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1.
Synapse ; 78(4): e22304, 2024 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-38896000

RESUMO

The goal of this report is to explore how K2P channels modulate axonal excitability by using the crayfish ventral superficial flexor preparation. This preparation allows for simultaneous recording of motor nerve extracellular action potentials (eAP) and intracellular excitatory junctional potential (EJP) from a muscle fiber. Previous pharmacological studies have demonstrated the presence of K2P-like channels in crayfish. Fluoxetine (50 µM) was used to block K2P channels in this study. The blocker caused a gradual decline, and eventually complete block, of motor axon action potentials. At an intermediate stage of the block, when the peak-to-peak amplitude of eAP decreased to ∼60%-80% of the control value, the amplitude of the initial positive component of eAP declined at a faster rate than that of the negative peak representing sodium influx. Furthermore, the second positive peak following this sodium influx, which corresponds to the after-hyperpolarizing phase of intracellularly recorded action potentials (iAP), became larger during the intermediate stage of eAP block. Finally, EJP recorded simultaneously with eAP showed no change in amplitude, but did show a significant increase in synaptic delay. These changes in eAP shape and EJP delay are interpreted as the consequence of depolarized resting membrane potential after K2P channel block. In addition to providing insights to possible functions of K2P channels in unmyelinated axons, results presented here also serve as an example of how changes in eAP shape contain information that can be used to infer alterations in intracellular events. This type of eAP-iAP cross-inference is valuable for gaining mechanistic insights here and may also be applicable to other model systems.


Assuntos
Potenciais de Ação , Astacoidea , Axônios , Fluoxetina , Neurônios Motores , Animais , Astacoidea/efeitos dos fármacos , Astacoidea/fisiologia , Fluoxetina/farmacologia , Potenciais de Ação/efeitos dos fármacos , Potenciais de Ação/fisiologia , Neurônios Motores/efeitos dos fármacos , Neurônios Motores/fisiologia , Axônios/efeitos dos fármacos , Axônios/fisiologia
2.
Cortex ; 161: 51-64, 2023 04.
Artigo em Inglês | MEDLINE | ID: mdl-36905701

RESUMO

The prevalence of developmental prosopagnosia (DP), lifelong face recognition deficits, is widely reported to be 2-2.5%. However, DP has been diagnosed in different ways across studies, resulting in differing prevalence rates. In the current investigation, we estimated the range of DP prevalence by administering well-validated objective and subjective face recognition measures to an unselected web-based sample of 3116 18-55 year-olds and applying DP diagnostic cutoffs from the last 14 years. We found estimated prevalence rates ranged from .64-5.42% when using a z-score approach and .13-2.95% when using a percentile approach, with the most commonly used cutoffs by researchers having a prevalence rate of .93% (z-score, .45% when using percentiles). We next used multiple cluster analyses to examine whether there was a natural grouping of poorer face recognizers but failed to find consistent grouping beyond those with generally above versus below average face recognition. Lastly, we investigated whether DP studies with more relaxed diagnostic cutoffs were associated with better performance on the Cambridge Face Perception Test. In a sample of 43 studies, there was a weak nonsignificant association between greater diagnostic strictness and better DP face perception accuracy (Kendall's tau-b correlation, τb =.18 z-score; τb = .11 percentiles). Together, these results suggest that researchers have used more conservative DP diagnostic cutoffs than the widely reported 2-2.5% prevalence. We discuss the strengths and weaknesses of using more inclusive cutoffs, such as identifying mild and major forms of DP based on DSM-5.


Assuntos
Reconhecimento Facial , Prosopagnosia , Humanos , Prosopagnosia/diagnóstico , Prosopagnosia/epidemiologia , Prosopagnosia/complicações , Prevalência , Reconhecimento Psicológico , Análise por Conglomerados , Reconhecimento Visual de Modelos
3.
Acta Trop ; 143: 47-50, 2015 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-25553972

RESUMO

Chagas disease is an endemic, neglected tropical disease in Latin America that is caused by the protozoan parasite Trypanosoma cruzi. In vitro models constitute the first experimental approach to study the physiopathology of the disease and to assay potential new trypanocidal agents. Here, we report and describe clearly the use of commercial software (MATLAB(®)) to quantify T. cruzi amastigotes and infected mammalian cells (BeWo) and compared this analysis with the manual one. There was no statistically significant difference between the manual and the automatic quantification of the parasite; the two methods showed a correlation analysis r(2) value of 0.9159. The most significant advantage of the automatic quantification was the efficiency of the analysis. The drawback of this automated cell counting method was that some parasites were assigned to the wrong BeWo cell, however this data did not exceed 5% when adequate experimental conditions were chosen. We conclude that this quantification method constitutes an excellent tool for evaluating the parasite load in cells and therefore constitutes an easy and reliable ways to study parasite infectivity.


Assuntos
Doença de Chagas/parasitologia , Carga Parasitária/métodos , Trypanosoma cruzi/patogenicidade , Animais , Contagem de Células/métodos , Técnicas de Cultura de Células , Chlorocebus aethiops , Técnicas In Vitro , Software
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