ß2-adrenergic receptors protect axons during energetic stress but do not influence basal glio-axonal lactate shuttling in mouse white matter.

In vitro studies have demonstrated that ß2-adrenergic receptor activation stimulates glycogen degradation in astrocytes, generating lactate as a potential energy source for neurons. Using in vivo microdialysis in mouse cerebellar white matter we demonstrate continuous axonal lactate uptake and glial-axonal metabolic coupling of glutamate/lactate exchange. However, this physiological lactate production was not influenced by activation (clenbuterol) or blocking (ICI 118551) of ß2-adrenergic receptors. In two-photon imaging experiments on ex vivo mouse corpus callosum subjected to aglycemia, ß2-adrenergic activation rescued axons, whereas inhibition of axonal lactate uptake by α-cyano-4-hydroxycinnamic acid (4-CIN) was associated with severe axonal loss. Our results suggest that axonal protective effects of glial ß2-adrenergic receptor activation are not mediated by enhanced lactate production.

A spectroelectrochemical study of the reduction of a Schiff base cryptand.

The electrochemical reduction of a bicyclic hexaimino Schiff base cryptand 1 (N[(CH2)2N-CH-meta-C6H4-CH=N(CH2)2]3N) and that of one of its strands 2 ((CH3)2CH-N=CH-meta-C6H4-CH=N-CH(CH3)2) has been studied by visible and near infrared in-situ spectroelectrochemical techniques. These results are in good agreement with those obtained using alkali metals, but in this case the effect of the formation of ion pairs is minimized through the use of tetrabutylammonium cations. It is confirmed that 1- and 1= have the same visible and near IR spectrum. The spectrum of the products of the electrochemical reduction of 2 is similar to those of 1- or 1=.