward the ability of these compounds to inhibit GSK-3 and CDKs, kinases implicated in neurodegenerative conditions. Little information is available on effects of indirubins on chemically-induced neurodegeneration. Here we examined the influence of three indirubins on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)- and kainic acid (KA)-induced neurotoxicity in the mouse. The three indirubins examined were 6-bromoindirubin-3′-oxime (6BIO), 5-bromoindirubin-3′-oxime (5BIO) and 5-amino-6-bromoindirubin

(5A6BI). The first two derivatives were previously described indirubins with low nanomolar inhibitory activity against GSK-3 and CDKs. The third compound was synthesized by the dimerization of 5-amino-6-bromoisatin with 3-acetoxyindol. The synthesis of the key compound 5-amino-6-bromoisatin was based on the bromination of the ketal of 5-amino-isatin. All indirubins examined decreased various measures associated with dopaminergic neurotransmission in striatum. These effects occurred alone or over and above the Methocarbamol decrements seen following administration of the dopaminergic neurotoxicant, MPTP. Striatal serotonin and serotonin turnover were decreased by the indirubins in MPTP-treated mice. None of these striatal effects of the indirubins alone were associated with evidence of astrogliosis, an indicator of underlying neuropathology, nor did they potentiate the astrogliosis accompanying administration of MPTP. In general, the indirubins reduced KA-associated mortality and striatal but not hippocampal astrogliosis due to this toxicant. The data suggest that indirubins affect striatal biogenic amine levels and turnover in intact mice.