Using a stereroscopic infrared camera the tracking sensor was located 3-dimensionally and a tracking handle was used to guide the cryoprobe percutaneously based on preoperative preloaded computerized tomography. Demographic and perioperative data were added prospectively to an institutional review board approved database. Immediately after cryoprobe placement computerized tomography was repeated to confirm placement accuracy.

Results: A total of 13 tumors in 10 patients were successfully

cryoablated with the novel navigational system. Mean tumor size was 2.2 cm. Preoperative biopsy revealed renal cell carcinoma in 9 cases. Mean operative time was selleck 155 minutes. No intraoperative or postoperative complications were noted. Mean length of stay was 9.5 hours. Mean targeting registration error was 4.2 mm.

Conclusions: Stereotactic percutaneous

cryoablation for renal tumors offers the potential for safe, precise needle placement.”
“Several groups maintain that morphine tolerance and dependence correlate with increased activity of protein kinases ERK1/2 and P38 MAPK and PKC as well as elevated levels of the neuropeptides dynorphin (DYN), substance P (sP), and calcitonin gene-related peptide (CGRP) in spinal cord dorsal horn (SCDH). They demonstrate that tolerance and dependence can be prevented, and sometimes reversed, by constitutive genetic deletion or pharmacological inhibition of these factors. Batimastat ic50 Recently, we showed that mice with a constitutive deletion of the GluR5 subunit of kainate receptors (GluR5

KO) are not different from wild type (WT) littermates with respect to baseline nociceptive thresholds as well as acute morphine antinociception, morphine physical dependence and conditioned place preference. However, unlike WT, GluR5 KO mice do not develop antinociceptive tolerance following systemic morphine administration. In this report, we examined levels of these mediators in SCDH of WT and GluR5 KO mice following subcutaneous implantation of placebo or morphine pellets. Surprisingly, spinal DYN and CGRP, along with phosphorylated ERK2 (pERK2), P38 (pP38) and PKCgamma (pPKC gamma) are elevated by deletion of GluR5. Additionally, chronic systemic morphine administration increased spinal pERK2, pP38 this website and pPKC gamma levels in both tolerant WT and non-tolerant GluR5 KO mice. In contrast, while morphine increased spinal DYN and CGRP in WT mice, DYN remained unchanged and CGRP was reduced in GluR5 KO mice. These observations suggest that spinal ERK2, P38 and PKC gamma are likely involved in multiple adaptive responses following systemic morphine administration, whereas DYN and CGRP may contribute selectively to the development of antinociceptive tolerance. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.

5 mm Hg +/- 20.7 to 27.3 +/- 13.0 mm Hg (P

= .00073), pulmonary vascular resistance decreased from 929 +/- dynes . s . cm(-5) to 299 +/- 307 dynes . s . cm(-5) (P = .0012), and cardiac output improved from 3.8 +/- 1.1 L/min to 5.6 +/- 1.6 L/min (P = .0061). There were no deaths during surgery or 30 days after surgery, and long-term survival (5+years) was achieved in 87.5%. As compared to adults with chronic thromboembolic pulmonary hypertension, there was a higher rate of rethrombosis in pediatric patients (38% vs 1%-4%).

Conclusions: This study demonstrates that pulmonary Selleck QNZ thromboendarterectomy surgery in pediatric patients with chronic thromboembolic pulmonary hypertension is well tolerated with improved postoperative hemodynamics, functional status, minimal postoperative complications, and low perioperative mortality, similar to that reported for adults with chronic thromboembolic pulmonary hypertension, with the notable exception being a higher rate of rethrombosis in pediatric patients. (J Thorac Cardiovasc Surg 2011;141:624-30)”
“Food intake is regulated according to circadian activity, metabolic needs and the hedonic value of food. Rodents

placed on a fixed feeding schedule show behavioral and physiological anticipation of mealtime referred to as food-anticipatory activity (FAA). FAA is driven by the food-entrainable oscillator (FEDI), whose anatomical JAK inhibitor substrate is not yet known. Recent data have shown that restricted feeding schedules

