Reviving a failing sense of smell through training

January, 2012

A rat study reveals how training can improve or impair smell perception.

The olfactory bulb is in the oldest part of our brain. It connects directly to the amygdala (our ‘emotion center’) and our prefrontal cortex, giving smells a more direct pathway to memory than our other senses. But the olfactory bulb is only part of the system processing smells. It projects to several other regions, all of which are together called the primary olfactory cortex, and of which the most prominent member is the piriform cortex. More recently, however, it has been suggested that it would be more useful to regard the olfactory bulb as the primary olfactory cortex (primary in the sense that it is first), while the piriform cortex should be regarded as association cortex — meaning that it integrates sensory information with ‘higher-order’ (cognitive, contextual, and behavioral) information.

Testing this hypothesis, a new rat study has found that, when rats were given training to distinguish various odors, each smell produced a different pattern of electrical activity in the olfactory bulb. However, only those smells that the rat could distinguish from others were reflected in distinct patterns of brain activity in the anterior piriform cortex, while smells that the rat couldn’t differentiate produced identical brain activity patterns there. Interestingly, the smells that the rats could easily distinguish were ones in which one of the ten components in the target odor had been replaced with a new component. The smells they found difficult to distinguish were those in which a component had simply been deleted.

When a new group of rats was given additional training (8 days vs the 2 days given the original group), they eventually learned to discriminate between the odors the first animals couldn’t distinguish, and this was reflected in distinct patterns of brain activity in the anterior piriform cortex. When a third group were taught to ignore the difference between odors the first rats could readily distinguish, they became unable to tell the odors apart, and similar patterns of brain activity were produced in the piriform cortex.

The effects of training were also quite stable — they were still evident after two weeks.

These findings support the idea of the piriform cortex as association cortex. It is here that experience modified neuronal activity. In the olfactory bulb, where all the various odors were reflected in different patterns of activity right from the beginning (meaning that this part of the brain could discriminate between odors that the rat itself couldn’t distinguish), training made no difference to the patterns of activity.

Having said that, it should be noted that this is not entirely consistent with previous research. Several studies have found that odor training produces changes in the representations in the olfactory bulb. The difference may lie in the method of neural recording.

How far does this generalize to the human brain? Human studies have suggested that odors are represented in the posterior piriform cortex rather than the anterior piriform cortex. They have also suggested that the anterior piriform cortex is involved in expectations relating to the smells, rather than representing the smells themselves. Whether these differences reflect species differences, task differences, or methodological differences, remains to be seen.

But whether or not the same exact regions are involved, there are practical implications we can consider. The findings do suggest that one road to olfactory impairment is through neglect — if you learn to ignore differences between smells, you will become increasingly less able to do so. An impaired sense of smell has been found in Alzheimer’s disease, Parkinson's disease, schizophrenia, and even normal aging. While some of that may well reflect impairment earlier in the perception process, some of it may reflect the consequences of neglect. The burning question is, then, would it be possible to restore smell function through odor training?

I’d really like to see this study replicated with old rats.

Reference: 

Related News

In the first mouse study, when young and old mice were conjoined, allowing blood to flow between the two, the young mice showed a decrease in

In a small study, 266 older adults with mild cognitive impairment (aged 70+) received a daily dose of 0.8 mg folic acid, 0.5 mg vitamin B12 and 20 mg vitamin B6 or a placebo for two years.

Comparison of 99 chimpanzee brains ranging from 10-51 years of age with 87 human brains ranging from 22-88 years of age has revealed that, unlike the humans, chimpanzee brains showed no sign of shrinkage with age. But the answer may be simple: we live much longer.

A study involving 105 people with Alzheimer's disease and 125 healthy older adults has compared cognitive function and brain shrinkage in those aged 60-75 and those aged 80+.

A three-year study following 1,262 healthy older Canadians (aged 67-84) has found that, among those who exercised little, those who had high-salt diets showed significantly greater cognitive decline.

In my book on remembering what you’re doing and what you intend to do, I briefly discuss the popular strategy of asking someone to remind you (basically, whether it’s an effective strategy depends on several factors, of which the most important is the reliability of the person doing the remindin

A study comparing activity in the dorsolateral prefrontal cortex in young, middle-aged and aged m

Dietary changes affect levels of biomarkers associated with Alzheimer's

Sleep apnea linked to later dementia

A study involving 298 older women with sleep problems found that those who had disordered breathing (such as sleep apnea) were significantly more likely to develop dementia or mild cognitive impairment.

Functional impairment good indicator of mild cognitive impairment

Pages

Subscribe to Latest newsSubscribe to Latest newsSubscribe to Latest health newsSubscribe to Latest news