Noradrenaline (NA) is a neurotransmitter found in various parts of the brain, including the hippocampus (an important centre for the creation of memories). It plays a vital role in controlling sleep patterns and levels of attention / awareness, and a lack of NA in the brain has been shown to cause a decrease in drive and motivation.

NA acts on a variety of receptors, including one type called the alpha 1b adrenergic receptor (a1b-AR). Studies have shown that too many a1b-ARs in the brain can lead to conditions such as drug addiction and the degeneration of neurons (hence brain damage). It has also been associated with the development of spontaneous seizures.

More research is needed into precisely how these consequences come about, and if they have any bearing on each other; but these findings suggest that if a1b-ARs are somehow stopped from functioning, seizures will be prevented and neurons will be protected from degeneration.

It was previously difficult to test this theory, because there are no drugs that effectively block a1b-ARs. However scientists have now managed to breed mice that do not have any a1b-ARs at all. In effect, the gene for a1b-ARs has been 'knocked out', so we will refer to these mice as KO. Mice have a very similar genetic make-up to humans, so they have a pivotal role in medical research.

In a recent study, a team from the University of Pisa exposed a group of KOs to two seizure-causing substances known as kinate and pilocarpine. They then measured their susceptibility to seizures and neurodegeneration.

The KOs resisted seizures completely when given a standard dose of either chemical, which is exactly what was expected.

When the scientists doubled the dose of kinate or pilocarpine given, they found that both caused severe and prolonged seizures. The lack of a1b-ARs had not, therefore, prevented seizures completely, but had raised the threshold at which they occurred. When they did take place, however, they were more serious and lasted longer than predicted. Presumably, the spontaneous seizures seen with excess a1b-ARs are partly due to this threshold being considerably lowered.

Interestingly, despite these seizures, the KOs showed no signs of neurodegeneration.

Put together these results suggest that a1b-ARs play a key role in controlling the onset, length and severity of seizures. Blocking a1b-ARs raises the threshold of neurological activity at which seizures take place, making them less likely to occur. It will also protect neurons from degeneration. The fact that this 'neuro-protective' trait remained even after severe seizures, indicates that the neurodegeneration seen where there are too many a1b-ARs is not a result of the spontaneous seizures that can also occur. As mentioned earlier, a lot more research is needed into precisely how these consequences of excess a1b-ARs come about.

These results are very promising. If they are consistent in humans, the a1b-AR will become a new target for the development of drugs; not only to curb seizures, but to prevent some cases of brain damage.

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