Molecular detection of Theileria cervi in equids from México.

Equine piroplasmosis is a parasitic illness caused by various protozoa of the Babesia and Theileria genera, which parasitize within red blood cells. The transmission of these pathogens occurs through certain genus of ticks, including Amblyomma, Haemaphysalis, Hyalomma, and Rhipicephalus. In recent times, an increase in the identification of new Theileria species and genotypes has been observed. This is further complicated by the presence of mixed Theileria infections in both mammals and tick vectors, particularly in regions where wildlife and livestock share habitats and vectors. Therefore, the objective of this study is to document the occurrence of Theileria cervi in a non-typical host. A total of 88 horses (Equus caballus) and 10 donkeys (Equus asinus) were sampled in three municipalities in Veracruz, Mexico. Molecular techniques were employed to identify Babesia/Theileria through the amplification of a segment of the 18S-rDNA and hsp70 genes. The phylogenetic reconstruction grouped the obtained sequences into a monophyletic cluster alongside sequences of T. cervi. This work represents the first documented occurrence of T. cervi in equids. These findings have significant implications from an epidemiological point of view. In addition, further studies are needed to determine the distribution and pathogenicity of this species for domestic animals and to develop effective control strategies.

First report of Babesia bigemina in Lama glama in a zoological garden of Veracruz, Mexico.

Zoological gardens represent specialised centres for the preservation of biological inventories and genetic diversity, allowing the recognition of multiple species in critical conservation categories. However, the close coexistence of multiple species of vertebrates that may be associated with various species of ectoparasites may be the cause of the transmission of multiple infectious agents, among which tick-borne pathogens stand out. In these areas, several animal species usually live in a small space and proximity to other wildlife, visitors and keepers. In Mexico, little is known about the disease agents transmitted by arthropods in zoological gardens. For this reason, the aim of this study was to identify the presence of Babesia/Theileria in animals maintained in captivity. As a part of a project identifying vector-borne pathogens in wildlife, 24 animals were sampled in the Miguel Angel de Quevedo zoo. Molecular identification of Babesia/Theileria was realised through amplification of a fragment of the mitochondrial cytB gene and the ribosomal 18S-rDNA. Two neotropical camelids (Lama glama) tested positive (2/3 = 66.6%) to Babesia bigemina. Our results represent the first record of B. bigemina in animals in captivity in a zoological garden in Mexico and the first finding of this haemoparasite in neotropical camelids in Mexico.

Neuronal KIF5b deletion induces striatum-dependent locomotor impairments and defects in membrane presentation of dopamine D2 receptors.

The process of locomotion is controlled by fine-tuned dopaminergic neurons in the Substantia Nigra pars-compacta (SNpc) that projects their axons to the dorsal striatum regulating cortical innervations of medium spiny neurons. Dysfunction in dopaminergic neurotransmission within the striatum leads to movement impairments, gaiting defects, and hypo-locomotion. Due to their high polarity and extreme axonal arborization, neurons depend on molecular motor proteins and microtubule-based transport for their normal function. Transport defects have been associated with neurodegeneration since axonopathies, axonal clogging, microtubule destabilization, and lower motor proteins levels were described in the brain of patients with Parkinson's Disease and other neurodegenerative disorders. However, the contribution of specific motor proteins to the regulation of the nigrostriatal network remains unclear. Here, we generated different conditional knockout mice for the kinesin heavy chain 5B subunit (Kif5b) of Kinesin-1 to unravel its contribution to locomotion. Interestingly, mice with neuronal Kif5b deletion showed hypo-locomotion, movement initiation deficits, and coordination impairments. High pressure liquid chromatography determined that dopamine (DA) metabolism is impaired in neuronal Kif5b-KO, while no dopaminergic cell loss was observed. However, the deletion of Kif5b only in dopaminergic neurons is not sufficient to induce locomotor defects. Noteworthy, pharmacological stimulation of DA release together with agonist or antagonist of DA receptors revealed selective D2-dependent movement initiation defects in neuronal Kif5b-KO. Finally, subcellular fractionation from striatum showed that Kif5b deletion reduced the amount of dopamine D2 receptor in synaptic plasma membranes. Together, these results revealed an important role for Kif5b in the modulation of the striatal network that is relevant to the overall locomotor response. OPEN SCIENCE BADGES: This article has received a badge for *Open Materials* because it provided all relevant information to reproduce the study in the manuscript. The complete Open Science Disclosure form for this article can be found at the end of the article. More information about the Open Practices badges can be found at https://cos.io/our-services/open-science-badges/.

Fast axonal transport of the proteasome complex depends on membrane interaction and molecular motor function.

Protein degradation by the ubiquitin-proteasome system in neurons depends on the correct delivery of the proteasome complex. In neurodegenerative diseases, aggregation and accumulation of proteins in axons link transport defects with degradation impairments; however, the transport properties of proteasomes remain unknown. Here, using in vivo experiments, we reveal the fast anterograde transport of assembled and functional 26S proteasome complexes. A high-resolution tracking system to follow fluorescent proteasomes revealed three types of motion: actively driven proteasome axonal transport, diffusive behavior in a viscoelastic axonema and proteasome-confined motion. We show that active proteasome transport depends on motor function because knockdown of the KIF5B motor subunit resulted in impairment of the anterograde proteasome flux and the density of segmental velocities. Finally, we reveal that neuronal proteasomes interact with intracellular membranes and identify the coordinated transport of fluorescent proteasomes with synaptic precursor vesicles, Golgi-derived vesicles, lysosomes and mitochondria. Taken together, our results reveal fast axonal transport as a new mechanism of proteasome delivery that depends on membrane cargo 'hitch-hiking' and the function of molecular motors. We further hypothesize that defects in proteasome transport could promote abnormal protein clearance in neurodegenerative diseases.

Long-term modulation of tyrosine hydroxylase activity and expression by endothelin-1 and -3 in the rat anterior and posterior hypothalamus.

Brain catecholamines are involved in the regulation of biological functions, including cardiovascular activity. The hypothalamus presents areas with high density of catecholaminergic neurons and the endothelin system. Two hypothalamic regions intimately related with the cardiovascular control are distinguished: the anterior (AHR) and posterior (PHR) hypothalamus, considered to be sympathoinhibitory and sympathoexcitatory regions, respectively. We previously reported that endothelins (ETs) are involved in the short-term tyrosine hydroxylase (TH) regulation in both the AHR and PHR. TH is crucial for catecholaminergic transmission and is tightly regulated by well-characterized mechanisms. In the present study, we sought to establish the effects and underlying mechanisms of ET-1 and ET-3 on TH long-term modulation. Results showed that in the AHR, ETs decreased TH activity through ET(B) receptor activation coupled to the nitric oxide, phosphoinositide, and CaMK-II pathways. They also reduced total TH level and TH phosphorylated forms (Ser 19 and 40). Conversely, in the PHR, ETs increased TH activity through a G protein-coupled receptor, likely an atypical ET receptor or the ET(C) receptor, which stimulated the phosphoinositide and adenylyl cyclase pathways, as well as CaMK-II. ETs also increased total TH level and the Ser 19, 31, and 40 phosphorylated sites of the enzyme. These findings support that ETs are involved in the long-term regulation of TH activity, leading to reduced sympathoinhibition in the AHR and increased sympathoexcitation in the PHR. Present and previous studies may partially explain the cardiovascular effects produced by ETs when applied to the brain.