for regular chow and daily limited access to palatable food in free-feeding rats activate distinct brain regions during FAA. The combination of a deprivation regimen and scheduled access to palatable food may give rise to a more global anticipatory mechanism because the Foretinib supplier temporal cycles of energy balance would be strongly modulated by the incentive properties of palatable food; however, the neuronal response to this combined treatment is not yet known. The present study investigated how adding palatable sucrose to feeding schedules affects the pattern of brain c-fos mRNA expression during FAA (0-3 h) and 1 h following feeding. The rats maintained on scheduled chow access increased their daily chow intake, while the rats maintained on scheduled sucrose and chow mainly increased their daily sucrose intake. Adding sucrose to scheduled feeding displaced c-fos mRNA expression from the dorsomedial and paraventricular hypothalamic nuclei and posterior lateral hypothalamus (LH) to the prefrontal cortex, lateral septum, nucleus accumbens and anterior LH. During refeeding, the rats on scheduled sucrose demonstrated higher activation of the nucleus of the solitary tract.

Of the estimated 440000 cases of MDR tuberculosis

that occurred in 2008, only 7% were identified and reported to WHO. Of these cases, only a fifth were treated according to WHO standards. Although treatment of MDR and XDR tuberculosis is possible with currently available diagnostic techniques and drugs, the treatment course is substantially more costly and laborious than for drug-susceptible tuberculosis, with higher rates of treatment failure and mortality. Nonetheless, a few countries provide examples of how existing technologies can be find more used to reverse the epidemic of MDR tuberculosis within a decade. Major improvements in laboratory capacity, infection control, performance of tuberculosis control programmes, and treatment regimens for both drug-susceptible and drug-resistant disease will be needed, together with a massive scale-up in diagnosis and treatment of MDR and XDR tuberculosis to prevent drug-resistant strains from becoming the dominant form of tuberculosis. New

diagnostic tests and drugs are likely to become available during the next few years and should accelerate control of MDR and XDR tuberculosis. Equally important, especially in the highest-burden countries of India, China, and Russia, will R428 solubility dmso be a commitment to tuberculosis control including improvements in national policies and health systems that remove financial barriers to treatment, encourage rational drug use, and create the infrastructure necessary to manage MDR tuberculosis on a national scale.”
“Neurodegenerative disorders are a group of hereditary and sporadic conditions that are characterized by progressive nervous system dysfunctions. These disorders are often associated with neuronal atrophy and are characterized by the presence of intra- or extra-neuronal inclusions in the central or peripheral nervous system. The emerging understanding on these apparently diverse set of disorders suggest that they share a few key pathomechanisms, one of which could be the abnormality in the protein quality control pathways. Recent studies have shown that selleckchem either an overload on the proteolytic pathways – the ubiquitin-proteasome

system and the autophagosome-lysosome system – or defects in the critical components of these pathways might underlie the neuropathology. Here, we review the recent advances in our understanding on the role of protein quality control systems in the pathomechanisms of neurodegenerative disorders, highlight the interdependence between the two pathways and their involvement in neuronal survival. (C) 2010 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.”
“During a severe local or systemic inflammatory response, immune mediators target lung tissue. This process may lead to acute lung injury and impaired diffusion of gas molecules. Although several mathematical models of gas exchange have been described, none simulate acute lung injury following inflammatory stress.

Both peripheral and intraganglionic BTX-A reduce phase II of formalin-induced pain. Antinociceptive effect of BTX-A was prevented completely by colchicine. BTX-A-truncated SNAP-25 in medullary A-1210477 chemical structure dorsal horn (spinal trigeminal nucleus) was evident 3 days following the peripheral treatment, even with low dose applied (3.5 U/kg). Presented data

provide the first evidence that axonal transport of BTX-A, obligatory for its antinociceptive effects, occurs via sensory neurons and is directed to sensory nociceptive nuclei in the CNS. (C)C 2011 IBRO. Published by Elsevier Ltd. All rights reserved.”
“The influence of pre-experimental autobiographical knowledge on recognition memory was investigated using as memoranda faces that were either personally known or unknown to the participant. Under a dual process theory, such knowledge

boosted both recollection- and familiarity-based recognition judgements. Under an unequal variance signal detection model, pre-experimental knowledge increased both the variance and the separation of the target and foil memory strength distributions, boosting hits and correct rejections. Thus, pre-experimental knowledge has profound effects on the multiple, interacting processes that subserve recognition memory, and likely in the neural systems that underpin them.”
“Sensory cortices show a decline in synaptic plasticity (e.g., long-term potentiation, LTP) during postnatal maturation. We

