Posts tagged insular cortex
Articles and news from the latest research reports.
Taste memory
Have you ever eaten something totally new and it made you sick? Don’t give up; if you try the same food in a different place, your brain will be more “forgiving” of the new attempt. In a new study conducted by the Sagol Department of Neurobiology at the University of Haifa, researchers found for the first time that there is a link between the areas of the brain responsible for taste memory in a negative context and those areas in the brain responsible for processing the memory of the time and location of the sensory experience. When we experience a new taste without a negative context, this link doesn’t exist.
The area of the brain responsible for storing memories of new tastes is the taste cortex, found in a relatively insulated area of the human brain known as the insular cortex. The area responsible for formulating a memory of the place and time of the experience (the episode) is the hippocampus. Until now, researchers assumed that there was no direct connection between these areas – i.e., the processing of information about a taste is not related to the time or the place one experiences the taste. The accepted thinking was that a negative experience – for example, being exposed to a bad taste – would be negative in the same way anywhere, and the brain would create a memory of the taste itself, divorced from the time or place.
But in this new study, conducted by doctoral student Adaikkan Chinnakkaruppan in the laboratory of Prof. Kobi Rosenblum of the Sagol Department of Neurobiology at the University of Haifa, in cooperation with the Riken Institute, the leading brain research institute in Tokyo, the researchers demonstrate for the first time that there is a functional link between the two brain regions.
In the study the researchers sought to examine the relationship between the taste cortex (which is responsible for taste memory), and three different areas in the hippocampus: CA1, which is responsible for encoding the concept of space (where we are located); DG, the area responsible for encoding the time relationship between events; and CA3, responsible for filling in missing information. To do this the researchers took ordinary mice and mice that were genetically engineered by their Japanese colleagues such that these three areas of the brain functioned normally but were lacking plasticity, which did not allow new memories reliant on them to be created.
“In brain research, the manipulation we do must be very delicate and precise, otherwise the changes can make the entire experiment irrelevant to proving or refuting the research hypothesis,” said Prof. Rosenblum.
The mice were exposed to two new tastes, one that caused stomach pains (to mimic exposure to toxic food) and another that didn’t cause that feeling. By comparing the two groups it emerged that when the new taste was not accompanied by an association with toxic food, there was no difference between the normal mice and those whose various functional areas in the hippocampus didn’t allow plasticity. But when the taste caused a negative feeling, there was clear involvement of the CA1 area, which is responsible for encoding the space.
“The significance of this is that the moment we go back to the same place at which we experienced the taste associated with a bad feeling, subconsciously the negative memory will be much stronger than if we come to taste the same taste in a totally different place,” explained Prof. Rosenblum. Similarly, the DG area, which is responsible for encoding the time between incidents, was involved the more time that passed between the new taste and the stomach discomfort. “This means that even during a simple associative taste, the brain operates the hippocampus to produce an integrated experience that includes general information about the time between events and their location,” he said.
The findings, which were recently published in the Journal of Neuroscience, expose the complexity and richness of the simple sensory experiences that are engraved in our brains and that in most cases we aren’t even aware of. Moreover, the study can help explain behavioral results and the difficulty in producing memories when certain areas of the brain become dysfunctional following and illness or accident. The better we understand the encoding of simple sensory experiences in the brain and the link between the feeling, time and place of the experiences; we will better understand the complex process of creating memories and storing them in our brains.
(Source: newmedia-eng.haifa.ac.il)
Hypersensitivity to Non-Painful Events May Be Part of Pathology in Fibromyalgia
New research shows that patients with fibromyalgia have hypersensitivity to non-painful events based on images of the patients’ brains, which show reduced activation in primary sensory regions and increased activation in sensory integration areas. Findings published in Arthritis & Rheumatology, a journal of the American College of Rheumatology (ACR), suggest that brain abnormalities in response to non-painful sensory stimulation may cause the increased unpleasantness that patients experience in response to daily visual, auditory and tactile stimulation.
Fibromyalgia is a chronic, musculoskeletal syndrome characterized by widespread pain, affecting roughly two percent of the world population, say experts. According to the ACR, five million people in the U.S. have fibromyalgia, which is more prevalent among women. In previous studies fibromyalgia patients report reduced tolerance to normal sensory (auditory, visual, olfactory, and tactile) stimulation in addition to greater sensitivity to pain.
For the present study, researchers used functional magnetic resonance imaging (fMRI) to assess brain response to sensory stimulation in 35 women with fibromyalgia and 25 healthy, age-matched controls. Patients had an average disease duration of 7 years and a mean age of 47.
