The organizing principle for all of these efforts must hearken back to the founding of modern neuroscience by AZD6244 supplier Ramon y Cajal (1899), who first saw and understood the fundamental importance of identification, characterization, and comparative analysis of the great diversity of cell types present in complex nervous systems. We thank Dr.

Charles Gerfen for the image appearing in Figure 1. We wish also to thank Melissa McKenzie, Danielle Van Versendaal, and Edmund Au for their help in creating Figure 2. N.H. was supported by a Howard Hughes Medical Institute (HHMI) Investigator Award, an NIH NINDS HSSN271200723701C GENSAT contract, a Simons Foundation SFARI 2009 Research Award, an NIH/NIDA ARRA Grand Opportunity Award, NIH/NIMH 5 P50 MH090963 P2 Conte Center Project 2, and NIH/NIDA P30 DA035756-01 Core Center of Excellence. G.F. was supported by NIH grants (RO1MH071679, RO1MH095147, R01NS081297, and P0NS074972), the Simons Foundation, and the State of New York through the NYSTEM initiative. “
“The term “glia” (from the ancient Greek for glue), coined by Rudolf Virchow in 1856, seems to carry both literal and figurative

connotations. Virchow thought glia to be support cells, a putty holding things together. However, it is perhaps pertinent that in Virchow’s time glue was a rather ignoble substance made from the hooves of knackered horses. Whether intentional or not, his descriptor implied a passive and uninteresting selleck function for glia, placing them low in the neural hierarchy. However, attitudes are shifting with new studies that show that glial and cells are essential modulators of brain function and health. In 2008, a previous Perspective on this topic in Neuron ( Barres, 2008) highlighted many then newly identified and unexpected functions of glia and predicted many more. A mere 5 years later, the list of developmental mechanisms of and roles for macroglia—i.e., oligodendrocytes, astrocytes, and their precursors—has expanded significantly. Progress in the field has been comprehensively covered in many outstanding recent reviews ( Aguzzi

et al., 2013, Attwell et al., 2010, Emery, 2010, Eroglu and Barres, 2010, Freeman, 2010, Molofsky et al., 2012 and Nave, 2010). This Perspective is not meant to be a comprehensive review of glial cell biology. Rather, we hope to highlight emerging ideas in the field, discuss how approaches are rapidly evolving, and suggest priorities for the future. We will focus primarily on macroglia (with apologies to microglia and Schwann cells) and adopt the speculative viewpoint that the long evolutionary time frame for codevelopment of neurons and glial cells, from simple organisms to higher organisms, indicates the fundamental importance of glia in invertebrates and predicts their increased diversity in vertebrates. We envisage that tools of developmental biology and cross-species analysis will yield exciting new insights into the precise functions of glial subtypes from the simplest invertebrates to man.

This issue is less of a concern for miRAP because Epigenetic inhibitor AGO2-miRNA interaction is very stable and of high affinity (Tang et al., 2008). In addition, comparison of FACS with miRAP in the Camk2α-Cre line suggests that

our method faithfully represent the miRNA profiles in this cell type. Discovered less than two decades ago, miRNAs have since been implicated in the regulation of almost all aspects of cellular processes. Despite their prominent expression in the mammalian brain, the role of miRNAs in brain development, function, and plasticity remains poorly understood. A major challenge is to link miRNA activity in defined neuron types to specific aspects of neuronal specification, development, and physiology; characterizing miRNA profiles in specific cell types is the first step. Using miRAP, we have obtained a set of miRNA expression profiles in defined neuron types in mouse brain. Our study reveals the expression of a large fraction of known miRNAs with distinct profiles in glutamatergic and GABAergic neurons and subtypes of GABAergic neurons. We have further PLX4032 in vitro detected putative novel miRNAs, tissue- or cell-type-specific strand selection of miRNAs, and miRNA editing. This generally applicable miRAP method will facilitate a systematic

analysis of miRNA expression and regulation in specific neuron types in the context of neuronal specification, development, physiology, plasticity, pathology, and disease models. Targeting of rare cell types may further reveal novel, low abundant miRNAs and link novel regulatory mechanisms

