Estradiol and luteinizing hormone regulate recognition memory following subchronic phencyclidine: Evidence for hippocampal GABA action.

The cognitive symptoms of schizophrenia are poorly understood and difficult to treat. Estrogens may mitigate these symptoms via unknown mechanisms. To examine these mechanisms, we tested whether increasing estradiol (E) or decreasing luteinizing hormone (LH) could mitigate short-term episodic memory loss in a phencyclidine (PCP) model of schizophrenia.

ERIN: A Portal to Resources for Higher Education in Neuroscience.

ERIN, Educational Resources in Neuroscience, is the Society for Neuroscience's web portal to selected, high-quality materials for higher education. A Board of Editors approves resources after describing them and classifying them by topic, subtopic, media type, author, and appropriate educational level. Some resources are also accompanied by reviews and ratings from faculty who have used the resource.

Luteinizing hormone as a key player in the cognitive decline of Alzheimer's disease.

This article is part of a Special Issue "SBN 2014". Alzheimer's disease is one of the most prevalent and costly neurological diseases in the world. Although decades of research have focused on understanding Alzheimer's disease pathology and progression, there is still a great lack of clinical treatments for those who suffer from it.

Identifying and using 'core competencies' to help design and assess undergraduate neuroscience curricula.

There has been a growing emphasis on the use of core competencies to design and inform curricula. Based on our Faculty for Undergraduate Neuroscience workshop at Pomona we developed a set of neuroscience core competencies. Following the workshop, faculty members were asked to complete an online survey to determine which core competencies are considered most essential and the results are presented.

Estradiol attenuates the cognitive deficits in the novel object recognition task induced by sub-chronic phencyclidine in ovariectomized rats.

Clinical studies have suggested that estrogens may affect the symptoms of schizophrenia. The novel object recognition task (NORT) in female rats treated with sub-chronic phencyclidine (PCP) was used as an animal model of the cognitive deficits in schizophrenia. The current studies investigated whether chronic estradiol (E) could alleviate sub-chronic PCP-induced cognitive deficits in the NORT.

The role of testicular hormones and luteinizing hormone in spatial memory in adult male rats.

Attempts to determine the influence of testicular hormones on learning and memory in males have yielded contradictory results. The present studies examined whether testicular hormones are important for maximal levels of spatial memory in young adult male rats. To minimize any effect of stress, we used the Object Location Task which is a spatial working memory task that does not involve food or water deprivation or aversive stimuli for motivation.

Low luteinizing hormone enhances spatial memory and has protective effects on memory loss in rats.

Though several studies have suggested that estradiol improves hippocampal-dependent spatial memory, the effects of other hormones in the hypothalamic-pituitary-gonadal axis on memory have largely been ignored. Estradiol and luteinizing hormone (LH) are generally inversely related and LH may significantly affect spatial memory. Ovariectomized (ovx) rats treated with Antide (a gonadotropin releasing hormone receptor antagonist) had low LH levels and showed enhanced spatial memory, comparable to treatment with estradiol.

Dihydrotestosterone increases hippocampal N-methyl-D-aspartate binding but does not affect choline acetyltransferase cell number in the forebrain or choline transporter levels in the CA1 region of adult male rats.

Testosterone, acting through its androgenic metabolite 5alpha-dihydrotestosterone (DHT), can increase dendritic spine density in the CA1 region of the male rat hippocampus. The mechanisms mediating this increase in spines are presently unknown. In female rats, estrogen (E) has been shown to increase spine density, which is in part mediated by increases in N-methyl-d-aspartate (NMDA) receptors in the CA1 region and cholinergic forebrain inputs to the hippocampus.