Posts tagged psychology

May 7, 2012 

(Medical Xpress) — An international study led by the University of Sydney and published in the Annals of Neurology has the potential to improve the design of clinical trials for the treatment of Charcot-Marie-Tooth disease, a disorder which affects the peripheral nervous system.

Charcot-Marie-Tooth disease (CMT) is among the most common inherited neurological disorders, affecting one in 2500 people. Symptoms such as leg weakness, foot pain, trips and falls develop in the first two decades of life, with some patients wheelchair bound by 21 years. Currently there is no treatment for any form of this disease, but clinical trials are increasingly occurring.

"While it is very positive that clinical trials are taking place in this area, it is vital that trials are based on appropriately selected patients and carefully chosen outcome measures," says Associate Professor Joshua Burns, Chief Investigator from the University of Sydney and The Children’s Hospital at Westmead. "This relies on being able to measure disease severity accurately, and in turn the patient’s response to treatment, which we were previously unable to do in children."

In response, Associate Professor Burns and colleagues from the USA, UK and Italy designed the CMT Pediatric Scale (CMTPedS), a patient-centred multi-item rating scale of disability for children with CMT.

"Rating scales used for adult patients are inappropriate for children and since most forms of CMT affect children there was an obvious need for a new clinical tool.

"Furthermore, it is during childhood that we anticipate that treatments for CMT may be most effective - before the disease progresses and makes repair more difficult."

During a 14-month test period the CMTPedS was administered to more than 170 children aged three to 20 with varying types of CMT in Australia and internationally via the Inherited Neuropathies Consortium. Analysis of these data supported the viability of CMTPedS as a reliable, valid and sensitive global measure of disability for children with CMT from the age of three years.

The CMTPedS can be completed in 25 minutes and will have broad application in clinical trials of rehabilitative, pharmacological and surgical interventions.

"There is growing international support for the rating scale to be implemented as the primary outcome measure in studies of children with CMT because the quality of the measure has the potential to influence the outcome of clinical trials and patient care," says Associate Professor Burns.

Provided by University of Sydney

Source: medicalxpress.com

May 7, 2012

Many of us love massages, but imagine a massage so deep that tissues, organs and cells could also be ‘massaged’.

That’s exactly what Vibroacoustic Therapy, a low frequency sound massage, is clinically proven to do, and new research at U of T suggests that it may help people with debilitating diseases.

“It is basically stimulating the body with very low sound – like sitting on a subwoofer,” said Professor Lee Bartel of the Faculty of Music.  “But it requires special speakers that carry sound almost too low to hear in a way that changes it basically to something you feel instead of hear.”

Bartel and his team in the new Music and Health Research Collaboratory (MaHRC) are exploring the medical effects of low frequency sound and have shown that this therapy can play a key role in reducing the symptoms of Parkinson’s disease.

Vibroacoustic therapy (VAT) consists of low sound frequencies that are transmitted to the body and mind through special transducers that convert the sound to inner body massage. MaHRC associates Heidi Ahonen and Quincy Almeida treated two groups of Parkinson’s patients (20 with dominant tremor symptoms and 20 with slow/rigid movement symptoms) with five minutes of 30 Hz vibration.

Both groups showed improvements in all symptoms, including less rigidity and better walking speed with bigger steps and less tremor.

“There have been several studies using vibration from sound with Parkinson’s,” said Bartel   “It has been known for over 100 years that vibration (like riding in a wagon on cobblestones) helped relieve some symptoms. So the scientific study of the effect of low frequency sound was a natural connection. Also known is that 40 Hz brain waves seem to be carriers of information between the parts of the brain that control movement. So adding extra stimulation in that zone should help that communication and so assist in movement control.”

Bartel, Founding and Acting Director of MaHRC, says the goal of low frequency sound studies with Parkinson’s is to determine which approach is most effective, how much and how often treatment is needed, and whether medication can be reduced. Vibroacoustic Therapy frequencies, between 20 and 100 Hz or pulses per second, correspond to brainwave activities and function that are currently being explored in neuroscience. 

But the effects of Vibroacoustic Therapy extend beyond the brain. It also provides deep physical cellular stimulation to skin, muscles and joints, resulting in decreased pain and increased mobility. Like hand/mechanical massage, vibroacoustic therapy aids circulation, relaxes muscles, and feels good.

Bartel points to research that shows that “several medical conditions including Parkinson’s and neuralgic pain like fibromyalgia, may be related to a common brain mechanism – a brain rhythm disorientation between the inner brain and the outer cortex. Since the rhythmic pulses of music can drive and stabilize these, we speculate that low frequency sound might help in fibromyalgia as well as Parkinson’s.”

