Conclusions: Ch-EVAR may extend the anatomical eligibility of end

Conclusions: Ch-EVAR may extend the anatomical eligibility of endovascular aneurysm repair using conventional devices. It appears to have similar mortality to open

repair with less morbidity. Long-term durability and stent patency remain to be determined. (J Vasc Surg 2011;53:895-905.)”
“Objective: Abdominal surgery in patients with advanced liver disease has been reported to be associated with high morbidity and mortality find more rates. However, the surgical risk of infrarenal abdominal aortic aneurysm (AAA) repair in cirrhotics remains ill-defined. We reviewed our experience to investigate the predictors of the outcome in cirrhotic patients after elective AAA open repair.

Methods: Between January 2001 and March 2006, 1189 patients underwent elective open repair of infrarenal AAA and 24 (2%) had a biopsy-proven cirrhosis (23 male, 1 female; mean age, 68 +/- 7 years). The latter were retrospectively stratified according to the Child-Turcotte-Pugh (CTP) score and the Model for End-Stage Liver Disease (MELD) TEW-7197 score.

Operative variables, perioperative complications, and survival were recorded and compared with those of 48 concurrent noncirrhotic controls matched (2:1) by gender, age, aneurysm size, preoperative glomerular filtration rate, and type of reconstruction. The effect of CTP and MELD scores on midterm survival was investigated in cirrhotics with the Kaplan-Meier log-rank method.

Results: No intraoperative or 30-day deaths were recorded. No significant differences in terms of major perioperative complications were observed between cirrhotic patients and controls. Operative time and intraoperative blood transfusion requirement were significantly higher in cirrhotics (162 +/- 49 vs 132 +/- 39 minutes; P = .007 and 273 +/- 364 vs 84 +/- 183 mL; P = .040, respectively). Hospital length of stay was nearly doubled in cirrhotic patients (11.0 +/- 2.8 vs 5.8 +/- 1.5 days; P < .0001). Twenty-two cirrhotic patients were XL184 mw classified as CTP A and two as CTP B. Median MELD score was 8 (range, 6-14).

CTP class B was associated with higher intraoperative blood transfusion requirement (941 +/- 54 vs 213 +/- 314 mL; P = .029). At a mean follow-up of 30.7 +/- 22.1 months, five deaths were recorded in cirrhotics, and three in controls. Actuarial survival at 2 years was 77.4% in cirrhotics and 97.8% in controls (log-rank test, P = .026). Both CTP B patients died within 6 months. CTP class B and a MELD score >= 10 were associated with reduced midterm survival rates (log-rank test, P < .0001 and P = .021, respectively).

Conclusions: In our experience, elective AAA open repair in relatively compensated cirrhotics was safely performed with an acceptable increase of the magnitude of the operation. However, the reduced life expectancy of cirrhotics with a MELD score >= 10 suggests that such a procedure may not be warranted in this subgroup of patients. (J Vasc Surg 2011;53:906-11.

We propose that the default response to uncertainty is the threat

We propose that the default response to uncertainty is the threat response and may be related to the well known negativity bias. We next review the evidence on the role of vagally mediated heart rate variability (HRV) in

the regulation of physiological, affective, and cognitive processes. Low HRV is a risk factor for pathophysiology and psychopathology. Finally we review recent work on the genetics of HRV and suggest that low HRV may be an endophenotype for a broad range of dysfunctions. (C) 2008 Elsevier Ltd. All rights reserved.”
“Purpose: We studied the safety and preliminary efficacy (marker tumor ablation) of 5 doses of BC-819 given as 6 intravesical infusions in patients with superficial bladder cancer in whom intravesical therapy with bacillus Calmette-Guerin had failed. BC-819 is a DNA plasmid that contains H19 gene regulatory BAY 63-2521 price sequences that drive the expression of an intracellular toxin.

Materials and Methods: A total of 18 patients in 4 groups of 3 and 1 group of 6 received escalating doses of BC-819 intravesically during 7 weeks. Patients had low grade superficial bladder cancer, which expressed H19. The effect on a marker tumor was examined 12 weeks after starting treatment. The escalating doses CH5424802 solubility dmso were 2, 4, 6, 12 and 20 mg plasmid per intravesical treatment. Responders continued to receive BC-819 once monthly every month for 1 year.

