In this manner, a systemic integration of time and food signals is achieved, balancing energy homeostasis. This concept is also illustrated by the finding that the regulation of dopaminergic transmission and reward is altered

in mice mutant for the gene Clock and associated with increased expression and phosphorylation of tyrosine hydroxylase (TH) ( McClung et al., 2005), INCB018424 molecular weight the rate-limiting enzyme for dopamine synthesis. Additionally, these mutants show elevated leptin levels ( Turek et al., 2005), which may be responsible for the elevated TH activity, because leptin increases the synthesis and activity of TH ( Fulton et al., 2006). As a consequence, these animals probably have elevated dopamine levels contributing to the mania-like behavior ( Roybal et al., 2007) and the increased firing rate of VTA dopaminergic neurons observed in these animals ( Mukherjee et al., 2010). The circadian system is strongly entwined with metabolism Imatinib (see above, Dallmann et al., 2012), organizing it in a temporal fashion that optimizes the organism’s performance over the day’s 24 hr. Concurrently, this organization ensures tissue homeostasis by keeping various physiological processes in balance. Perturbations of the circadian system caused by rotating shift work, frequent transmeridian

flights and stress lead to de-synchronization of the various body clocks. This is likely to be a confounding factor that favors the development of diseases such as metabolic syndrome (obesity, diabetes, cardiovascular problems) and neurological disorders. In these disorders, energy uptake and expenditure, and neuronal activation and inhibition become imbalanced. Studies in humans suggest that disruption of daily metabolic rhythms is an exacerbating factor in the metabolic syndrome (Gallou-Kabani et al., 2007). Shift-work and sleep deprivation are known to dampen rhythms in growth hormone

and Dichloromethane dehalogenase melatonin, reduce insulin sensitivity, and elevate circulating cortisol levels (Spiegel et al., 2009). These changes favor weight gain, obesity, and development of metabolic syndrome. Recently, forced circadian desynchronization (a simulation of shift work) in humans was shown to impact on neuroendocrine control of glucose metabolism and energetics (Scheer et al., 2009). Participants subjected to the shift-work protocol showed increased blood pressure, inverted cortisol rhythms accompanied by hypoleptinemia and insulin resistance (Scheer et al., 2009). Interestingly, patients with diabetes display dampened rhythms of glucose tolerance and insulin secretion (Boden et al., 1999), indicating that the relationship between circadian disruption and metabolic pathologies is bidirectional (Figure 1B, pink arrows). This suggests that circadian disruption may lead to a vicious cycle contributing to the augmentation and progression of metabolic syndrome.

The readout neuron is active when the weighted sum of the inputs is above a threshold. As in the exclusive-or (XOR) problem, there is no solution if inputs include only specialized neurons that encode the pictures separately. Even in the simplest case of two pictures (A, B) and their pairs (A′, B′), Veliparib solubility dmso the readout neuron cannot respond to the two related pairs (A, A′ and B, B′) and not to the other two (A, B′ and B, A′). The solution is to add neurons that respond to nonlinear mixtures of relevant variables. The task is

solved by simply adding a third neuron that adapts its selectivity according to the cue stimulus (it discriminates A′ versus B′ only when the cue was A). In a forthcoming paper, we demonstrate that mixed selectivity in PFC neurons BKM120 has critical computational advantages (Rigotti et al., 2013). It greatly increases the complexity and number of tasks that can be learned. Rather than “confuse” downstream readout neurons, increasing the number of mixed selectivity neurons exponentially increases the number of possible input-output mappings that readout neurons can implement. Networks without mixed selectivity have a limited capacity to learn a few simple tasks. Plus, mixed selectivity speeds and eases learning because only readout neurons need to be trained and, with high-dimensional neural representations, learning

algorithms converge more rapidly (Rigotti et al., 2010). Given these advantages, it is no wonder that mixed selectivity is so widely observed in the cortex. But does mixed selectivity not create problems? Do downstream neurons not sometimes receive signals that are irrelevant or counterproductive? One solution is the oscillatory brain rhythms. They could allow neurons to communicate different messages to different targets depending on what they are synchronized with (and how, e.g., phase and frequency). For example, rat hippocampal CA1 neurons preferentially synchronize to Isotretinoin the entorhinal or CA3 neurons at different

gamma frequencies and theta phases (Colgin et al., 2009). Different frequency synchronization between human cortical areas supports recollection of spatial versus temporal information (Watrous et al., 2013). Different phases of cortical oscillations preferentially signal different pictures simultaneously held in short-term memory (Siegel et al., 2009). Monkey frontal and parietal cortices synchronize more strongly at lower versus higher frequency for top-down versus bottom-up attention, respectively (Buschman and Miller, 2007). Entraining the human frontal cortex at those frequencies produces the predicted top-down versus bottom-up effects on behavior (Chanes et al., 2013). Thus, activity from the same neurons has different functional outcomes depending on their rhythmic dynamics. For years, experimentalists have observed that cortical areas central to cognition have large proportions of “weird” neurons with mixed selectivity that cannot be pinned to one particular message.