Bartel’s team is now looking at the role of vibroacoustic therapy as a treatment for patients with fibromyalgia.

“Although it is too early to form any conclusions, there is encouraging data indicating that treating fibromyalgia patients with doses of 40 Hz sound seems to reduce pain.” 

“It is truly an exciting time for music medicine – the idea of developing audioceuticals (prescribable sound) points to a whole new direction for music therapy, and the potential for MaHRC to lead in this is very exciting for me” said Bartel.      

Provided by University of Toronto

Source: medicalxpress.com

May 7, 2012

Erxi Wu, assistant professor of pharmaceutical sciences, and Shuang Zhou, a doctoral student in Wu’s lab, co-wrote the article, “Smilagenin Attenuates Beta Amyloid (25-35)-Induced Degeneration of Neuronal Cells via Stimulating the Gene Expression of Brain-Derived Neurotrophic Factor,” which will be published by Neuroscience. They collaborated with Yaer Hu lab at Shanghai Jiaotong University, China, for the publication.

According to the authors, the development of drugs that weaken neurodegeneration is important for the treatment of Alzheimer’s disease. They previously found that smilagenin, a steroidal sapogenin from traditional Chinese medicinal herbs that improves memory in animal models, is neither a cholinesterase inhibitor nor a glutamate receptor antagonist, but can significantly elevate the declined muscarinic receptor (M receptor density). In this paper, to clarify whether smilagenin represents a new approach for treating neurodegeneration disease, they first demonstrate that smilagenin pretreatment significantly attenuates the neurodegenerative changes induced by beta amyloid 25-35 (Aβ25-35) in cultured rat cortical neurons, including decreased cholinergic neuron number, shortened neurite outgrowth length and declined muscarinic receptor density. Brain-derived neurotrophic factor protein in the culture medium was also decreased by Aβ25-35 and significantly elevated by smilagenin. 

Parallel experiments revealed that when the trk receptors were inhibited by K252a or the action of brain-derived neurotrophic factor was inhibited by a neutralizing anti- brain-derived neurotrophic factor antibody, the effects of smilageninon the Aβ25-35 induced neurodegeneration in rat cortical neurons were almost completely abolished. In the all-trans retinoic acid-differentiated SH-SY5Y neuroblastoma cells, the brain-derived neurotrophic factortranscription rate measured by a nuclear run-on assay was significantly suppressed by Aβ25-35 and elevated by SMI, but the brain-derived neurotrophic factor degradation rate measured by half-life determination was unchanged by Aβ25-35 and smilagenin. Transcript analysis of the SH-SY5Y cells using quantitative RT-PCR showed that the IV and VI transcripts of brain-derived neurotrophic factor mRNA were significantly decreased by Aβ25-35 and elevated by smilagenin. 

“Taken together, this study concludes that smilagenin attenuates Aβ25-35-induced neurodegeneration in cultured rat cortical neurons and SH-SY5Y cells mainly through stimulating brain-derived neurotrophic factor mRNA transcription implicating that SMI may represent a novel therapeutic strategy for Alzheimer’s disease,” Wu said. “Collaborating with Dr. Hu at Shanghai Jiaotong University, China, we together would like to find better therapeutics and elucidate the mechanisms of the potential novel therapy for Alzheimer’s disease,” Wu said.

Provided by North Dakota State University

Source: medicalxpress.com

May 6, 2012 

Brain networks may avoid traffic jams at their busiest intersections by communicating on different frequencies, researchers at Washington University School of Medicine in St. Louis, the University Medical Center at Hamburg-Eppendorf and the University of Tübingen have learned.

"Many neurological and psychiatric conditions are likely to involve problems with signaling in brain networks," says co-author Maurizio Corbetta, MD, the Norman J. Stupp Professor of Neurology at Washington University. "Examining the temporal structure of brain activity from this perspective may be especially helpful in understanding psychiatric conditions like depression and schizophrenia, where structural markers are scarce."

The research will be published May 6 in Nature Neuroscience.

Scientists usually study brain networks — areas of the brain that regularly work together — using magnetic resonance imaging, which tracks blood flow. They assume that an increase in blood flow to part of the brain indicates increased activity in the brain cells of that region.

"Magnetic resonance imaging is a useful tool, but it does have limitations," Corbetta says. "It only allows us to track brain cell activity indirectly, and it is unable to track activity that occurs at frequencies greater than 0.1 hertz, or once every 10 seconds. We know that some signals in the brain can cycle as high as 500 hertz, or 500 times per second."

