For this analysis, we only considered sGFP cells within 400 μm from the PCs, because the probability for these interneurons to be connected becomes negligible this website beyond 400 μm (Figure 4C). We defined this probability as the number of common inputs divided by the total number of stimulated interneurons

and observed that it was similar between connected (0.42 ± 0.08, n = 8) and unconnected PCs (0.35 ± 0.03, n = 33; p = 0.36, Mann-Whitney; Figure 7F). This indicates that synaptically connected PCs, which are part of the same synaptic circuits, receive as many common sGFP inputs as unconnected PCs. These results overall suggest that sGFP cells appear to connect with PCs in a similar fashion, without discriminating whether these PCs are connected or not and therefore do not form specific subnetworks. We performed our initial mapping experiments with young animals (P11–P16), relatively early in the Cell Cycle inhibitor development of these circuits. It was therefore possible that the dense and unspecific

organization of inhibitory circuit would be a transitory developmental state and that similar mapping in older animals could yield sparser, perhaps more specific, functional maps. To test this hypothesis, we performed optical mapping experiments with older animals, in a range of developmental stages from P11 to P41, which encompass the normal maturation of mouse neocortical circuits through critical periods and into adulthood (Fagiolini and Hensch, 2000). We observed that the connection probability was similar throughout the range of ages examined (p > 0.05, one-way ANOVA): P11 to P12 (0.49 ± 0.04, n = 26), P13 to P14 (0.38 ± 0.03, n = 28), P15 to P17 (0.47 ± 0.06, n = 10), P18 to P20 (0.56 ± 0.06, n = 11), P22 to P23 (0.55 ± 0.05, n = 10), P26 to P30 (0.52 ± 0.12, n = 4), P34 to P35 (0.56 ± 0.04, n = 8), and P36 to P41 (0.54 ± 0.05, n = 7) (Figure 8A). It should be noted that there was a small significant

decrease in connection probability at P13–P14 (p = 0.04, compared to P11–P12; Mann-Whitney), which could indicate a potential remodeling of the connectivity in the those cortical circuits at the opening eyes stage of the development. The proportions of connected, unconnected interneurons and false positive were not significantly different for young (P11–P16) versus mature (P20–P41). The mature mapping revealed 55.8% ± 2.4% of connected sGFP cells (versus 43.2% ± 2.5% for young, p = 0.65, t test), 39.0% ± 2.5% of unconnected sGFP cells (versus 44.3% ± 2.6% for young, p = 0.85, t test) and 5.3% ± 1.0% of false positives (versus 12.5% ± 1.6% for young animals, p = 0.67, t test).

Pharmacological intervention remains largely powerless to treat stress-related illnesses, and far too often this lack of treatment efficacy results in attempts to self-medicate with alcohol or drugs of abuse. Without breakthroughs, the consequences of stressors that occur today will affect us long into the future. For these reasons, research that advances our understanding of the neurobiology of stress is of broad interest. In this issue of Neuron, Bruchas and colleagues describe an elegant series of studies that provides novel insight on the molecular pathways by which stress affects mood and motivation. The work is particularly

important because it identifies both familiar and novel targets for medications that may enable improved treatment—and perhaps even prevention—of 3-Methyladenine chemical structure stress-related illness. Corticotropin-releasing factor (CRF) is a peptide that is released in the brain in response to stress (Koob, 1999). Administration of CRF produces many of the same physiological and behavioral effects Pictilisib datasheet as stress in people and laboratory animals (Hauger et al., 2009). Recent evidence suggests that key stress-related effects of CRF are mediated by kappa-opioid receptors (KORs) (Land et al., 2009). The new work of Bruchas and colleagues provides exquisite detail on the nature of

this interaction, using an ethologically relevant form of stress (social defeat stress [SDS]) that recapitulates some of the physical and psychological consequences that are elements of many modern-day stressors and is known to cause persistent behavioral and molecular adaptations in mice (Krishnan et al., 2007). Focusing on the dorsal raphe Thymidine kinase nucleus (DRN), a brain region in which CRF, KOR, and serotonin (5-HT) systems converge, the authors show that SDS causes an increase in the activity (phosphorylation) of the intracellular signaling molecule p38α MAPK. This effect is mimicked by administration of a highly selective

