BAMS2 workspace: A comprehensive and versatile neuroinformatic platform for collating and processing neuroanatomical connections

We describe a novel neuroinformatic platform, the BAMS2 Workspace ( http://brancusi1.usc.edu ), designed for storing and processing information on gray matter region axonal connections. This de novo constructed module allows registered users to collate their data directly by using a simple and versatile visual interface. It also allows construction and analysis of sets of connections associated with gray matter region nomenclatures from any designated species. The Workspace includes a set of tools allowing the display of data in matrix and networks formats and the uploading of processed information in visual, PDF, CSV, and Excel formats. Finally, the Workspace can be accessed anonymously by third‐party systems to create individualized connectivity networks. All features of the BAMS2 Workspace are described in detail and are demonstrated with connectivity reports collated in BAMS and associated with the rat sensory‐motor cortex, medial frontal cortex, and amygdalar regions. J. Comp. Neurol. 522:3160–3176, 2014. © 2014 Wiley Periodicals, Inc.     

Mucosal Vaccination Shapes the Expression of Salivary Antibodies and Establishment of CD8+ T‐Cells

Background: Mucosal vaccination for preventing periodontitis shows promising results. However, various administration routes and adjuvants may have a substantial role in the efficacy of the vaccination. The aim of the study is to compare different modes of mucosal vaccination with whole‐cell Porphyromonas gingivalis and to test the role of various adjuvants as potential modifiers of this process. Methods: Mucosal vaccine was administered through oral or nasal routes to BALB/C mice. The tested adjuvants included Escherichia coli cholera toxin, E. coli labile toxin (LT), and unmethylated CpG dinucleotide (CpG). Control mice were vaccinated subcutaneously. Saliva and serum were collected; anti–P. gingivalis salivary immunoglobulin A (IgA) and serum IgG were quantified. A quantitative enzyme‐linked immunosorbent assay to measure anti–P. gingivalis IgA levels was established. In addition, cells were extracted from head and neck lymph nodes, and the relative CD8⁺ cells were quantified using flow cytometry. Results: All mucosal vaccination modes induced anti–P. gingivalis salivary IgA but not anti–P. gingivalis serum IgG. Subcutaneous vaccination induced both salivary IgA and serum IgG against P. gingivalis. Mucosal vaccination also induced greater establishment of CD8⁺ cells compared to the subcutaneous vaccination. Oral mucosal vaccinations with LT or CpG were the most efficient for salivary IgA expression and CD8 cell establishment in lymph nodes. Conclusions: Oral and nasal mucosal vaccination induced a local host response with little systemic effect. The use of CpG or LT as adjuvants with the oral mucosal vaccination was the most efficient vaccination mode in the present mouse model.     

Role of nitric oxide in the rat hippocampal CA1 area on morphine-induced conditioned place preference

Effects of intrahippocampal CA1 injections of L-arginine, a nitric oxide (NO) precursor, and N(G)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, on morphine-induced conditioned place preference in male Wistar rats were investigated. Animals received subcutaneous (s.c.) injections of saline (1.0 ml/kg) or morphine (0.5-7.5 mg/kg) once daily for 3 days to induce conditioned place preference. The administration of L-arginine (0.3, 1.0, and 3.0 microg/rat), but not L-NAME (0.3, 1.0, and 3.0, microg/rat), prior to administration of morphine (5.0 mg/kg) during acquisition of morphine-induced conditioned place preference increased morphine-induced conditioned place preference, but the interaction between the response to morphine and/or L-arginine was not statistically significant. The response to L-arginine was blocked by L-NAME pre-administration. L-Arginine or L-NAME by itself did not induce conditioned place preference. The administration of L-arginine but not L-NAME, 1 min before conditioned place preference testing, increased the expression of morphine-induced conditioned place preference. Pre-administration of L-NAME blocked the L-arginine response. It is concluded that NO in the rat hippocampal CA1 area may be involved in morphine-induced conditioned place preference.     

Influence of nitric oxide on morphine-induced conditioned place preference in the rat central amygdala

Effects of intra-central amygdala injections of L-arginine, a nitric oxide (NO) precursor, and N(G)-nitro-L-arginine methyl ester (L-NAME), a NO synthase (NOS) inhibitor, on morphine-induced conditioned place preference in rats were investigated by using an unbiased 3-day schedule of place conditioning design. Animals receiving once daily injections of morphine (0.5-7.5 mg/kg, subcutaneously, s.c.) or saline (1.0 ml/kg, s.c.) showed a significant place preference in a dose-dependent manner. The maximum response was observed with 5.0 mg/kg of the opioid. Co-administration of morphine (5.0 mg/kg) with L-arginine (0.3, 1.0 and 3.0 microg/rat), but not with L-NAME (0.3, 1.0 and 3.0 microg/rat), during the acquisition of morphine-induced conditioned place preference increased morphine-induced conditioned place preference. The response to L-arginine was blocked by L-NAME preadministration. L-arginine and L-NAME by themselves did not induce conditioned place preference. When L-arginine or L-NAME at 0.3-3.0 microg/rat was administered 1 min before conditioned place preference testing, L-arginine but not L-NAME caused an increase in the expression of morphine-induced conditioned place preference, the effect that was blocked by L-NAME preadministration. A dose of L-arginine (0.3 microg/rat), but not L-NAME, during expression of morphine-induced conditioned place preference produced an increase in locomotion compared with that in the control group. It may be concluded that an increase in the NO levels in the central amygdala may have an effect on the acquisition and expression of morphine-induced conditioned place preference.     