According to the study, patients reported increased unpleasantness in response to multisensory stimulation in daily life activities. Furthermore, fMRI displayed reduced activation of both the primary and secondary visual and auditory areas of the brain, and increased activation in sensory integration regions. These brain abnormalities mediated the increased unpleasantness to visual, auditory and tactile stimulation that patients reported to experience in daily life.
Lead study author, Dr. Marina López-Solà from the Institute of Cognitive Science, University of Colorado Boulder said, “Our study provides new evidence that fibromyalgia patients display altered central processing in response to multisensory stimulation, which are linked to core fibromyalgia symptoms and may be part of the disease pathology. The finding of reduced cortical activation in the visual and auditory brain areas that were associated with patient pain complaints may offer novel targets for neurostimulation treatments in fibromyalgia patients.”
(Source: eu.wiley.com)
(Image credit: The insular cortex of an autism mouse model is already so strongly activated by a single sensory modality (here a sound), that it is unable to perform its role in integrating information from multiple sources. Credit: © MPI of Neurobiology / Gogolla)
Insular cortex alterations in mouse models of autism
The insular cortex is an integral “hub”, combining sensory, emotional and cognitive content. Not surprisingly, alterations in insular structure and function have been reported in many psychiatric disorders, such as anxiety disorders, depression, addiction and autism spectrum disorders (ASD). Scientists from Harvard University and the Max-Planck Institute of Neurobiology in Martinsried now describe consistent alterations in integrative processing of the insular cortex across autism mouse models of diverse etiologies. In particular, the delicate balance between excitation and inhibition in the autistic brains was disturbed, but could be pharmacologically re-adjusted. The results could help the development of novel diagnostic and therapeutic strategies.
Autism is a neurodevelopmental disorder characterized by impaired social interaction, verbal and non-verbal communication, and by restricted and repetitive behaviors. Diagnosis is solely based on behavioral analysis as biological markers and neurological underpinnings remain unknown. This makes the development of novel therapeutic strategies extremely difficult.
As the cellular basis of autism spectrum disorders cannot be addressed in human patients, scientists have developed a number of mouse models for the disease. Similar to humans, mice are social animals and communicate through species-specific vocalizations. The mouse models harbor all diagnostic hallmark criteria of autism, such as repetitive, stereotypic behaviors and deficits in social interactions and communication.
Nadine Gogolla and her colleagues in the laboratory of Takao Hensch at Harvard University have now searched for common neural circuit alterations in mouse models of autism. They concentrated on the insular cortex, a brain structure that contributes to social, emotional and cognitive functions. ‘We wanted to know whether we can detect differences in the way the insular cortex processes information in healthy or autism-like mice’, says Nadine Gogolla, who was recently appointed Leader of a Research Group at the Max Planck Institute of Neurobiology.
As the researchers now report, the insular cortex of healthy mice integrates stimuli from different sensory modalities and reacts more strongly when two different stimuli are presented concomitantly (e.g. a sound and a touch). ‘We recognize a rose more easily when we smell and see it rather than when we just see or smell it’ says Nadine Gogolla. This capacity of combining sensory stimuli was consistently affected in all autism models the researchers looked at. Interestingly, often one sense alone elicited such a strong response that adding a second modality did not add further information. This is very reminiscent of the sensory hyper-responsiveness experienced by many autistic patients. The scientist further discovered that the insular cortex of adult autism-model mice resembled the activation patterns observed in very young control mice. ‘It seemed as if the insular cortex of the autism-models did not mature properly after birth’, says Gogolla.
For proper brain function, excitation and inhibition have to be in equilibrium. In the now identified part of the insular cortex, the scientists found that this equilibrium was disturbed. In one of the mouse models, inhibitory contacts between nerve cells were strongly reduced.
To test the influence of this reduction on sensory processing, the researchers gave mice the drug Diazepam, which is also known under the trade name Valium, to boost inhibitory transmission in the brain. Indeed, this treatment transiently rescued the capacity of the insular cortex to combine stimuli of different sensory modalities. The balance between excitation and inhibition in the brain is established after birth. The scientists thus treated young animals over several days with Diazepam. This treatment was efficient in reestablishing the insular cortex capacity for sensory integration permanently, even in adult mice that did not received any further treatment. Interestingly, also the stereotypic grooming of the animals was significantly reduced.
All autism models investigated showed alterations in inhibitory molecules. However, the alterations were very diverse. While in some models certain molecules were reduced, the opposite was true in another model. These results suggest that the disequilibrium between excitation and inhibition may be an important factor in the neuropathology of autism. However, future therapies will need to be carefully tailored to each particular subgroup of autism. For instance, an artificial boost of inhibition through a drug like Diazepam in healthy mice can throw the delicate equilibrium off and create changes in the insular cortex similar to those seen in the autism models. Whether a therapeutic strategy aimed on keeping the brain’s equilibrium between excitation and inhibition could be useful and if so, how to test the individuals’ status of the excitation/inhibition balance and how to implement individually tailored treatments, would need to be established through further studies and pre-clinical tests.
