Important limitations of this study are that TCD examinations we

Important limitations of this study are that TCD examinations were performed only depending on the clinical condition of the patient, and without previous measurements of the thickness of the temporal bone to distinguish between patients with ideal or nonideal TWs, a factor related to the absorption and/or scattering of the ultrasound energy (Aaslid et al. 1982). Also, some conditions such as renal failure or diabetes, that Inhibitors,research,lifescience,medical are associated

with suboptimal windows were not analyzed, as the effect of transducers with frequencies of less than 2 MHz, which could increase the detection of arterial signals in inadequate temporal bone windows, was not explored. Additionally, simply because a single operator performed all of the examinations does not necessarily imply that the results of this study are not reproducible. Finally, we do not know to what extent echo-contrasting agents would have improved the results in our population and whether Inhibitors,research,lifescience,medical our results could be applied to transcranial color-coded duplex sonography, a neurosonographic examination that is becoming progressively more popular, based on the fact that reliably

identifies blood flow in the intracranial Inhibitors,research,lifescience,medical arteries by allowing direct visualization of the vessels insonated; and it offers the opportunity for angle corrections resulting in more accurate measurement of flow velocities. Furthermore, it enables the detection of midline Inhibitors,research,lifescience,medical shifts in ischemic strokes and detection of intracerebral hemorrhages (Nedelmann et al. 2009). Conclusion The Hispanic–Mestizo population has a TW detection rate similar to those of European populations, and the rate of optimal insonation is mainly

affected by patient characteristics, Inhibitors,research,lifescience,medical such as age and sex. Acknowledgments Arnold Hoppe has been paid honoraria and received travel grants as part of research projects by AstraZeneca and Servier. Conflicts of Interest Alejandro M. Brunser this website reports no conflicts of interest. Claudio Silva reports no conflicts of interest. Daniel Cárcamo reports no conflicts of interest. Paula Muñoz reports no conflicts of interest. Arnold Hoppe has been paid honoraria and Bay 11-7085 received travel grants as part of research projects by Astra Zeneca and Servier. Veronica V. Olavarría reports no conflicts of interest. Violeta Díaz reports no conflicts of interest. Juan Abarca reports no conflicts of interest.
Cranial electrotherapy stimulation (CES) is a noninvasive therapeutic device that applies pulsed, alternating microcurrent (<1000 μA) transcutaneously to the head via electrodes placed on the earlobes, mastoid processes, zygomatic arches, or the maxillo-occipital junction. The U.S. Food and Drug Administration (FDA) granted approval in 1979 for CES for the treatment of insomnia, depression, and anxiety, and it is commercially available for personal use.

* Over the last several years, these techniques have been used in

* Over the last several years, these techniques have been used increasingly to study the neurobiology of depression and as potential antidepressant therapies. *Editor’s note: see also the article by Eitan and Lerer (this issue, p 241) for a detailed review of these techniques. Transcranial magnetic stimulation Transcranial magnetic stimulation (TMS) uses a current passed through an electromagnetic coil on the scalp to create

a brief, rapidly changing magnetic field. This magnetic field experiences Inhibitors,research,lifescience,medical little to no impedance from the scalp, skull and air, and is able to induce a small, focal electrical current within the underlying cortex, resulting in depolarization of cortical neurons. Although singlepulse TMS is an established diagnostic and research tool in humans,146 repetitive TMS (rTMS) has been most extensively Inhibitors,research,lifescience,medical studied as a possible treatment for depression. By convention, high-frequency or “fast” rTMS refers to stimulation delivered at a rate higher than 1 Hz, and low-frequency or “slow” rTMS refers to stimulation at frequencies Inhibitors,research,lifescience,medical of 1 Hz or slower. No anesthesia is needed when giving rTMS (except in the

case of magnetic seizure therapy [MST] discussed separately below). rTMS has been associated with behavioral changes in animals similar to those achieved with electroconvulsive shock and suggestive Inhibitors,research,lifescience,medical of an antidepressant effect,147,148 and functional imaging studies have confirmed that TMS can modulate function in several brain regions (including subcortical structures) implicated in