such as miRNA editing to specific neuronal and circuitry function. Identification of mRNA targets in defined cell types is key to understanding the biological function of miRNAs. As miRNA activity requires base-pairing with only 6–8 nucleotides of mRNA, target prediction through bioinformatics has proven to be challenging. Recently, Ago HITS-CLIP has been used to profile miRNA-mRNA targets in the mouse brain (Chi et al., 2009). Genetically targeted miRAP provides a possibility for cell-type-specific Ago2 HITS-CLIP using the MYC or GFP antibody. To generate mouse line that conditionally express GFP –myc-Ago2, a cassette containing LoxP-STOP -LoxP-GFP-myc-Ago2 was cloned in to a Rosa26-CAG targeting vector which contains DTA negative selection marker. GFP-myc-Ago2 is Montelukast Sodium a gift from Dr. Richard M. Schultz in University of Pennsylvania. The STOP cassette contains Neo gene which confers G418 resistance. The targeting vector was linearized by PacI digestion and transfected into C57BL/6 mouse ES cell line. G418-resistant ES clones were screened by PCR first using a forward primer upstream of 5′ homologous arm and a reverse primer in the transgene promoter region, then confirmed by Southern blot of EcoRV digested DNA, which was probed by a 134 bp genomic fragment upstream of the 5′ targeting arm. All PCR positive clones were also positive for Southern blot.

aru function is needed in the circadian PDF-expressing neurons for normal ethanol sensitivity, a feature shared with PI3K but not Egfr. In addition, aru mutants 17-AAG in vivo show increased synapse number in both larval and adult neurons, a phenotype also observed upon activation of PI3K, but not Egfr ( Martín-Peña et al., 2006). We propose that aru regulates

ethanol sensitivity of adult Drosophila by two distinct mechanisms, one involving the Egfr/Erk pathway and the other involving regulation of synapse number in conjunction with the PI3K/Akt pathway. Finally, we show that social isolation, which reduces the number of synaptic terminals in PDF neurons ( Donlea et al., 2009), causes a dramatic decrease in ethanol sensitivity in wild-type flies. This environmental manipulation also restores normal ethanol sensitivity and PDF synapse number to aru mutants. In summary, our results Galunisertib in vitro suggest that the regulation of synapse number is a mechanism of central importance in the regulation of

ethanol sensitivity. aru is a predicted adaptor protein containing PTB and SH3 domains ( Tocchetti et al., 2003) and probably forms protein complexes that mediate signal transduction. aru is orthologous to vertebrate Eps8L3, the atypical member of the Eps8 family ( Tocchetti et al., 2003). Interestingly, a mouse knockout (KO) of the founding family member, Eps8, shows reduced ethanol sensitivity and enhanced consumption, which is mediated in part by direct regulation of actin dynamics by Eps8 ( Offenhäuser et al., 2006). Since normal ethanol sensitivity ( Offenhäuser et al., 2006 and Rothenfluh et al., 2006) and synapse formation ( Hotulainen and Hoogenraad, 2010) require complex actin remodeling, aru may also affect ethanol sensitivity of and synapse number by regulating actin dynamics. However, this effect is probably indirect, since Aru, like Eps8L3,

lacks the predicted actin-binding and -capping domains found in Eps8 ( Offenhäuser et al., 2004). We uncover several differences in the ways the Egfr/Erk and PI3K/Akt pathways regulate ethanol sensitivity. Neuronal activation of the Egfr/Erk pathway reduces, while inhibition enhances ethanol sensitivity (Corl et al., 2009). Conversely, neuronal perturbations of the PI3K/Akt pathway alter ethanol sensitivity such that activation of the pathway enhances, whereas inhibition reduces ethanol sensitivity. In addition, both pathways have different temporal requirements: the Egfr/Erk pathway is required continuously (in development and adulthood), whereas the PI3K/Akt pathway is only required during development (which includes metamorphosis). The continuous requirement of Egfr function in neurons to affect ethanol sensitivity suggests that the previously described acute effects of Egfr inhibitors on adult ethanol behaviors ( Corl et al.