The role of histamine in estradiol-induced conditioned consumption reductions

Conditioned consumption reductions (CCRs) develop toward novel taste stimuli as a consequence of associating those tastes with certain physiological changes. Few studies have focused on the neurochemical basis of this learned behavior. The purpose of these experiments was to reexamine the role of histamine in CCRs elicited by estradiol. Previous studies have suggested that histamine mediates CCRs induced by radiation, centrifugal rotation, and estradiol. However, because the animals were trained in a drug state, but tested in a nondrug state, it is possible that state-dependent learning confounded the results of these studies. The following series of experiments was performed to test this possibility for estradiol-induced CCRs. Implementing our own methodologies in Experiment 1, we demonstrated that an estradiol-induced CCR was blocked by treatment with the histamine 1 receptor blocker, chlorpheniramine maleate, before sucrose consumption during acquisition. In Experiment 2, identical states were maintained during acquisition and extinction by administering chlorpheniramine prior to sucrose exposure during both phases. The results indicated that chlorpheniramine blocked the estradiol-induced CCR. However, circumventing state-dependency in Experiment 3 by administering chlorpheniramine following exposure to sucrose during acquisition augmented the estradiol CCR. Taken together, the results of these experiments suggest that the ability of chlorpheniramine to abolish estradiol-induced CCRs is not due to state-dependency or to the antihistaminergic properties of chlorpheniramine. It is proposed that the results of all of the experiments can be accounted for by the aversive properties of chlorpheniramine.     

Effect of cyclohexenonic long-chain fatty alcohol on rat overactive bladder induced by bladder neck obstruction

We attempted to clarify the preventive effects of cyclohexenonic long-chain fatty alcohol on detrusor overactivity induced by mild bladder neck obstruction. Bladder neck obstruction was created by partial ligation of the urethra. Female Sprague-Dawley rats were divided into three groups: those with bladder neck obstruction treated without long-chain fatty alcohol, those with bladder neck obstruction with long-chain fatty alcohol (8 mg/kg, i.p., every day) and the sham-operated control group (A, B, and C groups, respectively). Six weeks after the induction of bladder neck obstruction, voiding behavior was observed in the metabolic cage, and a cystometrogram was performed in the experimental animals. Furthermore, Hematoxylin and Eosin, Azan-Mallory, and Bodian stainings were performed in these bladders. Bladder weight, voiding behaviors and a cystometry indicated that rats in the A group showed detrusor overactivity, which was improved by treatment with long-chain fatty alcohol. The proportion of connective tissue and the density of bundles of neurofibers in the bladder of the A group was significantly less than that in the other bladders. Mild bladder neck obstruction induces detrusor overactivity, which is improved by treatment with long-chain fatty alcohol.     

Detection of necrotic neural response in super‐acute cerebral ischemia using activity‐induced manganese‐enhanced (AIM) MRI

Immediate and certain determination of the treatable area is important for choosing risky treatments such as thrombolysis for brain ischemia, especially in the super‐acute phase. Although it has been suggested that the mismatch between regions displaying ‘large abnormal perfusion’ and ‘small abnormal diffusion’ indicates a treatable area on an MRI, it has also been reported that the mismatch region is an imperfect approximation of the treatable region named the ‘penumbra’. Manganese accumulation reflecting calcium influx into cells was reported previously in a middle cerebral artery occlusion (MCAO) model using activity‐induced manganese‐enhanced (AIM) MRI. However, in the super‐acute phase, there have been no reports about mismatches between areas showing changes to the apparent diffusion coefficient (ADC) and regions that are enhanced in AIM MRI. It is expected that the AIM signal can be enhanced immediately after cerebral ischemia in the necrotic core region due to calcium influx. In this study, a remote embolic rat model, created using titanium‐oxide macrospheres, was used to observe necrotic neural responses in the super‐acute phase after ischemia. In addition, images were evaluated by comparison between ADC, AIM MRI, and histology. The signal enhancement in AIM MRI was detected at 2 min after the cerebral infarction using a remote embolic method. The enhanced area on the AIM MRI was significantly smaller than that on the ADC map. The tissue degeneration highlighted by histological analysis corresponded more closely to the enhanced area on the AIM MRI than that on the ADC map. Thus, the manganese‐enhanced region in brain ischemia might indicate ‘necrotic’ irreversible tissue that underwent calcium influx. Copyright © 2009 John Wiley & Sons, Ltd.