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The onset of puberty is a concerted action of many factors which leads to cyclic LHRH release in rats. It has been demonstrated that; in common with vasoactive intestinal polypeptide (VIP), pituitary adenylate cyclase activating polypeptide (PACAP) is also involved in the differentiation of the central nervous system. In our previous work, it was shown that a single PACAP injection into neonatal female rats delayed puberty. In the present work, neonatal administration of PACAP delayed the vaginal opening and decreased the weight of anterior pituitaries, the number of expelled ova at the first ovulation and the intensity of LHRH immunostaining in the septo–preoptico–infundibular system. PACAP antiserum had a reverse effect on LHRH immunoreactivity. The other studied parameters in the latter group remained unchanged compared to control rats. It was concluded that neonatal PACAP administration delayed the onset of puberty through the influence of the LHRH neuronal system. [Copyright &y& Elsevier]

Abstract: The analysis of the auditory scene begins from the moment we hear sounds, making it possible for the infant to distinguish the mother’s voice from other sounds in the environment. The purpose of the study was to determine, in two experiments, whether the frequency separation threshold, at which the perception of a mixture of sounds turns from being perceived as one stream to two streams, differs between two groups of school-aged children (ages 5–8 and 9–11 years) and adults. The results show a developmental course for the perception of auditory streams that is not simply dependent upon frequency discrimination. This suggests that maturation of the stream segregation process follows a longer developmental course than maturation of simple feature discrimination. The data indicate that the ability to hear distinct sound streams in the environment takes time to develop and becomes sharpened with experience and maturity. [Copyright &y& Elsevier]

Abstract: Alzheimer’s disease is characterized by the presence of senile plaques in the brain, composed mainly of aggregated amyloid-β peptide (Aβ), which plays a central role in the pathogenesis of Alzheimer’s disease and is a potential target for therapeutic intervention. Amyloid plaques occur in an increasing number of brain structures during the progression of the disease, with a heavy load in regions of the temporal cortex in the early phases. Here, we investigated the cognitive deficits specifically associated with amyloid pathology in the entorhinal cortex. The amyloid peptide Aβ1–42 was injected bilaterally into the entorhinal cortex of rats and behavioral performance was assessed between 10 and 17 days after injection. We found that parameters of motor behavior in an open-field as well as spatial working memory tested in an alternation task were normal. In contrast, compared with naive rats or control rats injected with saline, rats injected with Aβ1–42 showed impaired recognition memory in an object recognition task and delayed acquisition in a spatial reference memory task in a water-maze, despite improved performance with training in this task and normal spatial memory in a probe test given 24 h after training. This profile of behavioral deficits after injection of Aβ1–42 into the entorhinal cortex was similar to that observed in another group of rats injected with the excitotoxic drug, N-methyl-d-aspartate. Immunohistochemical analysis after behavioral testing revealed that Aβ1–42 injection induced a reactive astroglial response and plaque-like deposits in the entorhinal cortex. These results show that experimentally-induced amyloid pathology in the entorhinal cortex induces selective cognitive deficits, resembling those observed in early phases of Alzheimer’s disease. Therefore, injection of protofibrillar-fibrillar Aβ1–42 into the entorhinal cortex constitutes a promising animal model for investigating selective aspects of Alzheimer’s disease and for screening drug candidates designed against Aβ pathology. [Copyright &y& Elsevier]