Results: No selleck kinase inhibitor dose limiting

toxicity was observed. The most frequent adverse events were mild to moderate bladder discomfort, dysuria, micturition urgency, urinary tract infection, diarrhea, hypertension and asthenia. Intravesical administration of BC-819 resulted in complete ablation of the marker tumor without any new tumors in 4 of the 18 patients for a 22% overall complete response rate. Eight of the 18 patients (44%) had complete marker tumor ablation or a 50% reduction

of the marker lesion. Nine patients received monthly maintenance, of whom 4 and 1 were disease-free at 35 and 49 weeks, respectively.

Conclusions: Intravesical BC-819 causes tumor ablation following intravesical administration at doses that were well tolerated. It is worthy of continued clinical investigation.”
“Essential hypertension is idiopathic although it is accepted as a complex polygenic trait with underlying genetic components, which remain unknown. Our supposition is that hypertension involves activation of the sympathetic nervous system. One pivotal region controlling arterial pressure set point is nucleus tractus solitarii (NTS). We recently identified that pro-inflammatory molecules, such as junctional adhesion molecule-1 (JAM-1), were over expressed in endothelial cells of the microvasculature supplying the NTS in an animal model of human hypertension (the spontaneously hypertensive rat) compared to normotensive Wistar-Kyoto rats (WKY).

Investigations leading to the detailed identification, expansion,

Investigations leading to the detailed identification, expansion, maintenance and function of CD alpha alpha(+) Tregs should result in new therapeutic strategies for human inflammatory diseases.”
“Smokers have a twofold increased risk to develop Crohn’s disease (CD). However, little is known about the mechanisms through which smoking affects CD pathogenesis. Especially Crohn’s ileitis is negatively influenced by smoking. Interestingly, the ileum and, more in particular, the Peyer’s patches in the terminal ileum are also the sites where

the Selleckchem AZD3965 first CD lesions are found. Several chemokines are implicated in the pathogenesis, among which is the CCL20-CCR6 pathway. Here, we studied the gut-associated lymphoid tissue in C57BL/6 wild-type mice and in CCR6-deficient mice after exposure to air or cigarette smoke for 24 weeks. Apoptotic index of the follicle-associated epithelium overlying the Peyer’s Selleckchem AZD1480 patches was evaluated. We found that chronic smoke exposure induced apoptosis in the follicle-associated epithelium. Furthermore, immune cell numbers and differentiation along with chemokine expression were determined in Peyer’s

patches. Important changes in immune cell composition were observed: total dendritic cells, CD4+ T cells (including regulatory T cells) and CD8+ T cells increased significantly after smoke exposure. The CD11b+ dendritic cell subset almost doubled. Interestingly, these changes were accompanied by an upregulated click here mRNA expression of the chemokines CCL9 and CCL20. However, no differences in the increase of dendritic cells were observed between wild-type and CCR6-deficient

mice. Our results show that cigarette smoke exposure increases apoptosis in the follicle-associated epithelium and is associated with immune cell accumulation in Peyer’s patches. Laboratory Investigation (2011) 91, 1056-1067; doi:10.1038/labinvest.2011.74; published online 2 May 2011″
“microRNA (miRNA)-mediated RNA interference has been identified as a novel mechanism that regulates protein expression at the translational level. Recent publications have provided compelling evidence that a range of miRNAs are involved in the regulation of immunity, including the development and differentiation of B and T cells, proliferation of monocytes and neutrophils, antibody switching and the release of inflammatory mediators. In this review, we examine what is presently known of the function and mechanism of action of these miRNAs in the regulation of the innate and acquired immune response.”
“There is evidence that people with schizophrenia show specific deficits in theory of mind (TOM). However, it is a matter of debate whether these are trait or state dependent, and the nature of the relationship between ToM deficits and particular symptoms is controversial.