mood regulation.149,150 Several studies have shown antidepressant effects for fast rTMS applied to the left dorsolateral prefrontal cortex151,152; a smaller number have shown efficacy for slow rTMS applied to the right Inhibitors,research,lifescience,medical dorsolateral prefrontal cortex.153,154 Although meta-analyses of these studies generally agree that rTMS appears to have statistically significant antidepressant effects, the clinical significance of these effects has yet to be convincingly demonstrated.155 rTMS appears to be safe and reasonably well-tolerated. Magnetic seizure therapy (MST) DNA ligase uses a modified rTMS system to induce a generalized seizure similar to that obtained with ECT The goal is obtain the same efficacy as with more focal forms of ECT (eg, right unilateral lead placement) but with fewer cognitive side effects. Indeed, there is some preliminary data to support an antidepressant effect for MST with fewer cognitive side effects compared with ECT,156,157 but confirmatory data are lacking. Future studies will help click here clarify whether TMS offers a clinically useful treatment alternative in depression. However, even if TMS proves to be ineffective as an antidepressant treatment, it will likely continue to be useful as a probe of neural function, especially when combined with neuroimaging.

However, the equivalent prevalence rates

for mental disor

However, the equivalent prevalence rates

for mental disorders were only 32% (at least one diagnosis over a lifetime Pazopanib in vivo period) and 20% (at least one diagnosis over a 12-month period) in the ECA study. Analysis of the lifetime prevalence rates for each clinical entity (in decreasing order) provides an explanation. The difference mainly lies in depressive disorders and addictions, whose prevalence could arguably have increased. The difference in data between the ECA and NCS studies concerning phobic disorders is comparable to that observed in data originating between different ECA study centers, and is probably attributable Inhibitors,research,lifescience,medical to semiological data recording methods. Finally, the prevalence Inhibitors,research,lifescience,medical of schizophrenia is lower, which could be partly due to a lower prevalence of schizophrenia and partly due to the fact that institutionalized

patients were excluded from the NCS study. On the other hand, Angst and Wicki12 conducted a study in Zurich to identify recurrent brief anxiety (RBA) syndromes. The concept of brief and transient psychiatric pathologies has long been known, but has received an increasing amount of attention Inhibitors,research,lifescience,medical in the past few years. The terms recurrent brief depression (RED), RBA, recurrent brief hypomania, neurasthenia, and insomnia have all been coined recently. All these syndromes last 1 to 3 days on average, and are highly recurrent (at least once a month over a whole year). The authors

who developed these concepts have defined Inhibitors,research,lifescience,medical them by means of the following diagnostic criteria12: Anxiety (fear of being alone, apprehension of impending doom, fear of the next day dawning). Three of the four GAD symptoms as described in DSM-III (motor tension, neurovegetative hyperactivity, apprehension, exacerbated awareness while exploring surroundings). Anxious mood for 1 to 13 days, at least once a month during the previous year. Subjective professional impairment of handicap. The authors12 noticed that RBA morbidity was often associated Inhibitors,research,lifescience,medical with PDs and RED, and that many RBA patients had past familial and personal history of anxiety and depression. Angst and Wicki therefore suggested that the association of RBA and RBD could reflect a shared genetic predisposition for depression and anxiety.12 The comorbidity rate of RBA Resveratrol with other diagnoses is such (>75% with depression, >25% with phobias, >16% with PD, and >6% with GAD) that one can understandably challenge the authenticity of this clinical entity. Furthermore, the symptomatic definition of RBA does not identify any distinctive characteristic from those of GAD, aside from duration. These concepts can be questioned in the same way that one can challenge the existence of subsyndromic states. These states are related to entities defined by classical criteria systems (DSM-III, DSM-IV, or ICD-10), but differ only because they consist of n-1 or n-2 symptoms.

Often, treatment of the coexisting condition can reduce the degre

Often, treatment of the coexisting condition can reduce the degree of impairment, and improve the quality of life. Dementia may also have multiple etiologies. For example, substance abuse and traumatic brain injur}’ can contribute to dementia of other etiologies as well as cause dementia in their own right, eg, dementia due to head trauma, Korsakoff syndrome, or substance-induced persisting dementia. Anoxia, another common contributing factor,

can result from heart, attack, severe asthma, smoke or carbon monoxide inhalation, high altitude Inhibitors,research,lifescience,medical exposure, strangulation, anesthetic accidents, or poisoning. Because an older individual may present with a complex history and multiple medical comorbidities, it is important to diagnose the Inhibitors,research,lifescience,medical patient, not the disease. What is the Trametinib etiology of the patient’s dementia? Finally, the clinician must determine the etiology of the dementia. Although there are innumerable causes of dementia, the initial diagnostic focus is usually on the conditions that are most common and those that are potentially Inhibitors,research,lifescience,medical modifiable. Dementia of the Alzheimer type is the most common form of dementia. Diagnostic criteria for Alzheimer disease include dementia with gradual onset, and progressive decline that