Tired and edgy? Sleep deprivation boosts anticipatory anxiety
UC Berkeley researchers have found that a lack of sleep, which is common in anxiety disorders, may play a key role in ramping up the brain regions that contribute to excessive worrying.
Neuroscientists have found that sleep deprivation amplifies anticipatory anxiety by firing up the brain’s amygdala and insular cortex, regions associated with emotional processing. The resulting pattern mimics the abnormal neural activity seen in anxiety disorders. Furthermore, their research suggests that innate worriers – those who are naturally more anxious and therefore more likely to develop a full-blown anxiety disorder – are acutely vulnerable to the impact of insufficient sleep.
“These findings help us realize that those people who are anxious by nature are the same people who will suffer the greatest harm from sleep deprivation,” said Matthew Walker, a professor of psychology and neuroscience at UC Berkeley and senior author of the paper, which was published in the Journal of Neuroscience.
The results suggest that people suffering from such maladies as generalized anxiety disorder, panic attacks and post-traumatic stress disorder, may benefit substantially from sleep therapy. At UC Berkeley, psychologists such as Allison Harvey, a co-author on the Journal of Neuroscience paper, have been garnering encouraging results in studies that use sleep therapy on patients with depression, bipolar disorder and other mental illnesses.
“If sleep disruption is a key factor in anxiety disorders, as this study suggests, then it’s a potentially treatable target,” Walker said. “By restoring good quality sleep in people suffering from anxiety, we may be able to help ameliorate their excessive worry and disabling fearful expectations.”
While previous research has indicated that sleep disruption and psychiatric disorders often occur together, this latest study is the first to causally demonstrate that sleep loss triggers excessive anticipatory brain activity associated with anxiety, researchers said.
“It’s been hard to tease out whether sleep loss is simply a byproduct of anxiety, or whether sleep disruption causes anxiety,” said Andrea Goldstein, a UC Berkeley doctoral student in neuroscience and lead author of the study. “This study helps us understand that causal relationship more clearly.”
In their experiments, performed at UC Berkeley’s Sleep and Neuroimaging Laboratory, Walker and his research team scanned the brains of 18 healthy young adults as they viewed dozens of images, first after a good night’s rest, and again after a sleepless night. The images were either neutral, disturbing or alternated between both.
Participants in the experiments reported a wide range of baseline anxiety levels, but none fit the criteria for a clinical anxiety disorder. After getting a full night’s rest at the lab, which researchers monitored by measuring neural electrical activity, their brains were scanned via functional MRI as they waited to be shown, and then viewed 90 images during a 45-minute session.
To trigger anticipatory anxiety, researchers primed the participants using one of three visual cues prior to each series of images. A large red minus sign signaled to participants that they were about to see a highly unpleasant image, such as a death scene. A yellow circle portended a neutral image, such as a basket on a table. Perhaps most stressful was a white question mark, which indicated that either a grisly image or a bland, innocuous one was coming, and kept participants in a heightened state of suspense.
When sleep-deprived and waiting in suspenseful anticipation for a neutral or disturbing image to appear, activity in the emotional brain centers of all the participants soared, especially in the amygdala and the insular cortex. Notably, the amplifying impact of sleep deprivation was most dramatic for those people who were innately anxious to begin with.
“This discovery illustrates how important sleep is to our mental health,” said Walker. “It also emphasizes the intimate relationship between sleep and psychiatric disorders, both from a cause and a treatment perspective.”
(Source: newscenter.berkeley.edu)
‘Disgusted’ Rats Teaching Scientists About Nausea, Work May Lead to New Cancer Treatments
Nausea is a common and distressing side effect of many drugs and treatments. Unlike vomiting, nausea is not well understood, but new research by University of Guelph scientists may soon change that.
Guelph PhD student Katharine Tuerke, neuroscience researcher Cheryl Limebeer and Prof. Linda Parker in the Department of Psychology believe they’ve found the mechanism in the brain that is responsible for the sensation of nausea – with the help of some “disgusted” rats.
Their study was published this week in Journal of Neuroscience.
“Although everyone has experienced nausea at some point, its neurobiology is poorly understood due to a lack of animal models,” said Parker, who holds the Canada Research Chair in Behavioural Neuroscience.
“We know about vomiting. The vomiting reflex is very well characterized, but the experience of nausea is something that little is known about. How is it generated? Where is it generated?”
Although rats can’t vomit, they do display a disgust reaction called gaping when re-exposed to a taste that made them feel nauseous in the past. Therefore, these gaping reactions in rats provide a model to understand brain mechanisms that produce nausea in humans.