A significant, cortex-specific testosterone-but not estradiol-att

A significant, cortex-specific testosterone-but not estradiol-attenuated effect (increase) of gonadectomy on monoamine oxidase’s

A but not B isoform was also observed. Although none of these actions suggest potential roles in the reguation/dysregulation of prefrontal dopamine, the suppressive effects of testosterone on cortical CHIR-99021 mw monoamine oxidase-A that were observed could have bearing on the increased incidence of cognitive deficits and symptoms of depression and anxiety that are repeatedly observed in males in conditions of hypogonadalism related to aging, other biological factors or in prostate cancer where androgen deprivation is used as a neoadjuvant treatment. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Tegument is a unique structure of herpesvirus, which surrounds the capsid and interacts with the envelope. Morphogenesis of gammaherpesvirus is poorly understood due to lack of efficient lytic replication for Epstein-Barr virus and Kaposi’s sarcoma-associated herpesvirus/human herpesvirus 8, which are etiologically associated with several selleckchem types of human malignancies. Murine gammaherpesvirus 68 (MHV-68) is genetically related to the human gammaherpesviruses and presents an excellent model for studying de novo lytic replication of gammaherpesviruses. MHV-68 open reading frame 33 (ORF33) is conserved among Alpha-, Beta-, and Gammaherpesvirinae subfamilies. However,

the specific role of ORF33 in gammaherpesvirus replication has not yet been characterized. We describe here that ORF33 is a true late gene and encodes a tegument protein. By constructing an ORF33-null MHV-68 mutant, we demonstrated that ORF33 is not required for viral DNA replication, early and late gene expression, viral DNA packaging or capsid assembly but is required for virion morphogenesis and egress. Although the ORF33-null virus was deficient in release of infectious virions, partially tegumented capsids produced by the ORF33-null mutant accumulated in the cytoplasm, containing conserved capsid proteins, ORF52 tegument protein, but virtually no ORF45 tegument Selleckchem MK-4827 protein and the 65-kDa

glycoprotein B. Finally, we found that the defect of ORF33-null MHV-68 could be rescued by providing ORF33 in trans or in an ORF33-null revertant virus. Taken together, our results indicate that ORF33 is a tegument protein required for viral lytic replication and functions in virion morphogenesis and egress.”
“A number of in vitro and in vivo studies using selective agonists have indicated a neuroprotective role for group-II metabotropic glutamate (mGlu2/3) receptors in various models of neuronal injury. Although an interplay among neurotrophic factors and mGlu2/3 receptors signalling system has been suggested as possible mechanism involved on neuroprotection, at present poor information are available concerning the in vivo regulation by mGlu2/3 receptors activation of specific neurotrophic factors.

Using the described methodology, we show that a ninth segment can

Using the described methodology, we show that a ninth segment can also be incorporated by manipulation of the PB2 or PA segment-specific packaging signals. This approach offers a means of generating a bivalent influenza virus vaccine.”
“Neuronal ceroid lipofuscinoses (NCLs) are a group of inherited neurodegenerative disorders characterized by epilepsy, progressive motor and cognitive decline, blindness, and by the accumulation of autofluorescent lipopigment. Late-infantile onset forms (LINCL) include those linked to mutations in CLN8 gene, encoding a transmembrane protein at the endoplasmic reticulum (ER). In the motor neuron degeneration (mnd) mouse model check details of the CLN8-LINCL (CLN8(mnd)),

we carried out an analysis of ER stress-related molecules in CN5 structures that exhibit a variable rate of disease progression (early retinal

degeneration and delayed brain and motoneuron dysfunction). At the presymptomatic state of 1-month-old CLN8(mnd) mice, we found an upregulation of GRP78 and activation of the transcription factor-6 (ATF6) in Nec-1s all structures examined, an activation of a CHOP-dependent pathway in the cerebellum, hippocampus and retina, a caspase-12-dependent pathway in the retina and no activation of these two pathways in the cerebral cortex and spinal cord. An increased CHOP expression was detected in the cortex and spinal cord at the early symptomatic state (4 months). Caspase-3 cleavage occurred presymptomatically in the cerebellum, hippocampus and retina, and symptomatically in the cerebral cortex and spinal cord. We also monitored activation of NF-kappa B, which is engaged in the alarming phase of ER stress, together with increased levels of TRAF2, TNF-alpha and TNFR1, and no activation of ASK-1/JNK signalling pathway, all over mnd structures. The results suggest that early ER-stress responses distinctly combined

and ER-stress pathways integrated with inflammatory responses may contribute to the progression of the CLN8(mnd) disease in CNS structures. (C) 2010 Elsevier Ireland Ltd. All rights reserved.”
“The PF299804 mouse structures of polio-, coxsackie-, and rhinovirus polymerases have revealed a conserved yet unusual protein conformation surrounding their buried N termini where a beta-strand distortion results in a solvent-exposed hydrophobic amino acid at residue 5. In a previous study, we found that coxsackievirus polymerase activity increased or decreased depending on the size of the amino acid at residue 5 and proposed that this residue becomes buried during the catalytic cycle. In this work, we extend our studies to show that poliovirus polymerase activity is also dependent on the nature of residue 5 and further elucidate which aspects of polymerase function are affected. Poliovirus polymerases with mutations of tryptophan 5 retain wild-type elongation rates, RNA binding affinities, and elongation complex formation rates but form unstable elongation complexes.