Our results are based on a Cabozantinib order series of gene knockdown and knockout experiments, showing that BAD and BAX are required to activate caspase-3 in NMDA receptor-dependent LTD, and on the infusion of active BAD and caspase-3, showing that the BAD-BAX-caspase-3 cascade is sufficient for induction of synaptic depression in hippocampal neurons. We further demonstrate that activation of the BAD-BAX-caspase-3 cascade is initiated

by PP2B/calcineurin, PP1, and PP2A. Although in both LTD and apoptosis, the same group of phosphatases is responsible for BAD activation, it is likely that phosphatases respond differently to different Docetaxel manufacturer stimulations. LTD-inducing stimulations are brief and mild, while stimulations used to induce apoptosis (e.g., high concentrations of actinomycin D or NMDA) are prolonged

and strong. In fact, one would expect that mild, LTD-inducing NMDA stimulations would cause a lower level of calcium influx than strong, death-inducing NMDA stimulations. In turn, lower levels of calcium could lead to lower levels of PP2B/calcineurin activation and therefore only weak and brief activation of BAD. The level and duration of BAD activation determine the characteristics of BAX activation during LTD, because our results suggest that the primary mechanism for BAX activation in LTD is activation by BAD. In apoptosis, however, translocation of BAX from the cytosol to mitochondria plays a major Cytidine deaminase role in enhancing mitochondrial permeabilization and cytochrome c release, because under physiological conditions, BAX predominantly resides in the cytosol, with only a minor fraction being present on mitochondrial membranes (Hsu et al., 1997). Why the level of BAX

in mitochondria is not elevated in LTD remains unclear. In fact, even during apoptosis, the mechanism leading to BAX translocation to mitochondria is elusive. It has been suggested that some apoptotic stimulations induce sequential phosphorylations of BAX, for instance, by AKT and GSK3β (Arokium et al., 2007). Phosphorylation could then trigger a conformational change in BAX, thereby allowing it to interact with BAX-binding proteins, such as the p53 upregulated modulator of apoptosis (PUMA), which promotes BAX translocation (Zhang et al., 2009). Among the known proteins that regulate BAX translocation, only GSK-3β is known to be activated in NMDA receptor-dependent LTD (Peineau et al., 2007). It is conceivable that additional BAX-interacting proteins necessary to enable BAX translocation are not sufficiently activated by stimulations that induce LTD, leading to a lack of BAX accumulation in mitochondria.

, 2007). However, by extending the analysis GSK1349572 in vitro to all 12 sequenced Drosophila species, Gardiner and colleagues (2008) found that the proportion of pseudogenized genes did not differ between the specialist and generalist taxa, whereas the endemic species showed significantly more losses than

the mainland species. In their view, small effective population size and genetic drift may rather account for OR gene loss than ecological specialization. Firmly categorizing these species in terms of ecology and demography is however difficult. For example, although D. erecta is specialized upon fruit from Pandanus spp. screwpines, this resource is not continuously available in the habitat. Accordingly, this species must also utilize other resources. Moreover, D. erecta has a restricted and patchy distribution and may thus in fact have a small Volasertib cell line effective population size ( Lachaise et al., 1988). Consequently, examining OR repertoires of additional drosophilid taxa is undoubtedly necessary before any firm conclusions can be drawn. In short, the molecular basis of insect olfaction shows a number of unique features and is characterized by two large gene families, the OBPs and the ORs, which are presumably exclusive to this group of animals. When these two gene families first appear in the insect lineage and whether the initial conquest of land or the diversification

of land plants drove their evolution remains to be determined. All insect genomes to date stem from derived orders. Deep sequencing of species from basal insect orders, as well as from allied hexapod

orders is thus needed in order to understand the evolutionary history of these gene families. Insects have to detect specific volatile information crotamiton in a very complicated chemical environment. How is this feat accomplished? In the vinegar fly and the African malaria mosquito, more or less the complete OR repertoires have been deorphaned, i.e., their key odorant stimuli have been identified. In both species, the ORs display a varying degree of specificity, with certain receptors showing a high degree of selectivity, while others respond to a broad spectrum of compounds (Carey et al., 2010 and Hallem and Carlson, 2006). Response profiles of OSNs, obtained through single sensillum recordings (SSRs) from numerous other insects also suggest a spectrum of OR binding affinities. Perhaps the most well-known specialist OSNs are those detecting pheromones, where OSNs capable of separating two enantiomers with a specificity spanning over more than four decadic concentration steps have been found (Wojtasek et al., 1998). Highly specialized OSNs tuned to host volatiles have been identified from a number of insect species (e.g., Mustaparta et al., 1979, Todd and Baker, 1993 and Tanaka et al., 2009).