These results indicated that GPC1 is capable of binding Shh. Based on previous studies in flies and vertebrates, GPC1 and Shh could cooperate in two different (but not necessarily exclusive) manners to mediate postcrossing commissural axon guidance: (1) GPC1 could directly promote or inhibit Shh’s interaction with its axon guidance receptors (Beckett et al., 2008, Capurro et al., 2008 and Williams et al., 2010), and/or

(2) the presence of GPC1 within a receptor complex could regulate Gli-dependent transcription and subsequent gene expression in response to Shh (Chan et al., 2009), which in turn would specify the expression of guidance receptors on commissural LY294002 in vitro axons. Here, we investigated the latter. Gene transcription has been demonstrated to regulate discrete steps in postcommissural axon guidance (Condron, learn more 2002), and Shh has been speculated to be an appropriate floorplate-derived signal that could induce such an activity (Sánchez-Camacho and Bovolenta, 2009). However, so far evidence for such a mechanism has been elusive. Our previous studies identified Hhip as a mediator of the repulsive guidance response to Shh (Bourikas et al., 2005). Hhip messenger RNA (mRNA) is detectable transiently in dI1 neurons at the time when postcrossing axons turn into the longitudinal axis ( Figure S5; Bourikas et al., 2005). Interestingly, Hhip is a transcriptional target of Shh (

Chuang and McMahon, 1999 and Buttitta et al., 2003), suggesting that commissural neurons might begin to upregulate Hhip as they encounter high levels of Shh in the floorplate. Thus, we hypothesized that transcriptional activity in response

to Shh, in a GPC1-dependent manner, could modulate the responsiveness of the commissural growth cone at this intermediate target. To investigate this idea, we analyzed Hhip mRNA expression patterns in the spinal cord following GPC1 knockdown. Strikingly, we found that embryos electroporated with βact-hrGFPII-mi7GPC1 ( Figure 4A) or βact-hrGFPII-mi4GPC1 (data not shown) displayed a specific until loss of Hhip expression in the dorsal spinal cord on the electroporated side. In contrast, ventromedial Hhip expression was unaffected by the loss of GPC1, demonstrating a cell-type-specific requirement for GPC1 in Hhip induction. Electroporation of a control plasmid, βact-hrGFPII-mi2Luc, did not affect Hhip expression ( Figure 4B). Rescue experiments, as described above, revealed that dorsal expression of Hhip could be restored by the expression of GPC1ΔmiR ( Figures 4C–4F). We quantified these effects using two methods. First, we calculated the percentage of sections in each condition displaying “symmetrical” versus “asymmetrical” Hhip levels in the dorsal spinal cord ( Figures 4C–4F, percent values indicate the number of sections with symmetrical expression).

V.S. and M.S.), the Gatsby Charitable Foundation (M.S.), and the following awards to K.V.S.: NIH Director’s Pioneer Award (1DP10D006409), the Burroughs Wellcome Fund Career Award in the Biomedical Sciences, the Center for Integrated Systems at Stanford, the NSF Center for Neuromorphic Systems Engineering at Caltech, the Sloan Foundation, and the Whitaker Foundation. “
“Neurons are bombarded by ongoing excitatory and inhibitory inputs. What are the mechanisms that allow a neuron to detect the arrival of an

input carrying an important message requiring an immediate specific response? In this issue of Neuron, Kuo and Trussel (2011) reveal a robust mechanism that begins to answer this question CX 5461 by exploring the effects of noradrenaline (NA) on inhibitory inputs at fusiform cells, the principal cells of the mouse dorsal

