Learning and memory deficits consequent to reduction of the fragile X mental retardation protein result from metabotropic glutamate receptor-mediated inhibition of cAMP signaling in Drosophila.

Loss of the RNA-binding fragile X protein [fragile X mental retardation protein (FMRP)] results in a spectrum of cognitive deficits, the fragile X syndrome (FXS), while aging individuals with decreased protein levels present with a subset of these symptoms and tremor. The broad range of behavioral deficits likely reflects the ubiquitous distribution and multiple functions of the protein. FMRP loss is expected to affect multiple neuronal proteins and intracellular signaling pathways, whose identity and interactions are essential in understanding and ameliorating FXS symptoms.

Neuralized is expressed in the alpha/beta lobes of adult Drosophila mushroom bodies and facilitates olfactory long-term memory formation.

Memory formation involves multiple molecular mechanisms, the nature and components of which are essential to understand these processes. Drosophila is a powerful model to identify genes important for the formation and storage of consolidated memories because the molecular mechanisms and dependence of these processes on particular brain regions appear to be generally conserved. We present evidence that the highly conserved ubiquitin ligase Neuralized (Neur) is expressed in the adult Drosophila mushroom body (MB) alpha/beta lobe peripheral neurons and is a limiting factor for the formation of long-term memory (LTM).

Characterisation of the calcium paradox in the isolated perfused pigeon heart: protection by hypothermia, acidosis and alkalosis.

The aim of the present investigation was to examine the conditions inducing a calcium paradox in the isolated perfused pigeon heart. Loss of mechanical and electrical activity, creatine phosphokinase and total protein release were used to define cell damage. Perfusion was performed at 36, 38, 40 and 42 degrees C and calcium deprivation lasted 5, 10, 20 or 40 min.