KOR agonist (U50,488) and blocked by a highly selective KOR antagonist (norBNI), demonstrating dependence on KOR function. Using viral-mediated gene transfer and genetic engineering, they demonstrate that p38α MAPK activation within the DRN is responsible for the ability of stress to trigger depressive- and anxiety-like states, including dysphoria (aversion) and drug-seeking behavior. Since p38α MAPK is expressed ubiquitously, they used selective promoters to further isolate these effects to 5-HT-containing neurons. Importantly, they then used neurochemistry and immunoblotting techniques to demonstrate that p38α MAPK activation causes translocation of the serotonin transporter (SERT) from intracellular stores to neuronal membranes, thereby increasing clearance of extracellular 5-HT (Figure 1). These data raise the possibility that the therapeutic effects of selective serotonin reuptake inhibitors (SSRIs) could be related, at least in part, to an ability to offset stress-induced enhancements of SERT function within the DRN.

The central subfield thickness, which is the average thickness within the central 1 mm of the fovea, was used as a measure of CRT for all OCT devices. Scans were acquired using the fast macular scan protocol on Stratus (Carl Zeiss Meditec), which consists of 6-line B-scans (each consisting of 128 A-scans per line), each 6 mm long, centered on the fixation point and spaced 30 degrees apart around a circle. Scans were acquired using the high-speed spectral-domain GSK126 chemical structure OCT volume mode on the Heidelberg Spectralis, which

consists of 25 horizontal-line B-scans (each consisting of 512 A-scans per line; the line scans were saved for analysis after 9 frames and averaged) covering a total area of 20 × 20 degrees of the macula with a distance of 240 μm between the horizontal lines. OCT images were analyzed and graded by the Central Reading Center (Bern Photographic Reading Center, Bern, Switzerland). Digital images at the 30- to 40-degree setting (depending on the device) were taken using the Heidelberg HRA System (Heidelberg Engineering); click here MRP OphthaVision (MRP Group, Waltham, Massachusetts, USA); Ophthalmic Imaging Systems (OIS) WinStation (Sacramento, California, USA); Topcon IMAGEnet (Capelle a/d Ijssel, Netherlands); or Zeiss Visupac digital systems (Carl Zeiss Meditec). The fluorescein angiogram contained stereoscopic views of 2 fields at specified times (up to 10 minutes) after fluorescein injection. These fields included

the macula (ETDRS Field 2) of both eyes and the disc field (ETDRS Field 1M) of the study eye. Stereoscopic red-free photographs were taken of ETDRS Field 2 in each eye prior to the injection of the fluorescein dye. FA images were analyzed and graded by the Central Reading Center (Bern Photographic Reading Center). No formal significance or analytic testing was performed due to the small sample size. Continuous variables were summarized using descriptive statistics, and categoric variables were described using counts and percentages. Of the Resveratrol 45 patients screened, 32 met the inclusion/exclusion criteria and received a single intravitreal injection of MP0112 in the study eye (0.04 mg, 9 patients; 0.15 mg,

7 patients; 0.4 mg, 6 patients; 1.0 mg, 6 patients; 2.0 mg, 4 patients). All 32 patients completed the study. The baseline characteristics of the study population are summarized in Table 1. AEs that were considered to be drug related were reported in13 of 32 (41%) patients and included anterior chamber inflammation (5/13 patients); vitritis (4/13 patients); anterior chamber cell flare (3/13 patients); and endophthalmitis (1/13) (Table 2). Ocular inflammation resolved without consequence in all eyes; in 36% (4/11), this occurred without treatment, and all others received local anti-inflammatory medication (betamethasone, dexamethasone, tropicamide, or dexamethasone-tobramycin). One serious AE (3%) was reported during the study: a patient who received 2.

, 2011). Injections of graded concentrations of NaCl (0.3, 0.9, and 2.1 Osm/l) were delivered through an internal carotid artery (ICA) catheter in a volume of 300 μl over a period of 10–15 s. For microdialysis, microdialysis probes Gemcitabine molecular weight were stereotaxically implanted with the U-shaped tip located within or adjacent to the right SON, as previously described (Ludwig et al., 2002): 1.0 mm posterior to bregma, 1.7 mm