Most intervention studies in HD patients, such as statin therapy

Most intervention studies in HD patients, such as statin therapy and increased dialysis dose, have failed to show improvement in CVD outcomes. SN-38 chemical structure Two intervention trials using different antioxidants have found CVD benefits, suggesting that this line of therapy is effective in this resistant population. These studies

require validation in larger, adequately powered trials. Kidney International (2012) 81, 233-246; doi: 10.1038/ki.2011.341; published online 5 October 2011″
“The immune system is composed of networks of interacting cells and molecules; therefore, to understand and control immune behavior we need to adopt the thinking and tools of systems immunology. This review describes the use of an antigen microarray device and informatics to profile the repertoires of autoantibodies in health and disease. Autoantibody profiling provides an insight into the biomarkers used by the immune system in its dialog with the body. Heat shock PSI-7977 manufacturer protein 60 (HSP60) and HSP70 are cited as examples of key hubs in physiological regulatory networks; HSP molecules and peptides can be viewed as natural regulators because the immune system itself deploys them to modulate inflammatory reactions. The discovery of such natural biomarkers

paves the way towards natural control.”
“We previously identified a novel molecule “”Shati/Nat8l”" from the nucleus accumbens of mice. However, the physiological roles of the SHATI protein are not clear. To investigate selleck chemicals the effect of SHATI on the

central nervous system and behavior, we studied knockout mice of this protein. We carried out various behavior tests using Shari-knockout mice. Shati-knockout mice did not differ from wild type mice in learning and memory. In the open field test, Shari-knockout mice did not differ from wild-type mice in time of stay in the outer, middle and center areas. On the other hand, Shari-knockout mice showed increases in rearing and grooming time in the open field test, and exploration time of novel objects. These results suggested that knockout of the Shari gene may increase exploration in specific circumstances. Interestingly, the Shati-knockout mice avoided social interaction with unfamiliar mice out of their home cage, although there was no difference in social interaction in their home cage compared with wild type mice. Lack of the Shari gene increased brain-derived neurotrophic factor (BDNF) mRNA in the prefrontal cortex and hippocampus, and decreased glial cell line-derived neurotrophic factor (GDNF) mRNA in the striatum and hippocampus, and lipopolysaccharides-induced TNF-alpha factor (LITAF) mRNA in the striatum. Since these factors play important roles in behavior, alteration of expression of these factors may be related to the induction of exploration and reduction of social interaction in Shari-knockout mice. (C) 2012 Elsevier Ireland Ltd. All rights reserved.

“Deep brain stimulation (DBS) as a therapy in neurological

“Deep brain stimulation (DBS) as a therapy in neurological and psychiatric disorders is widely applied in the field of functional and stereotactic neurosurgery. In this respect, experimental DBS in animal models is performed to evaluate new indications and new technology. In this article, we review our experience with the concept of experimental DBS, including its development and validation. An electrode construction was developed using clinical principles to perform DBS unilaterally or bilaterally in freely moving rats. The stimulation parameters were adjusted for the rat using current density calculations. We performed validation

PD0332991 in vivo studies in 2 animal models: a rat model of Parkinson’s disease (bilateral 6-hydroxydopamine infusion in the striatum) and a rat model of Huntington’s disease (transgenic rats). The effects of DBS were evaluated in different behavioral tasks measuring motor and cognitive functions. The electrode construction developed allows experimental DBS to be performed in freely moving rats. With the current setup,

electrodes are placed in the target in 70% to 95% of the cases. Using a rat model, we showed that bilateral DBS of the subthalamic nucleus improves parkinsonian motor disability, but can induce behavioral side effects, similar BAY 11-7082 order to the clinical situation. In addition, we showed that DBS of the globus pallidus can improve motor and cognitive symptoms in a rat model of Huntington’s disease. Nevertheless, during the process of the development and validation of experimental DBS, we encountered specific problems., These are discussed in detail. Experimental DBS in freely moving animals is an adequate tool to explore new indications for DBS and to refine DBS technology.”
“BACKGROUND: Tuberculosis (TB) remains an important public health problem in developing countries.