cochlear nucleus (DCN). Inhibitory inputs in DCN fusiform cells occur as spontaneous IPSCs (sIPSCs) or as feedforward inhibition generated by parallel fiber excitation of cartwheel cells (eIPSCs). Surprisingly, NA dramatically reduced sIPSCs while increasing eIPSCs. Cartwheel cells are the source of both the spontaneous and the evoked IPSCs in fusiform principal cells. Thus, Kuo and Trussell systematically investigated the synaptic mechanisms between cartwheel cells and DCN principal cells to explain the opposing effects of NA. First, they examined the possibility Selumetinib supplier that NA enhances parallel fiber input at cartwheel cells. However, they demonstrated TCL that NA does not affect excitatory postsynaptic (EPSC) inputs in cartwheel cells. Next, they examined whether cartwheel connection with fusiform cells is modulated by NA. Paired recordings between presynaptic cartwheel cell and postsynaptic fusiform cells indicated that this synapse is also insensitive to NA. They further showed that changes in the membrane potential of cartwheel cells do not affect sIPSCs in fusiform cells. Thus, NA does not appear to act via its conventional presynaptic mechanisms (Berridge and Waterhouse, 2003 and Waterhouse and

Woodward, 1980). Next, they considered the possible impact of NA on spontaneous spiking of cartwheel cells. They first showed that cartwheel to fusiform cells exhibit activity-dependent synaptic depression. Further using paired recordings, they showed that the recovery from synaptic depression is slow (time constants of 5–6 s). Given that cartwheel cells exhibit spiking at about 8–13 Hz (Davis and Young, 1997 and Golding and Oertel, 1997), their synapses are not allowed to recover and exhibit ongoing depression. Thus, spontaneous spiking in cartwheel cells has two consequences. First, this activity generates sIPSCs in their postsynaptic cells, i.e., fusiform cells, and second, this ongoing spiking activity generates persistent synaptic depression. Using cell-attached recording, Kuo and Trussell showed that the spontaneous spiking of cartwheel cells is silenced by application of NA.

Addition of exogenous astrocytes, which are known to supply essential factors for synaptogenesis in other primary neuron culture models (Eroglu and Hydroxychloroquine Barres, 2010 and Ullian et al., 2004), “rescued” this phenotype. More recently, the issue of functional maturity has also been addressed by altering the composition of the neurogenic factor cocktail. For instance, transduction of a cocktail of factors that includes miR-124—a highly expressed neuronal microRNA that modulates expression of antineuronal gene regulatory factors, such as REST, during CNS development (Ambasudhan et al., 2011) —appeared effective in generating mature neurons with evidence of spontaneous synaptic activity.

In a related approach, repression of poly-pyrimidine-tract binding protein (PTB), which is

thought to normally oppose the action of miR-124, appeared sufficient to convert fibroblasts to a neuronal phenotype (Xue et al., 2013). Circumventing the need for ASCL1 or other additional exogenous regulatory factors significantly simplifies the conversion process. Extrinsic cues also play a major regulatory role in the neuronal fate conversion process. Withdrawal of serum, and inclusion of neurotrophic factors, is a common feature in the directed reprogramming protocols. Small molecule antagonists of glycogen synthase kinase-3β (GSK-3β) and SMAD signaling—signaling pathways implicated in CNS neurogenesis in vivo—have been Ulixertinib purchase reported to significantly improve the efficiency of reprogramming (Ladewig et al., 2012). Addition of exogenous primary astrocytes, which likely provide essential factors for synaptic maturation (Ullian et al., 2004), effectively promote synaptic activity in the iN cultures (Pang et al., 2011, Qiang et al., 2011, Vierbuchen from et al., 2010 and Yoo et al., 2011). A reduction in oxygen tension to physiological levels (Davila et al., 2013) may also promote the generation of mature neurons in vitro

by directed conversion. A particularly intriguing and potentially clinically relevant application is the directed conversion of nonneuronal cells to neurons in the adult CNS environment in vivo. In the adult mammalian CNS, switching cell fates has appeared to be particularly restricted, even from one neuronal type to another, although such switching has been described during late development (Rouaux and Arlotta, 2013). Genetic studies in the nematode C. elegans have achieved the efficient in vivo directed conversion of mature germ cells directly into neurons, by elimination of chromatin regulatory factors ( Tursun et al., 2011); it is unclear whether such a strategy would promote directed fate interconversion in the adult mammalian CNS. Another drawback to the directed generation of mature, postmitotic hiNs, is that these cells cannot be further propagated.