lateral to midline, 9.3 mm below the surface of the skull. After an equilibration period of at least 1 hr, consecutive 30 min dialysis samples were collected at a flow rate of 3 μl/min. After two 30 min baseline periods, rats were stimulated osmotically as described above, and a further two consecutive dialysate samples were collected, frozen, and stored at −20°C until assay for VP. The VP content in the microdialysates was measured by a highly sensitive and selective radioimmunoassay (Landgraf et al., 1995). Rats were anesthetized with pentobarbital (50 mg kg−1) and perfused transcardially in 4% paraformaldehyde in 0.01 M PBS. Brains were then removed, and coronal slices (30 μm) containing the PVN were cut and incubated with one or a combination of the following primary antibodies: rabbit (1:100; Millipore) or goat (1:50; Santa Cruz Biotechnology) anti-V1a receptor; goat anti-CTB (1:2500; List Biological Laboratories); rabbit anti-TRPM4 (1:2,000;

kindly PD-1/PD-L1 inhibition donated by Dr. Teruyama, LHSU); rabbit anti-MAP2 (1:500; Sigma-Aldrich); and mouse anti-DBH (1:20,000; Millipore). Incubation in primary antibodies was followed by specific fluorescently labeled secondary antibodies (1:250; Jackson ImmunoResearch Laboratories) for 4 hr. Slices were then

ADAMTS5 rinsed and visualized using confocal microscopy (Carl Zeiss MicroImaging; 63× oil immersion, zoomed ×2; single optical plane = 0.5 μm thick) (Biancardi et al., 2010). Single-cell RT-PCR was carried out as previously described with minor modification (Sonner et al., 2011). The cytoplasm of the patched neuron, taking care not to contain the nucleus, was pulled into a patch pipette containing 2 μl DEPC-treated water and then mixed with 1 μl of RNase inhibitor (Applied Biosystems). A nested approach was used to quantify V1a receptor mRNA. The primers used included first-nested PCR (5′-CGAGGTGAACAATGGCACTAAAAC-3′ and 5′-TGTGATGGAAGGGTTTTCTGAATC-3′), second-nested PCR (5′-TCATCTGCTACCACATCTGGCG-3′ and 5′-GTGTAACCAAAAGCCCCTTATGAAAG-3′), primers for TRPM4 (5′-CCTGCAGGCCCAGGTAGAGA-3′ and 5′-TTCAGCAGAGCGTCCATGAG-3′), and GAPDH primers (5′-TTCAACGGCACAGTCAAGG-3′ and 5′-TGGTTCACACCCATCACAAA-3′). All primers were synthesized by Integrated DNA Technologies. Final PCR products were electrophoresed on a 2% agarose gel in TAE buffer (40 mM Tris-acetate, 1 mM EDTA [pH 8]) containing 0.

We also used the GEO data set GSE15222 ( Myers et al., 2007) to analyze the association of MAPT, RFX3, SLC1A1, and PPAPDC2 genes and case-control status. None of the other genes (GLIS3, GEMC1, IL1RAP, OSTN, FOXP4) were found in this data set. This data set includes genotype and expression data from 486 late onset Alzheimer’s disease cases and 279 neuropathologically clean individuals. Association of mRNA levels with case control status or the different SNPs was carried out using ANCOVA.

Stepwise regression analysis selleck compound was used to identify the potential covariates (postmortem interval, age at death, site, and gender) and significant covariates were included in the analysis. SNPs were tested using an additive model

with minor allele homozygotes coded as 0, heterozygotes coded as 1, and major allele homozygotes coded as 2. Data used in the preparation of this article were obtained from the ADNI database (www.loni.ucla.edu/ADNI). The ADNI was launched in 2003 by the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, the Food and Drug Administration, private pharmaceutical companies, and nonprofit organizations, as a $60 million, 5 year public-private MG-132 order partnership. The Principal Investigator of this initiative is Michael W. Weiner, MD. ADNI is the result of efforts of many coinvestigators from a broad range of academic

institutions second and private corporations, and subjects have been recruited from over 50 sites across the US and Canada. The initial goal of ADNI was to recruit 800 adults, ages 55 to 90, to participate in the research—approximately 200 cognitively normal older individuals to be followed for 3 years, 400 people with MCI to be followed for 3 years, and 200 people with early AD to be followed for 2 years. For up-to-date information, see www.adni-info.org. This work was supported by grants from NIH (P30 NS069329-01, R01 AG035083, R01 AG16208, P50 AG05681, P01 AG03991, P01 AG026276, AG05136 and PO1 AG05131, U01AG032984, AG010124, and R01 AG042611), AstraZeneca, and the Barnes-Jewish Hospital Foundation. The authors thank the Clinical and Genetics Cores of the Knight ADRC at Washington University for clinical and cognitive assessments of the participants and for APOE genotypes and the Biomarker Core of the Adult Children Study at Washington University for the CSF collection and assays.