cannot, be attributed to other conditions.4 Inhibitors,research,lifescience,medical Typically, the first symptom is an inability to learn new information. Other early symptoms include visuospatial deficits, decreased verbal fluency, and subtle personality changes.11 Vascular dementia has a variable onset, presentation, and course due Inhibitors,research,lifescience,medical to the heterogeneity of cerebrovascular insults that can result in cognitive impairment, although onset is often abrupt with a stepwise progression.12 Vascular dementia is diagnosed when focal neurological signs and symptoms

or laboratory findings indicate the presence of cerebrovascular disease.4 Treatment of the underlying hypertension and vascular disease may prevent further progression of dementia. Dementia of combined vascular and Alzheimer etiology, or mixed dementia, may be more common than pure vascular dementia.13 Other common progressive dementing conditions include the frontotemporal dementias, such as isothipendyl Pick disease, in which patients often present initially with personality change rather than cognitive impairment, and Lewy body disease, including dementia due to Parkinson disease, which is associated with extrapyramidal signs. Symptoms of dementia due to the human immunodeficiency virus include forgetfulness, impairment, in attention and concentration, psychomotor slowing, poor balance, and tremor.

58 Third, the urge to void is a frequently experienced behavioral

58 Third, the urge to void is a frequently experienced behavioral state, and

generally increases with bladder distention in a complex manner. For example, at moderate bladder filling, urge to void appears to be under cognitive control and leads to a fluctuation of the conscious urge sensation. A recent fMRI study found significant brain activity associated with an increased urge to void in the insular cortex, frontal opercula, supplementary motor area, cingulate motor area, right posterior parietal cortex, left prefrontal cortex, and cerebellum.59 Fourth, Inhibitors,research,lifescience,medical anorectal continence is another urge-driven behavior that is under complex cerebral control A recent neuroimaging study showed that subjective sensation of discomfort increased during repeated rectal distension was associated with activation in the anterior cingulate gyrus, insula, Inhibitors,research,lifescience,medical thalamus, and

secondary somatosensory cortex. Moreover, voluntary contraction of the anal sphincter in response to anal distention was associated with activation of motor cortex and increased activity in supplementary motor as Inhibitors,research,lifescience,medical well as insular cortex.60 Thus, these neuroimaging studies have in common the involvement of the interoceptive system in the expression of diverse urge-related behaviors. Imagery-based techniques are frequently used to elicit memory of drug-related craving experiences,61 and some have even argued that stress imagery testing procedures may function as provocative tests for stress-induced drug craving.62 Inhibitors,research,lifescience,medical Several brain systems have been implicated in modulating the degree of drug-induced cravings. For example, the degree of drug-related craving by means of administration of presentation of conditioned stimuli has been related to activity in striatum,63 Inhibitors,research,lifescience,medical thalamus,64 anterior cingulate,65 inferior frontal cortex,66,67 and orbitofrontal cortex,68,70 but also with insula,71,72 amygdala,73 and cerebellum.74 For example, when viewing videos that display cocaine-related

stimuli users experience craving, which is associated with increases in amygdala and anterior cingulate cerebral Thalidomide blood flow relative to their responses to a nondrug video.75 Similarly, imagery-induced drug craving has been associated with bilateral activation of amygdala, insula, and anterior cingulate gyrus as well as the nucleus accumbens area.76 In alcohol-dependent individuals, cue-induced craving has been associated with activation in amygdala and hippocampal area as well as the cerebellum,77 but also visual and other limbic areas.78 Smoking-induced craving was associated with increased activation in left inferior frontal gyrus, left ventral anterior cingulate, and bilateral middle frontal gyrus.