Interestingly, although

Aoto et al. (2008) demonstrate that RA mimics mini blockade in driving protein synthesis-dependent postsynaptic recruitment of GluA1 to synapses and enhancing mEPSC amplitude, it had no effect on mEPSC frequency suggesting a selective role in postsynaptic compensation. Together with our findings, these results suggest that distinct releasable factors may be engaged for homeostatic adjustment of pre- and postsynaptic function. For homeostatic forms of plasticity induced by coincident blockade of APs and NMDARs, multiple studies have demonstrated enhanced synthesis of GluA1 in dendrites (Ju et al., 2004 and Sutton et al., 2006) or synaptic fractions (Aoto et al., 2008) and the incorporation of GluA2-lacking receptors at synapses click here (Ju et al., 2004, Sutton et al.,

2006 and Aoto et al., 2008). By contrast, blockade of APs alone induces a slower form of postsynaptic compensation characterized find protocol by enhanced expression of GluA2-containing AMPARs at synapses (Turrigiano et al., 1998, Wierenga et al., 2005 and Sutton et al., 2006), possibly owing to a decrease in receptor removal and an accumulation of existing synaptic receptors (e.g., O’Brien et al., 1998, Ehlers, 2003 and Ibata et al., 2008). These results support the notion that spontaneous and AP-mediated neurotransmission engage unique signaling pathways in neurons (Sutton et al., 2007 and Atasoy et al., 2008) and that miniature synaptic events in these neurons play an important role in the acute homeostatic regulation of synaptic strength. Frank et al. (2006) identified a similar role for spontaneous neurotransmission in rapid homeostatic adjustment of synaptic function at the Drosophila neuromuscular junction, suggesting Non-specific serine/threonine protein kinase that this role for miniature events may be conserved across

different synapse classes and species. In a similar vein, Thiagarajan et al. (2005) demonstrated the synaptic recruitment of GluA2-lacking AMPARs in response to chronic (∼24 hr) AMPAR blockade, suggesting that loss of AMPAR activity also engages mechanisms that recruit GluA2-lacking AMPARs to synapses. Our results extend these observations by demonstrating that AMPAR blockade induces rapid postsynaptic recruitment of GluA1 that is dependent on new protein synthesis. Moreover, we found that regardless of the presence or absence of background spiking, the increase in synaptic GluA1 and mEPSC amplitude induced by AMPAR blockade is indistinguishable. These results have two important implications. First, they demonstrate that although AP blockade reveals the functional impact of miniature neurotransmission (see also Sutton et al., 2006), this role extends to conditions where background spiking is permissive.

, 2004 and Emoto et al., 2006). In trc and fry mutants, dendrites of adjacent class IV da neurons

cross one another and thus have overlapping dendritic fields ( Emoto et al., 2004). Interestingly, trc and fry mutants also display extensive isoneuronal dendritic crossing of class IV da neurons. Time-lapse analyses in fry mutants showed that a much smaller percentage of dendrites display avoidance behaviors than in the wild-type, leading to the hypothesis that fry and trc directly regulate homotypic repulsion ( Emoto et al., 2004). In addition, Target of rapamycin (Tor), http://www.selleckchem.com/GSK-3.html SAPK-interacting protein 1 (Sin1), and rapamycin-insensitive companion of Tor (rictor), three components of TOR complex 2 (TORC2), act in the same pathway by phosphorylating and activating Trc ( Koike-Kumagai et al., 2009). Neuron-substrate interactions are important for neuronal development and function. Neuronal substrates typically derive from secreted molecules in the extracellular matrix (ECM). The ECM not only serves FG-4592 as an adhesive substrate permitting neurite outgrowth (Kapfhammer and Schwab, 1992), it also hosts guidance cues important for axon pathfinding (Nakamoto et al., 2004). A major class of cell membrane receptors

for ECM are integrins, which anchor to the actin cytoskeleton through cytosolic signaling and adaptor proteins, providing a linkage between the local ECM milieu and intracellular signaling events (Cabodi et al., 2010). In vivo studies have shown that integrins play pivotal roles in many aspects of neural development, such as axon guidance, neuronal migration, neurite growth, arborization, and maintenance (Denda and Reichardt, 2007). In Drosophila, integrins are known to regulate axon guidance and synaptic plasticity ( Grotewiel et al., 1998 and Stevens and Jacobs, 2002), but their role in patterning dendritic fields is largely unexplored. Class IV da neuron dendrites innervate

the larval body wall by attaching to the epidermis. Self-avoidance and tiling together ensure even spreading of the dendrites. Mephenoxalone In theory, contact-dependent repulsion requires dendrites to be restricted within a 2D space. Even though the receptive field of class IV da neurons, the larval epidermis, appears to be a 2D sheet, it is unclear whether the dendrites are indeed distributed within a 2D space. Specifically, how dendrites are positioned relative to epidermal cells is unknown. By using high-resolution confocal imaging, here we show that most dendrites of class IV da neurons are indeed distributed in a 2D space between the epidermal basal surface and the ECM. We further show that αPS1 and βPS integrins are cell-autonomously required in neurons for dendrites to attach to the ECM. Laminins secreted by the epidermis likely serve as ligands for integrins in the dendrite-ECM interaction.