Human tau protein as well as PHF1 tau could be detected in the EC and hippocampus of rTgTauEC (Figures S3A and S3B), confirming the histological data showing human tau protein present in the hippocampal formation. This observation of human tau protein and pathology in areas that largely do not express the human tau transgene indicates that tau pathology spreads from cells expressing the transgene to downstream neurons. Indeed, combined fluorescence in situ hybridization AZD8055 purchase (FISH) and immunofluorescent staining for both human tau protein and Alz50 revealed neurons with human tau and/or misfolded tau that do not have detectable

levels of human tau transgene in the EC (Figures 3D and 3E), hippocampal fields (Figures S3C and S3D), and anterior cingulate cortex (Figure S3E) showing a dissociation between htau expression and human tau protein accumulation. In the EC, quantification of human tau mRNA and Alz50-positive cells revealed that only 33.3% of the Alz50-positive neurons in EC expressed human tau mRNA at 12 months, indicating a spread of misfolded tau to neighboring neurons within the EC without detectable transgene expression (Figure 3F). By 24 months of age, an astonishing 97% of Alz50-positive neurons (96.4% ± 6.45% SD; p < 0.001)

did not have any detectable human transgene expression, showing that the propagation to neighboring cells increased with age (Figure 3F) and indicating that transgene expressing neurons may be lost Afatinib molecular weight (as will be discussed later). Alz50-positive aggregates were also found in large numbers of neurons

without detectable transgene expression in the DG, anterior cingulate cortex, CA1, and CA3, all major targets of the EC (Witter et al., 1988). Importantly, unlike the anterior cingulate cortex, cortical areas that showed limited transgene expression outside of the EC, but do not receive direct input from the EC, did not show any tau aggregation. Moreover, the cerebellum, which expresses human P301L tau mRNA, did not develop any fibrillar accumulation of htau in the soma. These experiments with FISH showing human tau protein and Alz50-positive aggregates in cells without PD184352 (CI-1040) detectable levels of human tau mRNA confirm the transmission of human tau from neuron to neuron and rule out the possibility that the transgene promoter was nonspecifically expressing human tau in these hippocampal neurons (i.e., becoming “leaky” in older animals). To confirm that the absence of human tau mRNA in the FISH experiments was not due to limited sensitivity of the technique, we used FISH to label human tau mRNA and immunofluorescence with HT7 to label human tau protein in sections from 17-month-old animals.

, 2009 and Sequeira et al., 2009). Such changes are predicted to disrupt the subunit composition of GABAARs and are consistent with the GABAergic

deficit hypothesis of major depression (Luscher et al., 2011). The neural response to GABAAR activation depends on the Cl− equilibrium (ECl) potential, which determines the electrochemical driving force for Cl−. ECl is determined chiefly by the relative expression of the Cl− transporters KCC2 and NKCC1, which increase and decrease, respectively, during animal development and neural differentiation (for reviews see Ben-Ari, 2002, Fiumelli and Woodin, 2007 and Andäng and Lendahl, 2008). The ensuing hyperpolarizing shift in ECl leads to a gradual conversion of GABAergic depolarization in immature neurons to mainly hyperpolarizing function in mature neurons. This Pfizer Licensed Compound Library in vitro switch in the function of GABAARs is essential for structural and

functional maturation of neurons (Tozuka et al., 2005, Ge et al., 2006 and Cancedda et al., 3-Methyladenine mw 2007) and for termination of interneuron migration in the developing neocortex (Bortone and Polleux, 2009). Recent evidence further suggests that the ECl of mature neurons may be subject to synaptic input-specific modulation by the voltage- and Cl−-sensitive Cl− channel ClC-2 (Földy et al., 2010). The proposed function of ClC-2 is to prevent excessive accumulation of intracellular Cl− following strong GABAergic stimulation. While crotamiton GABAergic inputs to mature neurons are mostly inhibitory, depolarizing GABAergic effects are also common (reviewed by Marty and Llano, 2005 and Kahle et al., 2008). In particular, the aforementioned

