RESUMO
This study aimed to determine the efficacy and parasite resistance of levamisole (LV) and ivermectin (IVM) in beef cattle naturally infected with gastrointestinal nematodes, as well as the effect on the liveweight gain in a tropical wet region of Oaxaca, Mexico. From November 2019 to January 2020, sixty-six grazing calves were randomly allocated into three groups of twenty-two animals each, treated with LV or IVM or an untreated control group (day 0). Feces were collected 1 day before treatment and 15 days after treatment. The liveweight gain from each animal was recorded at days 0, 15, 30 and 45 post treatment. The LV group presented the highest reduction of eggs per gram (EPG) of feces, followed by the IVM group. Resistance to IVM was detected, although LV resistance was also suspected. The IVM group had significantly higher effective treatment at 93.5%, resulting in an increase (P<0.05) of liveweight gain of 16.1kg, followed by the LV group (92.4%) with 17.1kg, compared to the untreated control group. A signiï¬cant (P < 0.05) negative correlation was observed between EPG and weight gain for the LV (r = -0.46) and IVM groups (r = -0.32). LV and IVM showed a lack of efficacy against gastrointestinal nematodes, as well as an adequate capacity for EPG reduction but with IVM resistance and detrimental effects on growth performance in grazing beef cattle.
Os nematódeos gastrointestinais do gado de pastoreio causam perdas econômicas substanciais em todo o mundo. Este estudo teve como objetivo determinar a eficácia e a resistência parasitária do levamisol (LV) e da ivermectina (IVM) em bovinos de corte naturalmente infectados com nematódeos gastrointestinais, bem como o efeito no ganho de peso vivo, em uma região tropical úmida de Oaxaca, México. De novembro de 2019 a janeiro de 2020, 66 bezerros de pasto foram distribuídos aleatoriamente em três grupos de 22 animais cada um, tratados com LV ou IVM, ou em um grupo controle sem tratamento (dia 0). As fezes foram coletadas 1 dia antes do tratamento e 15 dias após o tratamento. O ganho de peso vivo de cada animal foi registrado nos dias 0, 15, 30 e 45 pós-tratamento. O grupo do LV apresentou a maior redução de ovos por grama de fezes (EPG), seguido pelo grupo IVM. A resistência à IVM foi detectada, embora também se suspeitasse de resistência ao LV. O grupo IVM teve um tratamento eficaz significativamente maior, com 93,5%, resultando em um aumento (P < 0,05) do ganho de peso vivo de 16,1kg, seguido pelo grupo LV (92,4%), com 17,1kg, em comparação com o grupo controle sem tratamento. Foi observada uma correlação negativa (P < 0,05) entre o EPG e o ganho de peso para os grupos LV (r = -0,46) e IVM (r = -0,32). LV e IVM mostraram falta de eficácia contra nematódeos gastrointestinais, assim como uma capacidade adequada de redução de EPG, mas com resistência IVM e efeitos prejudiciais no desempenho de crescimento em gado de corte em pastagem.
Assuntos
Animais , Bovinos , Resistência a Medicamentos , Aumento de Peso , Doenças dos Bovinos/parasitologia , Anti-Helmínticos , Nematoides/patogenicidade , MéxicoRESUMO
The recombinant C-terminal domain of tetanus toxin (Hc-TeTx) is a new non-toxic peptide of the tetanus toxin that exerts a protective action against glutamate excitotoxicity in motoneurons. Moreover, its efficacy as a neuroprotective agent has been demonstrated in several animal models of neurodegeneration. The eleven amino acids in the ß amyloid peptide (Aß25-35) mimic the toxic effects of the full ß amyloid peptide (Aß1-42), causing the impairment of the cholinergic system in the medial septum (MS) which, in turn, alters the septo-hippocampal pathway and leads to learning and memory impairments. The aim of this study was to examine the neuroprotective effects of the Hc-TeTx fragment against cholinotoxicity. The Hc-TeTx fragment (100 ng) was injected into the rats intercranially, with the Aß(25-35) (2 µg) then injected into their MS. The animals were tested for spatial learning and memory in the eight-arm radial maze. The brains were removed to assess cholinergic markers, such as choline acetyltransferase (ChAT) and acetylcholinesterase (AChE), and to explore neurodegeneration in the MS and hippocampus, using amino-cupric silver and H&E staining. Finally, capase-3, a marker of apoptosis, was examined in the MS. Our results clearly demonstrate that the application of Hc-TeTx prevents the loss of cholinergic markers (ChAT and AChE), the activation of capase-3, and neurodegeneration in the MS and the CA1 and CA3 subfields of the hippocampus. All these improvements were reflected in spatial learning and memory performance, and were significantly higher compared with animals treated with Aß(25-35). Interestingly, the single administration of Hc-TeTx into the MS modified the ChAT and AChE expression that affect cognitive processes, without inducing neurodegeneration or an increase in capase-3 expression in the MS and hippocampus. In summary, our findings suggest that the recombinant Hc-TeTx fragment offers effective protection for the septo-hippocampal pathway, given that it reduces the neurodegeneration caused by Aß(25-35) and improves learning and memory processes.
Assuntos
Peptídeos beta-Amiloides/toxicidade , Fármacos Neuroprotetores/farmacologia , Fragmentos de Peptídeos/farmacologia , Toxina Tetânica/farmacologia , Acetilcolinesterase/metabolismo , Animais , Caspase 3/metabolismo , Colina O-Acetiltransferase/metabolismo , Hipocampo/efeitos dos fármacos , Hipocampo/metabolismo , Hipocampo/patologia , Imuno-Histoquímica , Masculino , Aprendizagem em Labirinto/efeitos dos fármacos , Aprendizagem em Labirinto/fisiologia , Nootrópicos/farmacologia , Fragmentos de Peptídeos/toxicidade , Distribuição Aleatória , Ratos Wistar , Septo do Cérebro/efeitos dos fármacos , Septo do Cérebro/metabolismo , Septo do Cérebro/patologia , Memória Espacial/efeitos dos fármacos , Memória Espacial/fisiologiaRESUMO
Several studies in rodents have shown that dysfunctions of the thalamic reticular nucleus (TRN) result in deficits of sensory gating and attentional processes, two core features of schizophrenia. TRN receives inputs from the prefrontal cortex (PFC) and hippocampal formation, two structures which send excitatory projections to the nucleus accumbens (NAcc) and are interconnected with the basolateral amygdala (BLA). Here we determined whether (and which) changes occurred four weeks after a TRN lesion in the dendritic morphology of pyramidal neurons of layers 3 and 5 of the PFC, neurons of ventral and dorsal hippocampus, BLA, and the medium spiny neurons of the NAcc. Dendritic morphology and characteristics were measured by using Golgi-Cox procedure followed by Sholl analysis. We also evaluated the effects of TRN lesion on exploratory behavior assessed by hole-board test and locomotor activity induced by a novel environment. We found that TRN damage induced a reduction in the exploratory behavior measured by hole-board test with neuronal hypotrophy in PFC (layer 5), CA1 ventral hippocampus and NAcc neurons. Taken together, these data suggest that the behavioral and morphological effects of TRN lesion are, at least partially, mediated by limbic subregions with possible consequences for schizophrenia-related behaviors.