In that sense, chemically fixed preparations reveal an underlying organization of the active zone that is missed in the cryo-EM studies, and the two EM approaches—EM on chemically fixed and on unfixed preparations—provide complementary Epacadostat ic50 insights in the organization of active zones. How then can we interpret the results obtained with EM studies of mutant synapses? For example, in Munc13-1 KO mice synaptic vesicle docking appears to be normal as analyzed by EM of chemically fixed synapses (Augustin et al., 1999) but impaired as analyzed by cryo-EM of unfixed samples (Siksou et al., 2009). A possible interpretation of this finding is that

docking analyzed with fixed samples is prone to artifacts, but the situation is not as straightforward as it seems. If in chemically fixed samples even nondocked vesicles always appear docked, no mutation should cause a loss of docking as analyzed by this method. However, in chemically fixed RIM mutant synapses,

vesicles are at least partially undocked (Kaeser et al., 2011). The fundamental problem here LY294002 in vitro is that docking as defined by EM is not a functional definition, and both EM approaches may provide a technique-dependent limited view, with neither allowing the claim of absolute conclusions. Short-term synaptic plasticity can increase or decrease the strength of a synaptic signal several-fold (Fioravante and Regehr, 2011). This change dramatically alters the size of a postsynaptic response elicited by a train of presynaptic action potentials. Many different mechanisms of short-term synaptic plasticity almost were identified, nearly all of which involve the active zone, although in different ways. At the most basic level, short-term plasticity of release

is due to the interplay between the buildup of residual Ca2+ and the loss of releasable vesicles from one action potential to the next. Ca2+ entering the active zone via Ca2+ channels is buffered away quickly, leading to Ca2+-transients of less than 1 ms (Meinrenken et al., 2003). However, during repeated action potentials, especially at frequencies of >10 Hz, residual Ca2+ accumulates because the decay of Ca2+-transients decelerates as Ca2+-buffers become saturated, resulting in an increase of the release probability and thus facilitation. At the same time, vesicles undergoing exocytosis need to be replenished. Although the precise rate of vesicle replenishment differs among synapses and is also regulated by Ca2+ (see discussion below), replenishment of release-ready vesicles can be rate-limiting during action-potential trains, leading to synaptic depression. Thus, short-term plasticity due to the interplay of residual Ca2+ and vesicle depletion depends on synapse-specific factors such as available Ca2+-buffers, the size of the readily releasable pool of vesicles, and the basal release probability.

The distance between the strips was chosen such that outgrowing temporal and nasal RGC axons came into contact within 24–36 hr. Strips were cut perpendicular to

the temporonasal DAPT clinical trial axis and thus contained either temporal or nasal RGCs. For the time-lapse analysis, we used a Nikon Eclipse Ti-E inverted microscope and Cool SNAP HQ2 camera. The interaction between temporal and nasal axons was analyzed for 3–10 hr. Pictures were taken with a 10× lens every minute with the entire area between the two strips documented. For this, pictures were taken from overlapping areas and stitched together using NIS software. Routinely, an area of about 4 × 2 mm was recorded. For data analysis, the area between nasal Selleck Lapatinib and temporal strips was subdivided into 10–18 regions of interest using ImageJ, analyzed individually, and then pooled. We only analyzed axons which could be clearly identified as single growing axons for > 30 min before contact with other axons. Only the first contact was counted for each axon. Furthermore, we only included axons in the analysis which clearly advanced prior to contact and which had a clearly visible growth cone. The interactions were scored as

follows: “0”, no growth cone collapse (axon crosses another axon without growth cone collapse and no/very little change in growth speed) (representative Movie S1); “0.3”, a short transient growth cone collapse after contact and/or a clear slowing down of growth speed, but eventual crossing of the other axon (Movie S2); “0.6”, a full growth cone collapse after contact (Movie Non-specific serine/threonine protein kinase S3); “1”, a full growth cone collapse with a strong retraction of the axon (Movie S4). The recordings were analyzed by two individuals independently and blind to the identity of the class of axons analyzed. Immunohistochemical analysis of frozen sections was performed using standard procedures. Nonspecific interactions were blocked with