For the new study, conducted at the University Medical Center at Hamburg-Eppendorf, the researchers used a technique called magnetoencephalography (MEG) to analyze brain activity in 43 healthy volunteers. MEG detects very small changes in magnetic fields in the brain that are caused by many cells being active at once. It can detect these signals at rates up to 100 hertz.

"We found that different brain networks ticked at different frequencies, like clocks ticking at different speeds," says lead author Joerg Hipp, PhD, of the University Medical Center at Hamburg-Eppendorf and the University of Tübingen, both in Germany.

For example, networks that included the hippocampus, a brain area critical for memory formation, tended to be active at frequencies around 5 hertz. Networks constituting areas involved in the senses and movement were active between 32 hertz and 45 hertz. Many other brain networks were active at frequencies between eight and 32 hertz. These “time-dependent” networks resemble different airline route maps, overlapping but each ticking at a different rate.

"There have been a number of fMRI studies of depression and schizophrenia showing ‘spatial’ changes in the organization of brain networks," Corbettta says. "MEG studies provide a window into a much richer ‘temporal’ structure. In the future, this might offer new diagnostic tests or ways to monitor the efficacy of interventions in these debilitating mental conditions."

Provided by Washington University School of Medicine

Source: medicalxpress.com

ScienceDaily (May 4, 2012) — Researchers in Spain have found that at least some of the individuals claiming to see the so-called aura of people actually have the neuropsychological phenomenon known as “synesthesia” (specifically, “emotional synesthesia”). This might be a scientific explanation of their alleged ability.

New research suggests that at least some of the individuals claiming to see the so-called aura of people actually have the neuropsychological phenomenon known as “synesthesia” (specifically, “emotional synesthesia”). This might be a scientific explanation of their alleged ability. (Credit: © Nikki Zalewski / Fotolia)

In synesthetes, the brain regions responsible for the processing of each type of sensory stimuli are intensely interconnected. Synesthetes can see or taste a sound, feel a taste, or associate people or letters with a particular color.

The study was conducted by the University of Granada Department of Experimental Psychology Óscar Iborra, Luis Pastor and Emilio Gómez Milán, and has been published in the journal Consciousness and Cognition. This is the first time that a scientific explanation has been provided for the esoteric phenomenon of the aura, a supposed energy field of luminous radiation surrounding a person as a halo, which is imperceptible to most human beings.

In basic neurological terms, synesthesia is thought to be due to cross-wiring in the brain of some people (synesthetes); in other words, synesthetes present more synaptic connections than “normal” people. “These extra connections cause them to automatically establish associations between brain areas that are not normally interconnected,” professor Gómez Milán explains. New research suggests that many healers claiming to see the aura of people might have this condition.

The case of the "Santón de Baza"

One of the University of Granada researchers remarked that “not all ‘healers’ are synesthetes, but there is a higher prevalence of this phenomenon among them. The same occurs among painters and artists, for example.” To carry out this study, the researchers interviewed some synesthetes including a ‘healer’ from Granada, “Esteban Sánchez Casas,” known as"El Santón de Baza".

Many local people attribute “paranormal powers” to El Santón, because of his supposed ability to see the aura of people “but, in fact, it is a clear case of synesthesia,” the researchers explained. According to the researchers, El Santón has face-color synesthesia (the brain region responsible for face recognition is associated with the color-processing region); touch-mirror synesthesia (when the synesthete observes a person who is being touched or is experiencing pain, s/he experiences the same); high empathy (the ability to feel what other person is feeling), and schizotypy (certain personality traits in healthy people involving slight paranoia and delusions). “These capacities make synesthetes have the ability to make people feel understood, and provide them with special emotion and pain reading skills,” the researchers explain.

In the light of the results obtained, the researchers remarked on the significant “placebo effect” that healers have on people, “though some healers really have the ability to see people’s ‘auras’ and feel the pain in others due to synesthesia.” Some healers “have abilities and attitudes that make them believe in their ability to heal other people, but it is actually a case of self-deception, as synesthesia is not an extrasensory power, but a subjective and ‘adorned’ perception of reality,” the researchers state.

Source: Science Daily

May 5, 2012 

In an effort to identify the underlying causes of neurological disorders that impair motor functions such as walking and breathing, UCLA researchers have developed a novel system to measure the communication between stem cell-derived motor neurons and muscle cells in a Petri dish.