axo-axonic synapses at the axon initial segment of cortical pyramidal cells (Szabadics et al., 2006), at hippocampal mossy fiber terminals (Jang et al., 2006), and on parallel fibers of the cerebellum (Stell et al., 2007 and Pugh and Jahr, 2011) are depolarizing and excitatory due to the local absence of KCC2 (Szabadics et al., 2006). Moreover, dynamic changes in the functional expression of KCC2 can lead to pathophysiological adaptations of neural excitability. For example, chronic stress-induced downregulation of KCC2 results in a depolarizing shift of the chloride reversal potential of neurons in the paraventricular nucleus of the hypothalamus, which renders GABA inputs ineffective (Hewitt et al., 2009). This posttranslational mechanism is thought to contribute to hypothalamus-pituitary-adrenal (HPA) axis hyperactivity and to the neuropathology of stress-associated neuropsychiatric disorders. Moreover, KCC2 mRNA and/or protein expression is downregulated following focal ischemia (Jaenisch et al., 2010) and status epilepticus (Pathak et al., 2007). The sustained loss of GABAergic inhibition observed following status epilepticus has been proposed to underlie injury-induced long-term increases in seizure susceptibility.

, 2007). Furthermore, diffusion within the synapse may display a complex behavior

swapping from one microdomain to another. This behavior needs to be aligned with the inhomogeneous distribution of scaffolding proteins (Fukata et al., 2013, MacGillavry et al., 2013, Nair et al., 2013 and Specht et al., 2013), thus defining subdomains within the PSD. Notably, the diffusion and the trapping of the receptor can be regulated by the activity of the neuron via phosphorylation events that tune the scaffold-scaffold (e.g., Charrier et al., Dinaciclib price 2010) or the receptor-scaffold (e.g., Opazo et al., 2010, Mukherjee et al., 2011 and Specht et al., 2011) interactions. The demonstration that the molecular dynamics of receptor-scaffold interactions can be regulated physiologically (Triller and Choquet, 2008) has reinforced

the notion that molecular movements can link physiology and morphology by providing access to the chemistry in the living cell. The measurement of dwell times and the knowledge of the number of copies of each molecular species together with the three-dimensional organization of the molecules will give access to a real chemistry in living cells, a chemistry “in cellulo.” In fact, the dwell time within a multimolecular assembly reflects association and dissociation constants. Furthermore, high-density single-molecule imaging and statistical approaches provided access to the energies involved in the trapping of receptors at synapses (Hoze et al., 2012, Masson et al., 2009 and Türkcan et al., BMS-777607 mw 2012). The diffusion

trapping of receptors and the dynamics of scaffolding proteins, each with specific physical constraints and properties, is at the origin of time-dependent fluctuations in molecule numbers referred to as a “molecular noise.” It reflects the rate of entry and exit of molecules from the PSD. Fluctuations in the number of receptors, which is one of the determinants of the amplitude of the postsynaptic potential (PSP), may account for part of the variability in PSP amplitudes observed between repeated identical patterns of stimulation (Heine et al., 2008a). However, other stochastic found processes such as vesicular release, transmitter diffusion, or channel kinetics also contribute to time-dependent PSP variability (Ribrault et al., 2011b). Thus, receptor-associated molecular noise is an important parameter not only in setting the robustness of the synaptic response, but also in accounting for the stochastic molecular interactions among the constituents of the PSD. This molecular dynamic approach imposes on our vision of synaptic function the need to incorporate new theoretical frameworks to integrate the cooperative effects between the molecular constituents of the PSD and their regulation, as well as to traverse the scale between the behavior of single molecules and tens-to-hundreds of molecules.

An afterimage is the illusory “photo negative” experienced immediately following exposure to a real stimulus. Afterimages used to be attributed exclusively to retinal adaptation, but a growing body of http://www.selleckchem.com/products/ABT-263.html work suggests that adaptation within cortical visual areas also contributes to afterimage formation (Brascamp et al., 2010; Ito, 2012; Shimojo et al., 2001; Tsuchiya and Koch, 2005). Of relevance for our purposes, a stimulus suppressed under rivalry causes weaker subsequent afterimages —a phenomenon believed to arise from

attenuated responses within phase-sensitive neural representations (Brascamp et al., 2010). We reasoned that if attention plays a critical role in modulating the shape of the contrast response under suppression, two key effects should emerge in the induction of afterimages under rivalry, depending