To break the CS-US contingency, Pavlov developed an experimental procedure in which the CS was presented alone (without the US) for several trials after the completion of conditioning (Pavlov, 1927). Not surprisingly, the earliest CS-alone trials produced a robust CR, but the CR gradually faded with subsequent CS presentations. Pavlov termed this phenomenon “extinction,” and it is now apparent that this form of learning is an important component of behavioral interventions for patients with pathological fear memories. For example, exposure therapy involves

the use of mental imagery and exposure to trauma-relevant cues in a safe environment to suppress the fear associated with the memory of the traumatic event (Craske et al., 2008, Powers et al., 2010 and Rothbaum AZD5363 and Davis, 2003). Given the importance of extinction learning as a mechanism for suppressing fear memory, there has been an explosion of work into the neural mechanisms of extinction (Bouton et al., 2006a, Herry et al., 2010, Myers and Davis, 2002, Pape and Pare, 2010 and Quirk and Mueller, 2008). Not surprisingly, much of this work has focused on the contribution of the amygdala to fear Smad inhibitor extinction and several reports indicate that the BLA is critical for the acquisition of

extinction memories. For example, infusing NMDA receptor antagonists into the BLA disrupts the acquisition of extinction (Falls et al., 1992,

Laurent et al., 2008 and Zimmerman and Maren, 2010), whereas blockade of NMDA receptors in the CEA does not affect extinction learning (Zimmerman and Maren, 2010). Intracellular signaling pathways downstream of BLA NMDA receptors are also critical for extinction learning (Herry et al., 2006, Lin et al., 2003a, Lin et al., 2003b, Lu et al., 2001 and Yang and Lu, 2005). In addition to the glutamatergic system, recent work indicates that other neurotransmitter systems contribute to extinction learning. For example, mice lacking endocannabinoid receptors (CB1 receptors, specifically) exhibit impairments in extinction learning and systemic administration of a CB1 antagonist (SR141716, rimonabant) Edoxaban inhibits extinction learning (Chhatwal et al., 2009 and Marsicano et al., 2002). Endocannabinoids modulate inhibitory GABAergic synaptic transmission in the amygdala, which is also essential for extinction learning (Chhatwal et al., 2005b, Harris and Westbrook, 1998, Laurent et al., 2008, Laurent and Westbrook, 2008 and Makkar et al., 2010). Collectively, these data suggest that changes in synaptic transmission within the BLA contribute to the suppression of conditional fear after extinction training. Indeed, depotentiation of amygdaloid synaptic transmission has been reported to occur after extinction training (Kim et al., 2007).

, 2009 and Ye et al., 2009).

Finally, Notch signaling activation by its downstream effectors (e.g., Hes1 and Hes5) was shown to inhibit the transition of OPCs to mature oligodendrocytes Dabrafenib mw and remyelination (Wang et al., 1998, Wu et al., 2003 and Zhang et al., 2009). As a potential mechanism to counter extrinsic suppressive signaling, a series of cell intrinsic factors, such as the basic helix-loop-helix transcription factors Olig1 and Olig2, have been identified to positively regulate differentiation of oligodendrocytes (Emery et al., 2009, He et al., 2007, Howng et al., 2010, Li et al., 2009, Wegner, 2008 and Ye et al., 2009). Olig2 directs early OPC specification and differentiation (Lu et al., 2002, Yue et al., 2006 and Zhou and Anderson, click here 2002); similarly, Olig1, whose expression is elevated during OPC differentiation, promotes oligodendrocyte maturation and is required for repair of demyelinated lesions (Arnett et al., 2004, Li et al., 2007 and Xin et al., 2005). This suggests that Olig1 and Olig2 have an overlapping function in regulating

myelination in the CNS. However, the underlying mechanisms that balance and coordinate extrinsic with intrinsic inhibitory cues to drive oligodendrocyte myelination are not fully understood. We hypothesized that the downstream effectors regulated by both Olig1 and Olig2 may function to coordinate the inhibitory pathways to promote myelination. By performing whole-genome chromatin immunoprecipitation (ChIP) sequencing Cytidine deaminase and gene profiling analysis, we identified a common target gene of Olig1 and Olig2 encoding