demonstrate a partial reversal of this decline in click here rat primary auditory cortex (A1) by pharmacological Tacrolimus (FK506) manipulations or modifications of the acoustic environment. In adult, anesthetized rats, field postsynaptic potentials (fPSPs) in A1 elicited by medial geniculate nucleus (MGN) stimulation consisted of two sequential peaks. Simultaneous application in A1 of a GABA(A) receptor agonist (muscimol) and GABA(B) receptor antagonist (SCH 50911), thought to result in a preferential inhibition of intracortical activity while preserving thalamocortical inputs, suggested that these two fPSP components largely reflect thalamocortical and intracortical synapses, respectively. Rats (postnatal day [PD]60-70) showed moderate LTP of fPSPs following theta-burst stimulation (TBS) of the MGN. Interestingly, repeated episodes (PD10-20 & 50-60) of patterned sound deprivation by continuous white noise exposure resulted in substantial LTP, an effect not seen with single exposure (PD10-20 or 50-60), or two episodes during adulthood (PD50-60 & 100-110). Thus, early sensory deprivation acts as a “”prime,”" allowing subsequent deprivation to reinstate juvenile-like levels of LTP. Older (>PD200) rats that no longer exhibit LTP in A1 showed LTP of the first fPSP peak when TBS occurred during cortical zinc application.

The agonist of P2X(7) receptor BzATP caused a sustained increase in [Ca2+](i) in both groups, but the effect was smaller in patients. The antagonist at the P2X(7) receptor KN-62 reduced [Ca2+](i) in patients, but had no effect in healthy subjects. In patients, the permeability of ethidium bromide through P2X(7) pores, as well as through BzATP-activated and KN-62-inhibited

pores, was distinct from permeability in healthy volunteers. Conclusions:These results demonstrate that the calcium signaling pathway in PBMCs of CKD patients is defective already in CKD stage 2-3, and the pore-forming P2X(7) receptors are involved in these pathophysiological processes. copyright (C) 2011 S. Karger AG, Basel”
“The sub-nanosecond structural dynamics of reduced and oxidized cytochrome c were characterized. Dynamic properties of the protein backbone measured by amide (15)N click here relaxation and side chains measured

selleck chemical by the deuterium relaxation of methyl groups change little upon change in the redox state. These results imply that the solvent reorganization energy associated with electron transfer is small, consistent with previous theoretical analyses. The relative rigidity of both redox states also implies that dynamic relief of destructive electron transfer pathway interference is not operational in free cytochrome c.”
“Sigma-1 receptors (Sig-1Rs) have been implicated in many neurological and psychiatric conditions.

Sig-1Rs PDK inhibitor are intracellular chaperones that reside specifically at the endoplasmic reticulum (ER)-mitochondrion interface, referred to as the mitochondrion-associated ER membrane (MAM). Here, Sig-1Rs regulate ER-mitochondrion Ca2+ signaling. In this review, we discuss the current understanding of Sig-1R functions. Based on this, we suggest that the key cellular mechanisms linking Sig-1Rs to neurological disorders involve the translocation of Sig-1Rs from the MAM to other parts of the cell, whereby Sig-1Rs bind and modulate the activities of various ion channels, receptors, or kinases. Thus, Sig-1Rs and their associated ligands may represent new avenues for treating aspects of neurological and psychiatric diseases.”
“The aim of the study was to collect retrospective data on renal anemia management, comorbidities and prospective data on 12-month standard care erythropoiesis-stimulating agent (ESA) therapy used in 398 hemodialyzed patients in selected Central and Eastern European countries (50 centers in 3 countries). Patients were divided into three groups according to ESA therapy start: group A-ESA (after start of hemodialysis, HD), B-ESA (within 3 months from start of HD), C-ESA (more than 3 months before HD). At the chronic kidney disease diagnosis, hemoglobin in all patients was 10.3 +/- 2.3 g/dl; however, ferritin, iron, TSAT were within reference limits.

