Primer describes current understanding of human taste perception and biology

Despite the significance of taste to both human gratification and survival, a basic understanding of this primal sense is still unfolding. Taste provides both pleasure and protection. Often taken for granted, the sense of taste evaluates everything humans put into their mouths. Taste mediates recognition of a substance and the final decision process before it is either swallowed and taken into the body, or rejected as inappropriate.

A new primer written by scientists at the Monell Center and Florida State University and published in the February 26 issue of Current Biology, provides a clear and accessible overview of recent advances in understanding human taste perception and its underlying biology.

Within the past few years, identification of receptors for sweet, bitter and umami (savory) taste has led to new insights regarding how taste functions, but many questions remain to be answered. The Current Biology primer reviews the current state of knowledge regarding how taste stimuli are detected and ultimately translated by the nervous system into the perceptual experiences of sweet, sour, salty, bitter, and umami.

Such perceptual evaluations are related to the function and ultimately, the consequences, of taste evaluation. These can range from pleasurable emotional reactions, for example the delight a child receives from a sweet candy, to the critical life-dependent response that causes a person to spit out a bitter potential toxin.

Author Paul A.S. Breslin, PhD, a sensory scientist at the Monell Center, observes, “For all mammals, the collective influence of taste over a lifetime has a huge impact on pleasure, health, well being, and disease. Taste’s importance to our daily lives is self-evident in its metaphors – for example: the ‘sweetness’ of welcoming a newborn child, the ‘bitterness’ of defeat, the ‘souring’ of a relationship, and describing a truly good human as the ‘salt’ of the earth.”

25 February 2008

Eric Chudler at Neuroscience for Kids has recently added Neuroscience on Stamps.

Scientific American -- Science Talk
(6 February 2008)

In this episode, University of California, Berkeley, linguist Alice Gaby talks about the relationships among language, culture, cognition and perception.

Queensland Brain Institute (QBI) scientists have found another important clue to why nerve cells die in neurodegenerative diseases, based on studies of the developing brain. Neuroscientists at The University of Queensland have just published findings, which add more weight to the "use it or lose it" model for brain function.

QBI's Dr Elizabeth Coulson said a baby's brain generates roughly double the number of nerve cells it needs to function; with those cells that receive both chemical and electrical stimuli surviving, and the remaining cells dying. In research published in the "Journal of Neuroscience", Dr Coulson and her colleagues have identified a crucial step in the cell-death process. "It appears that if a cell is not appropriately stimulated by other cells, it self-destructs," Dr Coulson said.

This self-destruct process is also known to be an important factor in stroke, Alzheimer's and motor neuron diseases, leading to the loss of essential nerve cells from the adult brain. "We know that a lack of both chemical and electrical stimuli causes the cells to self-destruct," Dr Coulson said. "But we believe that nerve cells will survive if appropriate electrical stimuli are produced to block the self-destruct process that we have identified." The researchers' next step is to test whether dying cells receiving only electrical stimulation can be rescued.

More than three years' research has gone into understanding these crucial factors regulating nerve cell survival, but it is a major step in the long process of discovery needed to combat neurodegeneration. QBI Director, Professor Perry Bartlett said the research is an extremely exciting finding because it also provides the missing piece of information as to how the brain likely keeps alive the new neurons it generates in some brain areas as an adult. "Combining this with our knowledge of how to stimulate new neurons in the brain of adults following to disease processes such as stroke, it provides new mechanisms for the treatment of a variety of diseases from depression to dementia," he said.

Very young brains process memories of fear differently than more mature ones, new research indicates. The findings appear in the Feb. 6 issue of The Journal of Neuroscience. The work significantly advances scientific understanding of when and how fear is stored and unlearned, and introduces new thinking on the implications of fear experience early in life.

“This important paper raises questions that are the ‘tip of the iceberg’ related to the very complex series of events that occur as we learn to fear something. In the real world, we become fearful, extinguish that fear, reacquire it at another time, and then conquer it yet again,” says John Krystal, MD, of Yale University and director of the clinical neuroscience division of the VA National Center for Post-Traumatic Stress Disorder. “Typically, we think about long-term, negative impact of fear learning, such as lifelong problems with anxiety. But this work highlights an avenue for adapting to early stresses that apparently can occur only early in life: to erase a learned fear from memory.” Krystal was not affiliated with the research.

Study co-authors Jee Hyun Kim and Rick Richardson, PhD, of the University of New South Wales in Sydney, homed in on the amygdala, using anesthesia to temporarily inactivate it and therefore isolate its role. The amygdala is critical for emotional learning and plays a central role in dulling the memory of a fear. Kim and Richardson trained rats that were 16 and 23 days old—the human equivalent of children and budding adolescents—to associate a specific sound with a mild shock to the foot. After subsequent training, when the sound was not followed by a shock, the animals’ fearful reaction to hearing the sound faded. Technically, this is known as “extinction,” and depended on the function of the amygdala.

In a second round of training, the researchers reintroduced the fear and tried to re-extinguish it. This time around, they found, only the older rats were able to do so without the amygdala. The researchers concluded that the age at which the initial extinction training occurred was critical to whether or not the rats’ fear faded the second time independently of the amygdala. The authors suggest that in the very young, it is primarily the amygdala that extinguishes fearful memories, but that mechanisms independent of the amygdala develop later.