This test evaluates the mitochondrial function as a measurement

This test evaluates the mitochondrial function as a measurement

of cell viability, which allows the detection of dead cells before they lose their integrity and shape. The amount of viable cells after SLN exposure was performed by the MTT assay with Caco-2 cell models, which are a well-established in vitro model that mimics the intestinal barrier and is often used to assess the Inhibitors,research,lifescience,medical permeability and transport of oral drugs [122]. Other authors have also reported that SLN show biocompatibility, which increase their attractiveness for drug-delivery applications [120]. 6. Marketed Products and Current Studies Since early nineties, researchers turned their attention to lipid nanoparticles because of their nontoxicity and cost/effectiveness relationship [12]. In spite of the advantages, formulating with lipid nanoparticles has been suffering some drawbacks. Because of the GIT conditions, most of promising drugs do not Inhibitors,research,lifescience,medical reach clinical trials. The stability of particles must be comprehensively tested due to pH changes and ionic strength as well as the drug release upon enzymatic degradation Inhibitors,research,lifescience,medical [123]. Lipid nanoparticles absorption through GIT occurs via transcellular (through

M cells or enterocytes) or paracellular (diffusion between cells). If the major drug uptake occurs through M cells, the portal vein to the liver is bypassed, resulting in higher drug concentrations to the lymph rather than to plasma [124]. Despite the low number of lipid nanoparticles formulations on the market for drug delivery, Mucosolvan retard capsules (Boehringer-Ingelheim) is a story of success [125]. Mucosolvan Inhibitors,research,lifescience,medical retard capsules was the first generation. It was produced Inhibitors,research,lifescience,medical by high-speed stirring of a MAPK Inhibitor Library research buy melted

lipid phase in a hot surfactant solution obtaining an emulsion. This emulsion was then cooled down to room temperature obtaining the so-called “lipid nanopellets for oral administration” [126]. Successful in vivo studies also include rifampicin, isoniazid, and pyrazinamide that are used in tuberculosis treatment. These drugs achieved until higher bioavailability when incorporated into SLN compared to the free solutions. Rifampicin has poor cellular penetration which requires high doses to reach effective concentrations. Rifamsolin is a rifampicin-loaded SLN under preclinical phase by AlphaRx. The methodology employed for production is acceptable by the regulatory agencies and has been addressed by various papers and patents [127]. Poor water-soluble drugs, as camptothecin, vinpocetine, and fenofibrate, can have their solubilization improved if incorporated into SLN [124, 128]. Another example is insulin, commonly administered parenterally in the treatment of diabetes mellitus. Injections are often painful and must be administered daily, which result in low patient compliance [129].

2007] There is also some evidence to suggest that agomelatine i

2007]. There is also some evidence to suggest that agomelatine improves sleep efficiency and increases the total amount of slow wave sleep [Quera Salva et al. 2007]. It is also thought to improve ‘daytime alertness’ compared with venlafaxine [Lemoine et al. 2007]. Agomelatine has also been shown to prevent relapse at similar rates to other antidepressants [Goodwin et al.

2009]. It appears to be well tolerated, with less weight gain, sexual side effects, sleep problems and withdrawal syndrome compared with SSRIs [European Public Assessment Report; Inhibitors,research,lifescience,medical Montgomery et al. 2006; Rouillon, 2006]. There is evidence that agomelatine improves Hamilton Anxiety Rating Scale scores in patients with Natural Product Library price generalized

anxiety disorder [Stein et al. 2008]. In patients with seasonal affective disorder, Inhibitors,research,lifescience,medical 25 mg of agomelatine over 14 weeks was associated with significant improvements in the Structured Interview Guide for the HAM-D, with a particular improvement in sleep disturbance and daytime fatigue [Pjrek et al. 2007]. Adjunctive use in patients with bipolar type 1 disorder Inhibitors,research,lifescience,medical also showed improvement in HAM-D scores [Calabrese et al. 2007] and the risk of triggering a manic switch was similar to that seen with venlafaxine [Calabrese et al. 2007]. This small study involved 21 patients with type I bipolar disorder Inhibitors,research,lifescience,medical who were prescribed concurrent mood-stabilizing agents (either lithium or valporic acid). All the patients were followed up for 6 weeks and although the preliminary findings suggest 25 mg of agomelatine is efficacious, a RCT is planned to confirm the results. Given its apparent efficacy and favourable side-effect profile, some have regarded agomelatine as an ‘innovative treatment for major depressive disorder patients offering a new approach in the management of depressed patients’ [den Boer et al. 2006]. However, most of the evidence about the efficacy and tolerability

Inhibitors,research,lifescience,medical of agomelatine as an antidepressant is derived from RCTs which are of short duration (usually 6–12 weeks). Currently there are no published retrospective, naturalistic studies involving agomelatine in clinical PAK6 practice and there are no published studies looking at combinations of agomelatine with other antidepressants. Aims We aimed to determine the tolerability and clinical effectiveness of agomelatine in unipolar depression in clinical practice. We also aimed to discern whether being refractory to previous treatment altered outcome. Method A retrospective analysis of all psychiatric contacts in a discrete geographical area in Scotland was undertaken searching the electronic records using the keyword ‘agomelatine’.

