April 5 : Nicotine-based drugs to treat cognitive deficits in Alzheimer’s and Parkinson’s diseases, schizophrenia, and attention-deficit/hyperactivity disorder may have come closer to reality, thanks to researchers who have found the mechanism behind nicotine’s helpfulness in enhancing memory.

The study was conducted by researchers at Vrije Universiteit Amsterdam in Amsterdam, the Netherlands.

Nicotine, which is highly addictive, has also been known to enhance learning and memory. A key problem in designing such drugs has been that little was known about the detailed mechanism by which nicotine exerts its learning-enhancing effects.

Researchers have now discovered important details of how nicotine adjusts the signaling properties of neuronal wiring to enhance memory. Such signaling properties include the strength of the connections by which one neuron triggers another.

As part of the study, researchers analyzed the electrophysiological properties of neurons in slices of mouse brain, as they treated the slices with nicotine or with drugs that prevent nicotine’s action. Specifically, the researchers studied the neurons of the prefrontal cortex, which contain centers for learning and memory.

Researchers found that by activating acetylcholine receptors, nicotine affects a process called “spike-timing-dependent potentiation” that governs changes in strength of signaling connections among neurons.

The researchers also traced this effect to nicotine’s action on specific kinds of neurons, called GABAergic neurons, in the learning centers. In turn, the effects on GABAergic neurons affected signaling between neurons mediated by the key substance calcium.

Key details of the mechanisms by which nicotine excites different kinds of “interneurons” in the prefrontal cortex were also found by the researchers

Interneurons are the way-stations for neuronal impulses, passing neuronal signals from one neuron to another.

The findings of the research were published in the April 2007, issue of the journal Neuron, published by Cell Press. (ANI)