OBJECTIVE: To evaluate the clinical presentation, management, and long-term outcome in 6 patients with tuberculous brain abscesses (TBA), an uncommon form of central nervous system (CNS) TB.

METHODS: A search of medical records of

a single referral neurological center in Mexico City from 2002 to 2007 retrieved 149 patients with CNS TB; 6 of them (4%) met Whitener’s criteria for TBA and were included in this review.

RESULTS: Five of six patients had a previous history of TB. Three patients were referred to our center Selleck Thiazovivin under antituberculous treatment (ATT) for pulmonary and lymph node TB, and two patients were receiving ATT for TB meningitis at diagnosis of TBA. All presented with symptoms of intracranial hypertension and hemiparesis. On imaging studies, 3 patients had a single, deep multiloculated lesion and another three had separated lesions, all patients underwent surgery and received long courses of ATT. One patient died after surgery and the rest recovered with moderate to severe neurological sequelae. The residual lesions in 5 patients resolved in follow-up CT or MRI studies at a mean time of 10 months.

If C protein function is compromised, as in the case of F170S HPI

If C protein function is compromised, as in the case of F170S HPIV1, the resulting PKR activation and reduction in viral protein levels

enable the host to further reduce C protein levels and to mount a potent antiviral type I IFN response.”
“Gliotransmitters such as glutamate and ATP play an essential role in the prevention of the osmotic swelling of retinal ICG-001 glial (Muller) cells. It has been shown that vascular endothelial growth factor (VEGF) induces a Ca2+-dependent release of glutamate from the cells [Wurm et al. (2008), J Neurochem 104:386-399]. In the present study, we investigated with cell swelling experiments on freshly isolated retinal glial cells of the rat whether activation of voltage-gated Na+ (Na-v) and Ca2+ channels (VGCCs) is implicated

in mediating the VEGF-induced release of glutamate. We found that the inhibitory effect of VEGF on the osmotic swelling of retinal glial cells, used as an indicator of glutamate release, is prevented in the presence of selective blockers of T-type VGCCs (kurtoxin, mibefradil, Ni2+) and Na-v channels (TTX, saxitoxin, phenytoin). In contrast, the swelling-inhibitory effect of glutamate, that is mediated by a downstream release of ATP, remained unaffected in the presence of the blockers. The cells displayed immunolabeling for VGLUT3, Ca(v)1.2, Ca(v)3.1, and Na(v)1.6. In addition to VEGF, various other receptor agonists including neuropeptide Y, progesterone, erythropoietin, and endothelin-1 evoked a VGCC- and Na-v channel-dependent release of glutamate. It is concluded that activation of T-type VGCCs and Na-v channels is implicated in mediating the ligand-induced release of glutamate from retinal glial cells of the rat. The involvement of VLGUTs might suggest

that glutamate is released by vesicular exocytosis. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“West Nile virus (WNV) is transmitted to vertebrate hosts primarily by infected Culex mosquitoes. Transmission of arboviruses by the bite of infected mosquitoes can potentiate infection in hosts Urease compared to viral infection by needle inoculation. Here we examined the effect of mosquito transmission on WNV infection and systematically investigated multiple factors that differ between mosquito infection and needle inoculation of WNV. We found that mice infected with WNV through the bite of a single infected Culex tarsalis mosquito exhibited 5- to 10-fold-higher viremia and tissue titers at 24 and 48 h postinoculation and faster neuroinvasion than mice given a median mosquito-inoculated dose of WNV (10(5) PFU) by needle. Mosquito-induced enhancement was not due to differences in inoculation location, because additional intravenous inoculation of WNV did not enhance viremia or tissue titers.