Table V shows magnetic resonance imaging (MRI) neuroimaging techn

Table V shows magnetic resonance imaging (MRI) Epigenetic activity neuroimaging techniques. Nevertheless, significant challenges exist, in terms of summarizing existing findings and translating data to improve clinical practice. Studies often involve diverse cohorts (eg, mild TBI, combat, veterans), and employ different paradigms (symptom provocation, cognitive activation) and modalities (eg, diffusion tensor imaging [DTI], functional magnetic resonance imaging [fMRI],

single photon emission computed tomography [SPECT]).50 As such, findings have varied. Peskind and colleagues noted that Inhibitors,research,lifescience,medical fluorodeoxyglucose positron emission tomography (FDG-PET) abnormalities in those with PTSD versus those without this disorder have been “limited and conflicting” (p 5).51 In terms of validation, experiments supporting newer functional imaging techniques often rely on neuropsychological paradigms. For example, in response to findings regarding Inhibitors,research,lifescience,medical the positive relationship between DTI results and neuropsychological test performance among those with mild, moderate, and severe injuries, Kraus ct al3 suggested that white matter load may be a “useful index.“ Much work is being conducted to support, these new imaging techniques, and findings are

increasing our knowledge regarding those with TBI and/or PTSD. Table V. Magnetic resonance imaging (MRI) Inhibitors,research,lifescience,medical neuroimaging techniques. BOLD, blood oxygen level dependent; DTI, diffusion tensor imaging, fMRI, functional MRI; MRS, magnetic resonance spectroscopy; PW-MRI, perfusion weighted MRI; SWI, susceptibility-weighted imaging … TBI Although newer techniques have begun to allow clinicians to explore questions regarding pathogenesis, natural history, neuroplasticity, and treatment, response,52 historically, neuroimaging has been used to identify Inhibitors,research,lifescience,medical and manage acute modcratc-to-sevcre TBI. Less sophisticated structural imaging techniques such as computed tomography (CT) or MRI have been useful in identifying skull fractures or more severe injuries (eg contusion, intraparaenchymal hemorrhage); however, they generally fail to adequately Inhibitors,research,lifescience,medical detect DAI or brain volume loss. Moreover, in combat, or deployment,

settings these generally common diagnostic tools may not be available Rutecarpine to the clinician.53 Research among both Veteran and civilian populations suggests that, use of CT and MRI has limited utility in confirming acute or post-acute mild TBI.54-56 In looking at MRI results of veterans long postTBI, Brenner and colleagues55 found that those with moderate to severe TBI were significantly more likely to have trauma-related findings (physical) than those with mild TBI. In specific, 11 out of 16 veterans with moderate to severe TBI versus 0 out 16 with mild TBI had MRI findings. Research regarding newer functional imaging techniques (eg, FDG-PET, DTI, SPECT) suggests that in the future they may be of significant clinical utility, particularly in the context of mild TBI and/or post-acute injuries.

Discussion In the clinical samples, RNA is degraded rapidly by

.. Discussion In the clinical samples, RNA is degraded rapidly by RNase existing in any body fluids such as sweat, sputum, or blood. The effects of RNase should be, therefore, considered in the RNA-based analysis on clinical samples. Although several storage buffers inhibiting the effect of DNase and RNase were available, we have been investigating the CRC screening method based on the analysis using the colonocytes isolated from feces. In our preliminary study, the colonocytes could not be isolated from feces stored in the storage buffers. Therefore we have investigated the suitable storage condition

of fecal samples for our screening test. Recently it was reported that miRNA was secreted from tumor cells via Inhibitors,research,lifescience,medical exosome and was transported to endothelial cells by paracrine induction (35). This indicates that exosome is not only a secretory tool, Inhibitors,research,lifescience,medical but that

it also supports miRNA. We have been investigating the CRC screening method (30),(31). And then we thought that fecal miRNA (free miRNA) from fecal homogenates, exosomal miRNA from fecal exosomes, and colonocyte miRNA from fecal colonocytes might be candidates for Inhibitors,research,lifescience,medical the fecal miRNA test. Exfoliated colonocytes were isolated from feces by EpCAM beads, using a previously published method (28),(32)). Exosomes could be isolated using both the centrifugation method (19),(35) and the cell isolation method by anti-CD63 mAb conjugated immunomagnetic beads (36) In the present study, HT-29 cells cultured in the media