Adult NH cells can generate bipotent primary neurospheres but not secondary ones, suggesting that the structure contains glial progenitors but probably not stem cells. Finally, when the NH is stimulated by dehydration, we observe an increase in cell proliferation associated with an increase in cell death. By identifying the cells incorporating bromodeoxyuridine (BrdU) or positive for Ki67, we demonstrate that this increased proliferation concerns all glial cell types in the adult NH, including the pdgfr alpha+ cells. Our study shows that the NH is a complex structure composed of multiple glial subtypes, which all participate

in the physiological response to dehydration. (C) 2008 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Aims: The effects Sonidegib solubility dmso of ischemia and hypercholesterolemia on the function and morphological adaptation of the rabbit hindlimb were assessed. Methods: In rabbits on normal or cholesterol diet, experiments were performed on days 0-28 following bilateral femoral artery ligation. Calf blood pressure (CBP), exercise tolerance, flow reserve, agonist vasodilatation, angiography and capillary density were examined and modeled. Results: C BP decreased markedly post-ligation and returned to 41 and 68% of baseline by days 7 and 28. Exercise tolerance was attenuated 40% and flow reserve 50 60% on day 7, with recovery by day 28. Ligation caused decreases in selleck chemicals llc 5-hydroxytryptamine-induced

dilatation, while adenosine

and acetylcholine responses were unaffected. Hypercholesterolemia attenuated acetylcholine-elicited dilatation. There was marked loss of adenosine dilatation on days 7-14 in the ligation plus Cilengitide clinical trial hypercholesterolemia group. Ligation caused a doubling in the number of medium-sized collateral arteries. Hypercholesterolemia, either alone or combined with ligation, greatly augmented small vessel density. Capillary density was unaltered by any treatment. Conclusions: The rabbit hindlimb shows a remarkable ability to recover its muscle function through vascular adaptation and remodeling 4 weeks following ligation, with or without hypercholesterolemia. Exercise tolerance, flow reserve and vascular reactivity were mainly restored 28 days post-ligation. Copyright (C) 2008 S. Karger AG, Basel.”
“Methamphetamine (MA) is a drug of abuse as well as a dopaminergic neurotoxin. We have previously demonstrated that pretreatment with bone morphogenetic protein 7 (BMP7) reduced 6-hydroxydopamine-mediated neurodegeneration in a rodent model of Parkinson’s disease. In this study, we examined the neuroprotective effects of BMP7 against MA-mediated toxicity in dopaminergic neurons. Primary dopaminergic neurons, prepared from rat embryonic ventral mesencephalic tissue, were treated with MA. High doses of MA decreased tyrosine hydroxylase immunoreactivity (THir) while increasing terminal deoxynucleotidyl transferase-mediated dNTP nick end labeling.

One of the 2 silver coated catheters showed sparse but measurable inhibition zone activity on day 1 but not thereafter and no statistically significant

activity on adherence assay. The other lacked detectable activity using either test system. In the adherence assay the nitrofurazone coated catheter decreased the E. coli count as potently in inoculum broths as in post-sonication suspensions (median decrease more than 8 and more than 6 log(10) cfu/ml, respectively).

Conclusions: The nitrofurazone coated catheter showed significantly greater in vitro potency and durability of the antimicrobial effect against 9 E. coli strains than the 2 silver coated catheters, of which 1 appeared completely inert. No difference click here in antimicrobial effect was apparent between extended spectrum cephalosporin resistant and susceptible E. coli. The clinical relevance of these in vitro findings remains to be defined.”
“As acute ethanol exposure inhibits N-methyl-D-aspartate glutamate (Glu) receptors, sudden withdrawal

from chronic alcohol use may lead to an increased activation of these receptors with excitotoxic effects. In the longer term, brain levels of Glu and its metabolites, such as glutamine (Gln), are likely to be chronically altered by alcohol, possibly providing a measure of overall abnormal Glu-Gln cycling. However, few studies have assessed concentrations of these metabolites BMS202 concentration in clinical populations of individuals with alcohol use disorders. Glu and Gln levels were compared in groups of 17 healthy controls and in 13 participants with alcohol dependence. Within the alcohol-dependent group, seven participants had current alcohol use disorder (AUD), and six had AUD in remission for at least 1 year (AUD-R). Neurometabolite concentrations were measured with proton magnetic resonance spectroscopy ((1)H-MRS) in a predominantly gray matter voxel that included the bilateral anterior JIB04 molecular weight cingulate gyri. Tissue segmentation provided an assessment of the proportion of gray matter in the (1)H-MRS voxel. The Drinker Inventory of Consequences (DrInC) and Form-90 were administered to all participants to quantify alcohol consequences

and use. Glu level was lower and Gln level was higher in the AUD and AUD-R groups relative to the control group; creatine, choline, myo-inositol, and total N-acetyl groups, primarily N-acetylaspartate did not differ across groups. These results were not confounded by age, sex, or proportion of gray matter in the (1)H-MRS voxel. Neurometabolite concentrations did not differ between AUD and AUD-R groups. Subsequent regressions in the combined clinical group, treating voxel gray matter proportion as a covariate, revealed that total score on the DrInC was positively correlated with Gln but negatively correlated with both Glu and gray matter proportion. Regression analyses, including DrInC scores and smoking variables, identified a marginal independent effect of smoking on Gln.