1% BSA-TBST, primary antibody solution was applied overnight, and secondary antibody solution was applied for 2 hr, all at room temperature. RNA was extracted from littermate pups on the day of birth using standard protocols. For retina, RNA was extracted from the whole retina of one eye. For SC, RNA was extracted from the central third of the SC from one side. RNA was then reverse transcribed and PCR performed to detect the relative abundance of ephrinA5 expression levels (ephrinA5 FW: TTT GAT GGG TAC AGT GCC TGC GAC; ephrinA5 Rev: AAG CAT CGC CAG GAG GAA CAG TAG) or β-actin (β-actin FW: GAT GAC GAT ATC GCT GCG CTG GTC G; β-actin Rev: GCC TGT GGT ACG ACC AGA GGC ATA CAG) using the following protocol: 94°C, 5 min, 30× (94°C, 1 min; 60°C, 1 min; 72°C, 1 min) followed by 72°C, 10 min. Genomic DNA was extracted using the HotSHOT method (Truett et al., 2000), and genotyping reactions were performed for the presence of ephrinA5 wild-type, KO-first, and floxed alleles as well as rx:cre and en-1:cre alleles.

The loss of variant 1 expression in the GGGGCC repeat carriers was further confirmed by real-time RT-PCR using a custom-designed Taqman assay specific to variant 1. In lymphoblast cell lines of patients from family VSM-20 and in frontal cortex samples from unrelated FTLD-TDP patients carrying expanded repeats, the level of C9ORF72 variant 1 was approximately 50% reduced compared to nonrepeat carriers ( Figure 4C). Since C9ORF72 variants 1 and 3, which each contain a different noncoding first exon, both encode C9ORF72 isoform a (NP_060795.1), we next determined the effect of the expanded repeats on the total levels of transcripts encoding this

isoform (variants 1 and 3 combined) using an inventoried ABI Taqman assay (Hs_00945132). Significant mRNA reductions were observed in both lymphoblast cells (34% reduction) and frontal cortex samples (38% reduction) JAK inhibitor from expanded repeat carriers ( Figure 4D). In contrast, no appreciable changes in total levels of C9ORF72 protein could be observed by western blot analysis of lymphoblast cell lysates or brain ( Figure S2), or by immunohistochemical

Romidepsin mw analysis of C9ORF72 in postmortem brain or spinal cord tissue from expanded repeat carriers ( Figure S2). These protein expression data should, however, be considered preliminary since they are based on a limited number of samples using relatively uncharacterized commercially obtained C9ORF72 antibodies without detailed quantitative analyses. In recent years, intracellular accumulation of expanded nucleotide repeats as RNA foci in the nucleus and/or cytoplasm of affected cells has emerged as an important disease mechanism for the growing class of noncoding repeat expansion disorders (Todd and Paulson, 2010). To determine whether GGGGCC repeat expansions in C9ORF72 result in the Carnitine dehydrogenase formation of RNA foci, we performed RNA fluorescence in situ

hybridization (FISH) in paraffin-embedded sections of postmortem frontal cortex and spinal cord tissue from FTLD-TDP patients. For each neuroanatomical region, sections from two patients with expanded GGGGCC repeats and two affected patients with normal repeat lengths were analyzed. Using a probe targeting the GGGGCC repeat (probe (GGCCCC)4), multiple RNA foci were detected in the nuclei of 25% of cells in both the frontal cortex and the spinal cord from patients carrying the expansion, whereas a signal was observed in only 1% of cells in tissue sections from noncarriers ( Figures 5A–5C). Foci were never observed in any of the samples using a probe targeting the unrelated CCTG repeat (probe (CAGG)6), implicated in myotonic dystrophy type 2 (DM2) ( Liquori et al., 2001), further supporting the specificity of the RNA foci composed of GGGGCC in these patients ( Figure 5D).

Here, we extend these previous results, showing spindle phase locking of hippocampal ripple power similar to that reported in humans (Clemens et al., 2011) in SHAM animals (Figure 3). Embedded slow-wave, spindle, and ripple oscillations therefore coordinate the rhythmic firing of pyramidal cells in cortex and CA1, providing windows of opportunity for cross-structural synaptic plasticity. Indeed, oscillatory activity in both hippocampus and neocortex during NREM sleep is associated with selective reactivation of activity sequences seen during previous behaviors (Peyrache et al., 2009; O’Neill et al., 2010). The initiation of this replay SNS-032 solubility dmso through cortical delta wave-modulated