Furthermore, the autophagy induction was also characteristic hall

Furthermore, the autophagy induction was also characteristic hallmark of amyloid-beta-induced cytotoxicity. Morphological changes were positively correlated with the extent of phosphorylated glycogen synthase kinase-3 beta (phospho-Tyr(216)-GSK-3 beta, GSK-3 beta-P(Y216)). The activity of GSK-3 beta is believed to cause tau protein hyper-phosphorylation, increased amyloid-beta production and local plaque-associated microglial-mediated inflammatory responses. All of them are symptomatic for AD. In our studies, the highly significant Y216 phosphorylation and over-expression of total GSK-3 beta were observed in A beta PPsw-transfected PC12 cells. In addition, the immuocytochemical

analysis S63845 showed co-localization of GSK-3 beta-P(Y216) see more and amyloid-beta deposits. Thus, our data support a functional role of GSK-3 beta in A beta PP

processing, further implicating this kinase in the amyloid-beta-dependent pathogenesis. (C) 2009 Elsevier Inc. All rights reserved.”
“Extinction of fear requires learning that anticipated aversive events no longer occur. Animal models reveal that sustained phosphorylation of the extracellular signal-regulated kinase (Erk) in hippocampal CA1 neurons plays an important role in this process. However, the key signals triggering and regulating the activity of Erk are not known. By varying the degree of expected and delivered aversive

reinforcement, we demonstrate that Erk specifically responds to prediction errors of contextual aversive events. An increase of somatonuclear phospho-Erk (pErk) within principal CA1 neurons was observed only when the expectation of contextual Selleck ARS-1620 foot shock was violated, but not when the context was consistently nonreinforced or reinforced by foot shock. The rate of error detection, Erk signaling, and fear extinction markedly depended on shock expectancy and the aversive valence of the context, as revealed by comparison of groups trained with single, continuous, or partial reinforcement. On the basis of these findings, the hippocampal Erk response to prediction errors of aversive outcome is proposed as a unique mechanism of fear extinction. Improving the detection and processing of these errors has the potential to attenuate fear responses in patients with anxiety disorders.”
“Cadmium, mercury and rotenone are environmental pollutants whose neurotoxic mechanisms are not fully understood. We have shown previously that exposure of nerve cells to these agents produces oxidative stress which reversibly blocks growth factor and cytokine-mediated Janus kinase (Jak)/signal transducer and activator of transcription (STAT) signaling. Here we determined a critical role for mitochondrial dysfunction in inhibiting Jak/STAT activity in human BE(2)-C neuroblastoma cells.

This expression pattern was similar to that of cyclooxygenase-2 (

This expression pattern was similar to that of cyclooxygenase-2 (COX-2) following TMT administration. The P2X1 antagonist NF499 strongly prevented neuronal cell death induced by TMT in the CA1 region, and successfully suppressed locomotor hyperreactivity. Furthermore, NF449 administration also inhibited COX-2 expression in the CA1 region AMG510 on day 3 following TMT treatment, whereas no change was observed in the CA3. These findings suggest that P2X(1) plays a primary

role in TMT-induced neuronal cell death in the CA1 region. (C) 2011 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.”
“The relationship between “”connectivity”" measures such as DTI and the cellular alterations in the cortex that give rise to those connections remains unclear. Cytoarchitectural changes in the planum temporale (PT) suggest impaired layer III feedforward projection neurons in schizophrenia. Altered hemispheric asymmetry of the PT has been reported in patients, along with altered white matter density in the corpus callosum, and there

is anomalous activation of the PT during auditory hallucinations. We measured layer III cell density and pyramidal neuron size in PT of both hemispheres of post-mortem brains from patients with schizophrenia (n = 16) and control subjects (n = 16). We found reduced cell density and the loss of a correlation between magnopyramidal neuron density and axon number in the isthmus of the corpus callosum in schizophrenia. The normal asymmetry indicated PX-478 price that magnopyramidal neurons tend towards being larger and denser in the left PT but this asymmetry is significantly reduced in schizophrenia. The findings

offer cytoarchitectural insight into the relationship between PT cortex and callosal white matter abnormalities in MK-0518 schizophrenia. (C) 2011 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.”
“Neostriatum plays an important role in the pathophysiology of Parkinson’s disease (PD). However, the changes of sensitivity of dopamine receptors of neostriatal neurons in PD have been less addressed in vivo. In the present study, systemic exposure to paraquat and maneb induced Parkinsonian symptoms and neuronal loss of substantia nigra pars compacta. Using single-unit recording methods, three types of neostriatal neurons were recorded including medium spiny-like neurons, large aspiny-like neurons and fast-spiking interneurons. In the exposed rats, increased firing activity of neostriatal neurons was revealed when compared to control rats. Following D1 receptor agonist, SKF38393 and D2 receptor agonist, LY171555 iontophoretically administrated respectively, effects of increase and decrease in firing activity were both observed in neostriatal neurons.