containing RNase were analyzed, and fecal homogenates were treated by RNase. Although free miRNA (fecal miRNA) was degraded rapidly, cellular miRNA (colonocyte miRNA) was Inhibitors,research,lifescience,medical highly conserved. In the culture media, exosomal miRNA was conserved for a 30-min Pazopanib datasheet treatment of RNase, but degraded for a 90-min treatment. On the other hand, the fecal exosome could be conserved for a 90-min treatment of RNase. These indicated that cellular Inhibitors,research,lifescience,medical membrane prevented RNase from degrading miRNA in cells, but that the exosome partially prevented RNase from degrading miRNA in exosome. In this study, U6, miR-16, and miR-21 were analyzed because U6 and miR-16 were used for internal control as an expression of miRNA in several reports (31),(37) and miR-21 was one of the miRNAs important for CRC carcinogenesis (38),(39). The expression of miR-21 in the CRC tissue was higher than that in the normal colorectal mucosa; however, no significant difference was seen between the early stage of CRC and the advanced stage of CRC regarding the expression Rolziracetam of miR-21 (31). Recently fecal-based RNA tests have been noticed because of their simplicity and cost-effectiveness (33),(34),(40), however, fecal miRNA was unstable under the existence of RNase. For the clinical use of fecal miRNA, it was therefore necessary to store the fecal sample under strict conditions. On the other hand, exosomal miRNA or colonocyte miRNA were protected from RNase by exosome or cellular membrane.

The final data are presented as a mean value of the total number

The final data are presented as a mean value of the total number of each rat group. Brainstem sections were categorized according to their approximate rostrocaudal

location from the MDH subnucleus interpolaris junction. The pERK1/2-positive cells were counted under a 20× objective according to their location in the different laminae of the MDH from sections costained for PKCγ, a cellular marker that highlights the inner lamina II (Polgár et al. 1999). The delineation of the MDH was based on the Paxinos and Watson atlas. The data are expressed as the sum of the total number of labeled cells counted from all the sections analyzed in each animal. Tyrosine hydroxylase (TH) immunolabeling was performed using anti-TH primary antibody Inhibitors,research,lifescience,medical (Millipore, Molsheim, France), as described above. Quantification of the impact of the 6-OHDA lesion on the SNc was investigated as described previously (Paillé Inhibitors,research,lifescience,medical et al. 2007; Zengin-Toktas et al. 2013) using frozen coronal sections (40 μm) under a 20× objective. For each rat, TH-positive cells were counted at different rostrocaudal levels (every 0.12 mm; to Inhibitors,research,lifescience,medical −4.64 until −6.2 relative to bregma) using Image J software (ImageJ v1.41, National Institute of Health, Bethesda, MD). Split-cell counting errors were corrected using Abercrombie’s formula, where N = n [t/(t + d)] (N: total number of cells; n: number of cells counted; t: section thickness; and d: cell diameter). The total

number Inhibitors,research,lifescience,medical of cells in the SNc was calculated using Konigsmark’s formula, where Nt = Ns (St/Ss) (Nt total number of cells; Ns number of cells counted; St total number of sections through the SNc; Ss number of sections in which cells were counted (Paillé et al. 2007). Image analysis was Natural Product Library in vitro completed using ImageJ software. The point picker plugin available in ImageJ freeware can be used to mark cells with a colored cross by clicking with the mouse. The number of cells counted is displayed in a text box on completion. For each group Inhibitors,research,lifescience,medical of animals,

the data were the total number of cells in the section expressed as the percentage of the number of cell bodies measured for the shams (mean ± SD). Anatomical and behavioral analyses were performed by an experimenter blind to the treatments. Locomotor second impairment The rotarod test was performed 2 weeks after surgery. Locomotor impairment was determined on an accelerating rotarod treadmill (TSE systems GmbH, Bad Homburg, Germany). Before testing, the rats were habituated to the instrument at a constant (4 rpm, 5 min) and accelerated speed (40 rpm, 5 min, five times) for three consecutive half days. A testing session was performed on the fourth consecutive day. The rotarod was accelerated progressively from 4 rpm to 40 rpm over 5 min. The time that the rats remained balanced on the device was scored. The rotarod test results for each animal represent the average time (sec) spent on the rod for the last three sequences on the testing session (mean ± SD).