“
“The hippocampus is involved in both cognitive and emotional processing; these different functions are topographically distributed along its septo-temporal axis, the dorsal (septal) hippocampus being preferentially involved in cognitive NU7441 order processes such as learning and memory while the ventral (temporal) hippocampus participates in emotional regulation and anxiety-related behaviors. Newborn hippocampal neurons become functionally integrated into hippocampal networks and are likely to contribute to hippocampal functions, but whether their regulation and function are homogenous throughout this axis

is not clear. Here we investigate changes in cell proliferation and neurogenesis along the septo-temporal axis of the hippocampus induced by the Unpredictable Chronic Mild Stress model of depression (UCMS), chronic fluoxetine treatment and enriched environment.

Mice were either subjected to UCMS, learn more standard housing or enriched

environment. Stress-exposed mice were treated daily with fluoxetine (10 mg/kg) or vehicle. Effects of UCMS regimen, fluoxetine treatment and enrichment were assessed by physical measures and behavioral testing. Quantitative changes in cell proliferation and neurogenesis were assessed by immunohistochemistry using BrdU labeling.

Results indicate that UCMS decreased cell proliferation and neurogenesis preferentially in the ventral hippocampus, an effect that was reversed by fluoxetine treatment. Environmental enrichment on the other hand increased cell proliferation in both divisions but promoted neurogenesis only in the dorsal hippocampus. These results indicate that environmental factors can differentially regulate neurogenesis in a region-specific VE-822 cost manner. This may possibly underlie heterogeneous function of newborn neurons along the septo-temporal axis of the hippocampus and have functional significance as to their implication in stress related disorders and memory processes. (C) 2012 Elsevier Ltd. All rights reserved.”
“Human

exposure to arsenic and ionizing radiation (IR) occur environmentally at low levels. While the human health effects of arsenic and IR have been examined separately, there is little information regarding their combined effects at doses approaching environmental levels. Arsenic toxicity may be affected by concurrent IR especially given their known individual carcinogenic actions at higher doses. We found that keratinocytes responded to either low dose arsenic and/or low dose I R exposure; resulting in differential proteomic expression based on 2-DE, immunoblotting and statistical analysis. Seven proteins were identified that passed a rigorous statistical screen for differential expression in 2-DE and also passed a strict statistical screen for follow-up immunoblotting.

“
“Previous studies have shown that cerebral hypoxia results in increased activity of caspase-9, a key initiator of programmed cell death, in the cytosolic fractions of the cerebral cortex of newborn piglets. The present study tests the hypothesis that hypoxia. results in increased expression of procaspase-9 and procaspase-3 in neuronal nuclear, mitochondrial and cytosolic fractions of the cerebral cortex of newborn piglets. To test this hypothesis,

expression of procaspase-9 and procaspase-3 was determined in 10 newborn piglets divided into two groups: normoxic www.selleckchem.com/products/dinaciclib-sch727965.html (Nx, n = 5) and hypoxic (Hx, n = 5). The hypoxic piglets were exposed to an FiO(2) of 0.06 for 1 h. Tissue hypoxia was documented by ATP and phosphocreatinine (PCr) levels. Neuronal

nuclear, mitochondrial and cytosolic fractions were isolated and the expression of procaspase-9 and procaspase-3 was determined by immunoblotting using specific anti-procaspase-9 and anti-procaspase-3 antibodies. ATP levels (mu mol/g brain) were www.selleckchem.com/products/epz004777.html 4.34 +/- 0.36 in the Nx and 1.43 +/- 0.28 in the Hx (p < 0.001 vs. Nx) groups. PCr levels (mu mol/g brain) were 3.75 +/- 0.27 in the Nx and 0.69 +/- 0.26 in the Hx (p < 0.001 vs. Nx) group. Cytosolic procaspase-9 density (OD x mm(2)) was 88.82 +/- 17.55 in the Nx and 215.54 +/- 22.77 in the Hx (p < 0.001 vs. Nx). Mitochondrial procaspase-9 density (OD x mm(2)) was 104.67 +/- 12.75 in the Nx and 183.44 +/- 16.69 in the Hx (p < 0.001 vs. Nx). Nuclear procaspase-9 density (OD x mm(2)) was 135.56 +/- 15.36 in the Nx and 190.66 +/- 29.35 in the Hx (p < 0.001 vs. Nx). Cytosolic procaspase-3 density (OD x mm(2)) was 23.72 +/- 3.71 in the Nx and 92.44 +/- 8.46 in the Hx (p < 0.001 vs. Nx). Mitochondrial procaspase-3 density (OD x mm(2)) was 22.12 +/- 2.97 in the Nx and 51.22 +/- 10.67 in the Hx (p < 0.001 vs. Nx). Nuclear procaspase-3 density (OD x mm(2)) was 53.80 +/- 7.18 in the Nx and 84.67 +/-

