Synaptic physiology

Dendritic release of glutamate suppresses synaptic inhibition of pyramidal neurons in rat neocortex. Zilberter, Y. J. Physiol. 528 , 489–496 (2000) [PubMed]

Dendritic release of GABA can inhibit presynaptic glutamate release between pyramidal cells and bitufted interneurons in the neocortex. The story has now come full circle, as Zilberter shows that glutamate released from pyramidal cell dendrites can inhibit GABA release from fast-spiking interneurons by activation of presynaptic metabotropic glutamate receptors. As both examples of retrograde signalling would tend to favour excitation over inhibition in the cortex, it is possible that alterations of this process might contribute to the generation of epileptic activity.

Addiction

Reduced operant ethanol self-administration and in vivo mesolimbic dopamine responses to ethanol in PKCɛ-deficient mice.  Olive, M. F. et al. Eur. J. Neurosci. 12 , 4131–4140 (2000) [PubMed]

The authors explored the molecular mechanisms of ethanol reinforcement by studying the effects of a null mutation in PKCɛ. Mice lacking PKCɛ showed reduced ethanol self-administration. In addition, dopamine levels in the nucleus accumbens of the mutant mice were not increased by the acute administration of ethanol. These findings raise the possibility that selective PKCɛ antagonists could be used to treat alcohol abuse.

Memory

Auditory fear conditioning increases CS-elicited spike firing in lateral amygdala neurons even after extensive overtraining. Maren, S. Eur. J. Neurosci. 12 , 4047–4054 (2000) [PubMed]

The basolateral amygdala (BLA) is involved in the acquisition and storage of fear conditioning, but it is not clear whether BLA is a temporary or a permanent storage site. Maren overtrained rats in a fear-conditioning task and recorded action potential firing in the BLA upon presentation of the conditioned stimulus. Increase in firing commonly seen after conditioning also occurred in the overtrained animals, indicating that the BLA is indeed a long-lasting storage site of fear conditioning.

Neurodegeneration

Binding of disease-associated prion protein to plasminogen.  Fischer, M. B. et al. Nature 408 , 479–483 (2000) [PubMed]

The structural discrimination between PrPC and its abnormal variant PrPSc has remained problematic. The authors show that plasminogen can distinguish between the two proteins by binding selectively to PrPSc, and define some of the structural determinants that are important for binding. These data show that plasminogen could be used as a tool for the diagnosis of prion-related diseases.