An expanded task battery in the Morris water maze reveals effects of Toxoplasma gondii infection on learning and memory in rats.

Infection with the neurotropic parasite Toxoplasma gondii is widespread among human populations; however, the impacts of latent central nervous system (CNS) T. gondii infection have only recently come to light. Epidemiological evidence in humans and experimental studies in rodents have revealed a number of neurological and behavioral sequelae following the establishment of latent CNS toxoplasmosis. Here, we report alterations in learning and memory task performance in latently infected rats using the Morris water maze. While simple spatial reference learning was intact, infected rodents exhibited poor performance compared to controls in probe trials requiring spatial memory recall and progressively poorer performance with increasing time intervals before memory testing, but, surprisingly, enhanced performance in reversal learning tasks. Despite obvious changes to memory task performance, no cysts were detected in the hippocampi of infected rats. Instead, cysts were stochastically distributed across the entire brain, suggesting that behavioral alterations in this study were due to accumulated changes in neurophysiology across multiple anatomical regions. Together, these data provide new evidence that latent toxoplasmosis contributes to neurocognitive symptoms in mammalian hosts, and does so on a broad anatomical scale within the CNS.

Professional Autonomy in Medicine: Defending the Right of Conscience in Health Care beyond the Right to Religious Freedom.

Health-care professionals currently have the right to conscientiously object to any procedure that they deem as morally illicit or that, in their opinion, could harm the patient. However, the right of conscientious refusal in medicine is currently under severe scrutiny. Medical procedures such as abortion and physician-assisted suicide that are not commonly medically indicated, but that can be requested by the patient, represent a type of medical care that is the penultimate expression of patient autonomy. When a health-care provider exercises his or her conscience in a way that denies the patient immediate access to such procedures, many claim that patient autonomy has been oppressed by the religious convictions of the health-care professional. As such, there is a growing opposition to the protection of conscience rights in health care that deserves attention. A common strategy used to defend conscience rights has been to claim that under the United States Bill of Rights, the health-care professional must be allowed to exercise their religious liberties in the context of their profession. This rationale seems to ignite a more intense opposition to conscience rights as it seems to validate the sense that a health-care professional's religious convictions are protected at the cost of patient autonomy. This paper reviews the current status of this debate and proposes a defense of conscience rights in health care that considers both the autonomy of the health-care worker and that of the patient in the context of the patient-physician relationship.

NMDA-induced phosphorylation and regulation of mGluR5.

Glutamate regulates neuronal function by acting on ionotropic receptors such as the N-methyl-D-aspartate (NMDA) receptor and metabotropic receptors (mGluRs). We have previously shown that low concentrations of NMDA are able to significantly potentiate mGluR5 responses via activation of a protein phosphatase and reversal of phosphorylation-induced desensitization. While low concentrations of NMDA are able to potentiate mGluR5 responses, higher concentrations of NMDA are actually inhibitory. In this report, we show that NMDA receptors and mGluR5 are highly colocalized in cortical regions. We also show that in voltage-clamp recordings obtained from Xenopus oocytes expressing mGluR5 and NMDA receptors, high concentrations of NMDA (50-100 microM) that elicited large currents (>400 nA) caused an inhibition of mGluR5 currents. Additionally, agonist-induced phosphoinositide hydrolysis presumably mediated by activation of mGluR5, is inhibited by NMDA (30 microM and above). Additional data presented in this report suggest that the inhibitory effect of NMDA is caused by phosphorylation of mGluR5 at protein kinase C (PKC) sites since NMDA induces phosphorylation of the receptor as measured in a back phosphorylation assay.