This raises the possibility that fears unlearned at an early enough age are, in fact, erased. As brains develop, however, and related structures near the amygdala mature, these structures take on a greater role. Thus, fear in adolescence and later in life may not be erased, but instead be, for example, inhibited by a process of overlaying neutral memories on top of the initial fear reaction. The initial memory could still exist and be called on again. “Extinction in the young brain might forever erase early traumatic learning—but accepting this hypothesis will have to wait for more research,” says Mark Bouton, PhD, of the University of Vermont, who did not participate in the esearch. “What might change as the brain develops is where and how fear learning and extinction are stored and how they can be retrieved.”

In the first study to use imaging technology to see what goes on in the brain when we scratch, researchers at Wake Forest University Baptist Medical Center have uncovered new clues about why scratching may be so relieving – and why it can be hard to stop. The work is reported online in the Journal of Investigative Dermatology and will appear in a future print issue.

"Our study shows for the first time how scratching may relieve itch,” said lead author Gil Yosipovitch, M.D., a dermatologist who specializes in itch. “It’s important to understand the mechanism of relief so we can develop more effective treatments. For some people, itch is a chronic condition that affects overall health.” The study involved 13 healthy participants who underwent testing with functional magnetic resonance imaging (MRI) technology that highlights areas of the brain activated during an activity. Participants were scratched on the lower leg with a small brush. The scratching went on for 30 seconds and was then stopped for 30 seconds – for a total of about five minutes.

“To our surprise, we found that areas of the brain associated with unpleasant or aversive emotions and memories became significantly less active during the scratching,” said Yosipovitch. “We know scratching is pleasurable, but we haven’t known why. It’s possible that scratching may suppress the emotional components of itch and bring about its relief.” The reduced brain activity occurred in the anterior cingulate cortex, an area associated with aversion to unpleasant sensory experiences, and the posterior cingulate cortex, which is associated with memory. When participants reported that the scratching felt most intense, activation in these areas was lowest.

Yosipovitch said patients occasionally report that intense scratching – to the point of drawing blood – is the only thing that relieves chronic itch. “This is the first real scientific evidence showing that itch may be inhibited by scratching,” he said. “Of course, scratching is not recommended because it can damage the skin. But understanding how the process works could lead to new treatments. For example, drugs that deactivate this part of the brain might be effective.”

The imaging studies also showed that some areas of the brain were made more active by the scratching, including the secondary somatosensory cortex, a sensory area involved in pain, and the prefrontal cortex, which is associated with compulsive behavior. “This could explain the compulsion to continue scratching,” said Yosipovitch.

One drawback to the study is that the scratching occurred in the absence of itch. Yosipovitch’s team is continuing the research by evaluating whether the findings will apply to chronic itch. Understanding more about chronic itch is important, Yosipovitch said, noting that more than 30 million Americans suffer from eczema and that almost half (42 percent) of kidney dialysis patients are bothered by moderate to severe itch. In fact, those kidney dialysis patients with itch have a 17 percent higher mortality rate, likely from a loss of sleep, according to a report in Nephrology Dialysis Transplantation.


Wake Forest University Baptist Medical Center News
31 January 2008

Colorful, salty flame burns a chemical path to our hearts.
by Ted Alvarez at 60-Second Science
29 January 2008

Another crack at non-addictive opioids? Why we don't get hooked on our own endorphins.
by Maia Szalavitz at 60-Second Science
29 January 2008

Four days’ exposure to a REM sleep deprivation procedure reduces cell proliferation in the part of the forebrain that contributes to long-term memory of rats, according to a study published in the February 1 issue of the journal SLEEP. [abstract] The study, authored by Dennis McGinty, PhD, of the V.A. Greater Los Angeles Healthcare System, focused on male Sprague-Dawley rats.

REM sleep deprivation was achieved by a brief treadmill movement initiated by automatic online detection of REM sleep. A yoked-control (YC) rat was placed in the same treadmill and experienced the identical movement regardless of the stage of the sleep-wake cycle. According to the results, REM sleep was reduced by 85 percent in REM sleep deprived rats and by 43 percent in YC rats. Cell proliferation was reduced by 63 percent in REM sleep deprived rats compared with YC rats. Across all animals, cell proliferation exhibited a positive correlation with the percentage of REM sleep.

“Several studies have shown that sleep contributes to brain plasticity in general, and to adult neurogenesis, in particular,” said Dr. McGinty. “Neurogenesis is a concrete example of brain plasticity, suppression of adult neurogenesis is thought to be important in pathologies such as depression. One current question has to do with the relative contribution of the two sleep states, non-REM and REM, which have very different, even opposite, physiological properties. This study showed that REM sleep has a critical role in facilitating brain plasticity. The study does not exclude an equally important role for non-REM sleep. In other recent work, we have shown that sleep fragmentation can also suppress adult neurogenesis. How sleep affects the molecular mechanisms underlying neurogenesis remains to be explored.”

It is recommended that older adults get between seven and eight hours of nightly sleep. The American Academy of Sleep Medicine (AASM) offers the following tips on how to get a good night’s sleep:

• Follow a consistent bedtime routine.
• Establish a relaxing setting at bedtime.
• Get a full night’s sleep every night.
• Avoid foods or drinks that contain caffeine, as well as any medicine that has a stimulant, prior to bedtime.
• Do not bring your worries to bed with you.
• Do not go to bed hungry, but don’t eat a big meal before bedtime either.
• Avoid any rigorous exercise within six hours of your bedtime.
• Make your bedroom quiet, dark and a little bit cool.
• Get up at the same time every morning.