on whether attention is directed toward or away from the rival stimuli. Directing attention toward a small, high-contrast competitor viewed by one eye should elicit a response gain shift when the other eye’s competitor is small, but a contrast gain shift when that other eye’s competitor is large. For a high-contrast, suppressed stimulus, this should induce a weaker afterimage when the competitor stimulus viewed by the dominant eye is small compared to when that competitor is large. The model predicts that without attention the balance between excitation and inhibition will be preserved regardless of competitor size. Thus, diverting attention away from high-contrast, competing stimuli should transform the response Bortezomib cell line gain modulation associated with small stimuli into a contrast gain modulation. For a high-contrast stimulus, a contrast gain shift would be signified by an attenuation of the suppressive effects that rivalry has on afterimages, for all competitor sizes. To test afterimage strength, we implemented a psychophysical paradigm that quantitatively indexes the strength

of negative afterimages (Brascamp et al., 2010; Kelly and Martinez-Uriegas, 1993; Georgeson and Turner, 1985; Leguire and Blake, 1982). To induce heptaminol afterimages, observers were given brief, 2 s exposures to a sinusoidal grating (the inducer) presented to one eye while, at the same time, the other eye received one of three possible stimulus arrangements (Figure 7): (1) an uncontoured field that produced no suppression of the inducer, (2) a large (8°) competitor, or (3) small (1.5°) competitor, both of which suppress visibility of the inducer. Immediately following each brief induction period, the competitor grating, if present, was removed and the contrast of the inducer viewed by the other eye was ramped off and was replaced by a “nuller” stimulus, itself a sinusoidal grating presented to the same eye that received the inducer.

These include (1) vesicular transporters that localize to synaptic vesicles, actively driving transmitter into the vesicular lumen and (2) plasma membrane transporters that terminate neurotransmission by the uptake of neurotransmitter into either the presynaptic GSI-IX ic50 site of release or adjacent cells. The number of known vesicular transporters is surprisingly small and includes four distinct families for the transport of the following: (1) monoamines, such as dopamine and serotonin (VMAT1 and VMAT2); (2) GABA and glycine (VGAT or VIAAT); (3)

acetylcholine (VAChT); and (4) glutamate (VGLUT1-3; Chaudhry et al., 2008). Additional transporters for purine nucleotides (Sawada et al., 2008) and aspartate (Miyaji selleck screening library et al., 2008) have recently been identified as part of the SLC17 family, related to VGLUTs. Any other novel neurotransmitters

used by invertebrates and/or mammals would similarly require a distinct vesicular transporter for storage and exocytotic release. In Drosophila and other insects, the mushroom bodies (MBs) play a critical role in olfactory learning, as well as integrating information from other sensory modalities ( Davis, 2011, Keene and Waddell, 2007, Strausfeld et al., 1998 and Wessnitzer and Webb, 2006). Kenyon cells (KCs) form all of the intrinsic fiber tracts of the MBs, whereas several extrinsic neurons project into the MBs, providing input and output of information and/or regulating KC function ( Tanaka et al., 2008). To date, neither the neurotransmitter released from the intrinsic neurons nor the vesicular transporter responsible for

its storage has been identified. Of the known neurotransmitter systems, the vesicular transporters for amines (DVMAT), GABA (DVGAT), and glutamate (DVGLUT) are absent from KCs ( Chang et al., 2006, Daniels et al., 2008 and Fei et al., 2010). Although Farnesyltransferase expression data for the vesicular acetylcholine transporter is not available, the biosynthetic enzyme responsible for Ach synthesis is also absent from KCs ( Gorczyca and Hall, 1987 and Yasuyama et al., 2002). Several classical and peptide neurotransmitters have been identified in processes that project into the MBs ( Davis, 2011). In contrast, although multiple candidates have been suggested ( Schäfer et al., 1988, Schürmann, 2000 and Sinakevitch et al., 2001), the neurotransmitter released from the KCs is not known and could possibly constitute a previously undescribed neurotransmitter system. The MBs have been implicated in other behaviors, including sleep (Joiner et al., 2006), aggression (Baier et al., 2002), and motor activity (Serway et al., 2009). Furthermore, both the MBs and the central complex (CCX) have been linked to aspects of sexual behavior (O’Dell et al., 1995, Popov et al., 2003 and Sakai and Kitamoto, 2006).