input may mark the beginning of a looped circuit interaction, whereby cortical delta waves initiate hippocampal reactivation during ripples, which in turn triggers cortical reactivation during spindles (Marshall and Bortezomib Born, 2007). The lack of coupling between hippocampal ripples and cortical spindles in MAM-17 rats demonstrates the crucial role of synchronized cortical slow-waves in organizing the dialog between cortex and hippocampus by providing

a temporal framework for faster oscillations. Disrupting this dialog presumably constitutes the neurophysiological mechanism for behavioral deficits in long term learning and memory described in the MAM E17 model (Flagstad et al., 2004; Gourevitch et al., 2004; Moore et al., 2006), and may contribute to cognitive deficits in other models of sleep fragmentation (Tartar et al., 2006). Our study serves to emphasize that disrupted thalamic-cortical-limbic network activity during sleep must therefore be considered alongside waking activity as a therapeutic

Phosphoprotein phosphatase target in schizophrenia and related diseases. Since active entrainment of slow-waves through transcranial stimulation enhances both spindle density and declarative memory in humans (Marshall et al., 2006) one intuitive possibility would be to use transcranial stimulation as a possible therapy for relieving cognitive and sleep deficits found in patients. The MAM-E17 model provides a unique opportunity to study the detailed cellular, synaptic and network mechanisms that underpin such novel therapeutic approaches. All procedures were carried out in accordance with the UK Animals Scientific Procedures Act (1986) and University of Bristol and Lilly UK ethical review. Sprague-Dawley dams were obtained from Charles River (UK) on day 12 of gestation and injected on E17 with saline or MAM (22 mg/kg i.p.; Midwest Research Institute, Missouri). Fifteen saline-injected and 15 MAM-injected dams produced 51 SHAM and 49 MAM pups. No more than two animals used were derived from a single litter. In brief, 70–80 day old rats were prepared for either EEG recording (cranial implant of five stainless steel screws: 2× motor cortex +3.9 mm AP, ± 2.0 mm ML, 2× visual cortex −6.4mm AP, ±5.

A second Gal4 line, E605-Gal4, contains PERin and displays the same behavioral phenotypes upon neural inactivation or activation ( Figure S4). These data suggest that there is a reciprocal C646 price balance between feeding initiation and locomotion mediated by PERin activity. To test whether the act of proboscis extension sufficed to inhibit locomotion, we immobilized the proboscis in an extended or retracted position with wax. Wild-type flies with

extended proboscises moved significantly less (Figure 7D), arguing that motor activity or proprioceptive feedback from the proboscis inhibits locomotion. Consistent with this, immobilizing the proboscis in a retracted state partially rescued the locomotor defect of flies with inactivated PERin NLG919 purchase neurons (Figure 7D). Thus, proboscis extension feeds back onto circuits to inhibit locomotion, allowing for mutually exclusive behaviors. Many behaviors are mutually exclusive, with the decision to commit to one behavior excluding the selection of others. Here, we show that feeding initiation and locomotion are mutually

exclusive behaviors and that activity in a single pair of interneurons influences this behavioral choice. PERin neurons are activated by stimulation of mechanosensory neurons and activation of PERin inhibits proboscis extension, suggesting that they inhibit feeding while the animal is walking. Consistent with this, leg removal or immobilization enhances proboscis extension probability and this is inhibited by increased PERin activity. The opposite behavior is elicited upon inhibiting activity in PERin neurons: animals show constitutive proboscis extension at the expense of locomotion. This work shows that activity in a single pair of interneurons dramatically influences the choice between feeding initiation and movement. The precise mechanism Thalidomide of activation of PERin neurons remains to be determined. PERin dendrites reside in the first leg neuromere, suggesting that they process information from the legs. Stimulation of leg chemosensory bristles with sucrose or quinine or activation of sugar, bitter, or water neurons using

optogenetic approaches did not activate PERin neurons, nor did satiety state change tonic activity. Stimulation of sensory nerves into the ventral nerve cord and stimulation of mechanosensory neurons, using a nompC driver, activated PERin. In addition, by monitoring activity of PERin while flies moved their legs, we demonstrated that activity was coincident with movement. These studies argue that PERin is activated by nongustatory cues in response to movement, likely upon detection of mechanosensory cues. Additional cues may also activate PERin. Studies of behavioral exclusivity in other invertebrate species suggest two mechanisms by which one behavior suppresses others (Kristan and Gillette, 2007). One strategy is by competition between command neurons that activate dedicated circuits for different behaviors.