5.63 in the Hx (p < 0.001 vs. Nx). We conclude that procaspase-9 and procaspase-3 proteins increased in all cell compartments including cytosolic, mitochondrial and nuclear during hypoxia, indicating increased expression of procaspase-9 during hypoxia. We propose that following increased expression of procaspase-9 and procaspase-3, these molecules traffic among the various cell compartments STAT inhibitor and become available for their activation resulting in increased caspase-9 and caspase-3 activity. (C) 2008 Published by Elsevier Ireland Ltd.”
“In this article we investigate all possible three-dimensional structures for sialyl Lewis(a) (SLe(a)) in aqueous solution and we predict without a priori experimental information its conformation when bound to SelectinE by using a combination of long molecular dynamics (MD) simulations. Based on 10 ns MD studies, three structures differing in glycosidic conformations are proposed for SLe(a) in aqueous solution.

The hypothesized effect of type of loss was not supported. Conclusions: These preliminary findings encourage further investigations to elucidate pathways from sudden unexpected loss to biomarker changes that increase risk for morbidity and mortality.”
“The methodology of predicting sonication-induced unfolding proteins (SUP) is presented in this study. The methodology bases selleckchem on: (a) simulation of SUP by the

excessive deviations of protein domains in regime of damped forced vibrations caused by critical level of involved acoustic energy, which is associated with temperature rise and acoustic pressure; (b) simulation of stochasticity of SUP by failures in jobs service in the queueing system with Markovian fluxes. The assessments of probability of SUP accounting the complex of parameters of pulsed ultrasound, biophysical properties of tissue and macromolecular crowding of insonated zone of tissue are considered. (C) 2012 Elsevier Ltd. All rights reserved.”
“Aripiprazole (APZ) is regarded as a first-line atypical antipsychotic used for the treatment of first and multiple episodes of schizophrenia to improve positive- and negative-symptoms. Its therapeutic indications were extended to acute manic and mixed episodes associated with bipolar

disorder. In addition, APZ was approved as an adjunct therapy for major depressive disorder in 2007. Compared to other antipsychotic drugs. APZ has a unique pharmacological profile. It is a partial agonist at D-2 dopamine receptors and serotonin 5-HT1A and 5-HT7 receptors, whereas it is an antagonist at serotonin 5-HT2A and 5-HT6 receptors. Since epilepsy is often accompanied see more with neurological

click here comorbidities such as depression, anxiety and cognitive deficits caused by both the disease and/or drug treatment, we wished to examine the effects of a sub-chronic treatment (>14 consecutive days) with APZ (0.3, 1 and 3 mg/kg; i.p.) on both absence seizures and WAG/Rij rat’s behavior using different standard paradigms: Open field (OF) test, elevated plus maze (EPM) test, forced swimming (FS) test, sucrose consumption (SC) test and Morris water maze (MWM). WAG/Rij rats represent a validated genetic animal model of absence epilepsy with mild-depression comorbidity, also including other behavioral alterations. APZ treatment showed some anti-absence properties and regarding the behavioral comorbidity in this rat strain, we observed that APZ possesses clear antidepressant effects in the FS and SC tests also increasing memory/learning function in the Morris water maze test. In the two anxiety models used, APZ showed only minor effects. In conclusion, our results indicate that APZ might actually have a potential in treating absence seizures or as add-on therapy but more interestingly, these effect might be accompanied by positive modulatory actions on depression, anxiety and memory which might be also beneficial in other epileptic syndromes.

This article is part of a Special Issue entitled ‘Cognitive Enhancers’.