Smad-interacting protein-1 (Sip1; also named zinc finger homeobox protein 1b [Zfhx1b] or Zeb2). Our present studies reveal a critical role of the transcription factor Sip1 in governing CNS myelination. Sip1 inhibits BMP-Smad negative regulatory pathways while activating the expression of crucial myelination-promoting factors. In addition, we identify Smad7, a member of inhibitory Smads (I-Smads) in the Smad pathway, as a key target induced by Sip1. We show that Smad7 is required for oligodendrocyte differentiation and promotes myelination by blocking BMP and Wnt/β-catenin inhibitory pathways. Thus, by antagonizing activated BMP-Smads while inducing the I-Smad gene Smad7, Sip1 exerts dual-mode regulation of Smad signaling to control oligodendrocyte maturation. Our findings reveal a previously unrecognized role for Sip1 in governing myelination and, in addition, its direct modulation of two Smad pathways, pointing to Sip1 as a nodal point that integrates extrinsic signals and intrinsic regulators to control the myelinogenic program in the CNS. To identify the target genes directly regulated by Olig2, we carried out whole-genome ChIP sequencing using purified rat oligodendrocytes.

There was no association learn more between the presence of dogs and seropositivity for N. caninum, and this result

was similar to what has been observed in other surveys conducted in Brazil ( Figliuolo et al., 2004, Romanelli et al., 2007, Salaberry et al., 2010 and Soares et al., 2009), suggesting that this coccid is preferentially transmitted vertically, similar to bovine infections. The serological evidence found in this study indicates that infection due to N. caninum is widely distributed on sheep-rearing farms in the state of Minas Gerais, especially in the mesoregions of Metropolitana de Belo Horizonte (28.1%) and Alto Paranaíba/Triângulo (26.6%), which according to the official agriculture and livestock census ( IBGE, 2009), presented increases in sheep populations over the decade 1999–2009 of 249.3% and 64.1%, respectively. Further studies will be needed to

selleck kinase inhibitor determine the impact of N. caninum as a cause of reproductive problems in sheep in Minas Gerais. We thank the Instituto Mineiro de Agropecuária (IMA) and their veterinarians for their help in collecting serum samples and filling out questionnaires on sheep herds in Minas Gerais. Financial support was provided by the IMA and by the Research Support Foundation of the State of Minas Gerais (Fundação de Amparo à Pesquisa do Estado de Minas Gerais; FAPEMIG – No. CVZ APQ-7963-5.04/07). “
“Plasmodium juxtanucleare Versiani & Gomes, 1941, the agent that causes avian malaria in Gallus gallus Linnaeus, 1758, was observed for the first time in Brazil when researchers studying avian spirochetosis at a street market, while examining blood samples drawn from

live fowls, observed a small parasite with rounded or irregular shape, always found near the blood cell nuclei. For this reason, it was named P. juxtanucleare ( Versiani and Gomes, 1941). Besides domestic chickens, there are reports of other fowls being infected by P. juxtanucleare: Gallus lafayettei Linnaeus, 1758 (jungle fowl) in Sri Lanka ( Dissanaike, 1963); Bambusicola thoracica sonorivox Linnaeus, 1758 (bamboo partridge) in Taiwan ( Manwell, 1966); Mephenoxalone Francolinus spp. (partridge) in Africa ( Mohan and Manwell, 1966); Crysolophus pictus Linnaeus, 1758 (golden pheasant), Lophura nyctemera Linnaeus, 1758 (silver pheasant), Crysolophus amherstiae Linnaeus, 1758 (Lady Amherst’s pheasant) and Phasianus colchicus Linnaeus, 1758 (common pheasant) in Brazil ( Massard and Massard, 1981); and Meleagris galopavo Linnaeus, 1758 (Turkey), also in Brazil ( Serra-Freire and Massard, 1979). The invertebrate hosts of P. juxtanucleare are mosquitoes of the Culicini tribe ( Versiani and Gomes, 1941, Bennet et al., 1966, Garnham, 1966, Krettli, 1972 and Lourenço-de-Oliveira and Castro, 1991). The pathogenicity of P.