Incubation in shaded hatcheries biases sex-determination but preserves Lepidochelys olivacea hatchling physiology.

Some studies have associated ex situ conservation with cerebral and gonadal developmental delay, as well as decreased motor performance in Lepidochelys olivacea offspring. Ex situ management is also related to a more mature spleen and a differential leukocyte count in newly emerged Lepidochelys olivacea hatchlings. The physiological relevance of a more mature spleen is unknown in sea turtles, but studies in birds suggest an increased immune response. Because egg relocation to hatcheries is a common conservation practice, it is imperative to know its impact on hatchling physiology. Herein, plasma activity of superoxide dismutase, alkaline phosphatase and the alternative complement pathway, as well as total antioxidant capacity and hydrogen peroxide concentrations were quantified in hatchlings from in situ and ex situ nests under basal conditions at nest emergence. Toll-like receptor 4 (tlr4), heat shock proteins (hsp) 70 and hsp90 expression were quantified in the spleen and liver of the hatchlings. Hepatocyte density and nuclear area were quantified in histological sections of the liver and all turtles were sexed by histological sectioning of the gonads. Total antioxidant capacity and hydrogen peroxide concentrations in plasma were lower in turtles from ex situ nests, while tlr4 and hsp70 mRNA expression was higher in the spleen but not in the liver. Ex situ incubation produced 98% male hatchlings, whereas in situ incubation produced 100% females. There were no other differences in the attributes sampled between hatchlings emerging from ex situ and in situ treatments. The results suggest that ex situ relocated turtles may be less prone to oxidative stress than in situ incubated hatchlings and could have more mature splenic function. Together, the data suggest that ex situ relocation to shaded hatcheries biased sex determination but preserved the general physiological condition of sea turtle hatchlings.

Short communication: Ex-situ conservation in hatcheries is associated with spleen development in Lepidochelys olivacea turtle hatchlings.

Ex-situ conservation in hatcheries is a successful strategy for the recovery of sea turtle populations. However, it alters the ontogenesis of the brain and gonads, as well as body size and locomotor performance at nest emergence. Relocation to hatcheries may alter immune system development, since this depends highly on the nest environment. We hypothesized that ex-situ brooding would negatively associate with immune traits of Lepidochelys olivacea. Splenic cytoarchitecture and leukocyte quantification were used as proxies for the immune configuration. Body size, gonadal sex and sand temperature during incubation were determined. Additionally, the success of nest hatching and emergence was quantified. Linear mixed models of splenic cytoarchitecture, leucocyte proportions and body size, using sex and nest type as explanatory variables, evaluated the effects of ex-situ brooding. Generalized linear mixed models using quasibinomial distributions (log link) analyzed effects on hatching and emergence success. Hatchlings from ex-situ nests were heavier, larger and showed a greater spleen-somatic index. They showed more and better defined splenic periarteriolar lymphoid sheaths, as well as a higher proportion of heterophils but less monocytes. Moreover, ex-situ brooding increased hatching and emergence success. Sand temperatures in hatcheries favored male sex determination, while the opposite occurred for in-situ incubation. Interestingly, the immune configuration and body size were independent of sex but associated with ex-situ conservation. Greater body size promotes early hatchling survival, while better spleen development is related to a greater antibody production and a better immune response to pathogens. Altogether, the results suggest that ex-situ incubation is associated with a better immune configuration and higher survival success.

Synaptic Vesicle Protein 2A Expression in Glutamatergic Terminals Is Associated with the Response to Levetiracetam Treatment.

Synaptic vesicle protein 2A (SV2A), the target of the antiepileptic drug levetiracetam (LEV), is expressed ubiquitously in all synaptic terminals. Its levels decrease in patients and animal models of epilepsy. Thus, changes in SV2A expression could be a critical factor in the response to LEV. Epilepsy is characterized by an imbalance between excitation and inhibition, hence SV2A levels in particular terminals could also influence the LEV response. SV2A expression was analyzed in the epileptic hippocampus of rats which responded or not to LEV, to clarify if changes in SV2A alone or together with glutamatergic or GABAergic markers may predict LEV resistance. Wistar rats were administered saline (control) or pilocarpine to induce epilepsy. These groups were subdivided into untreated or LEV-treated groups. All epileptic rats were video-monitored to assess their number of seizures. Epileptic rats with an important seizure reduction (>50%) were classified as responders. SV2A, vesicular γ-aminobutyric acid transporter and vesicular glutamate transporter (VGLUT) expression were assessed by immunostaining. SV2A expression was not modified during epilepsy. However, responders showed ≈55% SV2A-VGLUT co-expression in comparison with the non-responder group (≈40%). Thus, SV2A expression in glutamatergic terminals may be important for the response to LEV treatment.

Synaptic vesicle protein 2A: basic facts and role in synaptic function.

In recent years, there has been considerable interest in determining the function of synaptic vesicle protein 2A and its role as a target for antiepileptic drugs. Although it is known that synaptic vesicle protein 2A is involved in normal synaptic vesicle function, its participation in synaptic vesicle cycling and neurotransmitter release in normal and pathological conditions is unclear. However, the experimental evidence suggests that synaptic vesicle protein 2A could be a vesicular transporter, regulate synaptic exocytosis as a gel matrix, or modulate synaptotagmin-1 activity. This review describes and discusses the participation of synaptic vesicle protein 2A in synaptic modulation in normal and pathological conditions.