January 2012

Current Related Research

The abolishment of anesthesia-induced cognitive impairment by timely protection of mitochondria in the developing rat brain: The importance of free oxygen radicals and mitochondrial integrity

Early exposure to general anesthesia (GA) causes developmental neuroapoptosis in the mammalian brain and long-term cognitive impairment. Recent evidence suggests that GA also causes functional and morphological impairment of the immature neuronal mitochondria. Injured mitochondria could be a significant source of reactive oxygen species (ROS), which, if not scavenged in timely fashion, may cause excessive lipid peroxidation and damage of cellular membranes. This study examines whether early exposure to GA results in ROS upregulation and whether mitochondrial protection and ROS scavenging prevent GA-induced pathomorphological and behavioral impairments. Read More

Ketamine-induced neuroapoptosis in the fetal and neonatal rhesus macaque brain

Exposure of rhesus macaque fetuses for 24 h or neonates for 9 h to ketamine anesthesia causes neuroapoptosis in the developing brain. The current study clarifies the minimum exposure required for and the extent and spatial distribution of ketamine-induced neuroapoptosis in rhesus fetuses and neonates. Read More

Propofol neurotoxicity is mediated by p75 neurotrophin receptor activation

Propofol exposure to neurons during synaptogenesis results in apoptosis, leading to cognitive dysfunction in adulthood. Previous work from the authors’ laboratory showed that isoflurane neurotoxicity occurs through p75 neurotrophin receptor (p75NTR) and subsequent cytoskeleton depolymerization. Given that isoflurane and propofol both suppress neuronal activity, we hypothesized that propofol also induces apoptosis in developing neurons through p75NTRRead More

Protective function of nicotinamide against ketamine-induced apoptotic neurodegeneration in the infant rat brain

During development, anesthetics activate neuroapoptosis and produce damage in the central nervous system that leads to several types of neurological disorders. A single dose of ketamine (40 mg/kg) during synaptogenesis in a 7-day-old rat brain activated the apoptotic cascade and caused extensive neuronal cell death in the forebrain. In this study, we investigated the protective effect of nicotinamide against ketamine-induced apoptotic neurodegeneration. Read More

Effects of metabotropic glutamate receptor 7 allosteric agonist N,N’-dibenzhydrylethane-1,2-diamine dihydrochloride on developmental sevoflurane neurotoxicity: role of extracellular signal-regulated kinase 1 and 2 Mitogen-activated protein kinase signaling pathway

The present study was designed to evaluate the possible neuroprotective effects of metabotropic glutamate receptor (mGluR7) allosteric agonist N,N’-dibenzhydrylethane-1,2-diamine dihydrochloride (AMN082) on developmental sevoflurane neurotoxicity. Read More

Upcoming Events

EURO-NEURO 2012: 7th International Update on Interdisciplinary Neuroscience

February 16-18, 2012, 
Vienna, Austria
Related Sessions

• Neuroprotection and Neurotoxicity

World Congress of Anesthesiologists

March 25-30, 2012,
 Buenos Aires, Argentina
Related Sessions

• Mechanisms of Perioperative Neurotoxicity
• Perioperative Cognitive Dysfunction

International Anesthesia Research Society 2012 Annual Meeting

May 18-21, 2012, Boston, Massachusetts
Related Sessions

• Pediatric Anesthesia Neurotoxicity
• Pediatric Anesthesia: Little People with Lots of Problems!
• Developmental Neurotoxicity: Are the Narcotics Safe?