The study provides an important proof of principle that functional motor circuits can be created outside of the body using stem cell-derived neurons and muscle cells, and that the level of communication, or synaptic activity, between the cells could be accurately measured by stimulating motor neurons with an electrode and then measuring the transfer of electrical activity into the muscle cells to which the motor neurons are connected.

When motor neurons are stimulated, they release neurotransmitters that depolarize the membranes of muscle cells, allowing the entry of calcium and other ions that cause them to contract. By measuring the strength of this activity, one can get a good estimation of the overall health of motor neurons. That estimation could shed light on a variety of neurodegenerative diseasessuch as spinal muscular atrophy and amyotrophic lateral sclerosis, or Lou Gehrig’s disease, in which the communication between motor neurons and muscle cells is thought to unravel, said study senior author Bennett G. Novitch, an assistant professor of neurobiology and a scientist with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

The findings of the study appear May 4, 2012 in PLoS ONE, a peer-reviewed journal of the Public Library of Science.

"Now that we have this method to measure the strength of the communications between motor neurons and muscle cells, we may be able to begin exploring what happens in the earliest stages of motor neuron disease, before neuronal death becomes prevalent," Novitch said. "This can help us to pinpoint where things begin to go wrong and provide us with new clues into therapeutic interventions that could improve synaptic communication and promote neuronal survival."

Novitch said the synaptic communication activity his team was able to create and measure using mouse embryonic stem cell-derived motor neurons and muscle cells looks very similar what is seen in a mouse, validating that their model is a realistic representation of what is happening in a living organism.

"That gives us a good starting point to try to model what happens in cells that harbor genetic mutations that are associated with neurodegenerative diseases,. To do that, we had to first define an activity profile of normal synaptic communication," he said. "Some research suggests that a breakdown in this communication can be an early indication of disease progression or possibly an initiating event. Neurons that cannot effectively transmit information to muscle cells will eventually withdraw their contacts, causing both the neurons and muscle cells to degenerate over time. Hopefully, we can now create disease models that will allow us to study what is happening."

In this study, Novitch and his team, led by Joy Umbach, an associate professor of molecular and medical pharmacology, used mouse embryonic stem cells to create the motor neurons and previously established lines of muscle precursors to produce muscle fibers. They put both cells together in a Petri dish, and the cells were cultured in such a way to encourage communication. Novitch said the team wanted to see if they would naturally form synaptic contacts and whether or not there was neural transmission between them.

In less than a week, the neurons had reached out to the muscle cells and assembled the protein networks needed for synaptic communication, Novitch said.

To measure the connections between the cells, the scientists used a technique called dual patch clamp recording. Pipettes containing stimulating and recording electrodes are inserted into the membranes of the motor neurons and muscle cells, being careful not to injure them. With this method, they were able send an electrical current into the motor neurons and measure responses in the muscle cells, as well as visualize the muscular contractions.

"The in vitro system developed here might accordingly be expanded to assess the underlying cellular and molecular mechanisms that contribute to this decline in synaptic input to motor neurons," the study states. "Thus, in addition to their utility for helping to answer fundamental biological questions, these co-cultures have clear applications in addressing problems of medical significance."

Going forward, Novitch and his team hope to recreate and confirm the work using human stem cell-derived motor neurons and muscle cells and measure the synaptic communications with newly developed optical recording methods, which are less invasive than the patch clamp techniques used in this study.

Provided by University of California, Los Angeles

Source: medicalxpress.com

ScienceDaily (May 3, 2012) — Malfunctioning single proteins can cause disruptions in neuronal junctions leading to autistic forms of behavior. A current study, published in the scientific journal Nature, comes to this conclusion after examining genetically altered mice.

The study, in which scientists from Charité — Universitätsmedizin Berlin and the NeuroCure Cluster of Excellence contributed, thus supports the hypothesis that disruptions in neuronal junctions, i.e. synapses, could be the cause of the development of neuropsychiatric illnesses like autism. The international research team, that included scientists from Ulm University and the Institut Pasteur in Paris, ascribes a key role to the excitatory synapses. This finding could become an important step stone for future autism therapies.

Nerve cells communicate with each other via signal transmission to synaptic junctions. These junctions are stabilized through structural proteins, including the so-called ProSAP1/Shank2 protein. In order to understand the role that this protein has on synapses and ultimately in the development of autism, the researchers genetically modified mice and disabled the relevant protein. The choice of this protein was not arbitrary: In preparation for the current study, a number of the scientists involved found evidence that the mutation of this protein can lead to autism in humans. Various neuronal developmental disorders manifested through distinctive social and communicative behavioral features, as well as stereotyped behaviors are combined under the term of “autism.”

The absence of this structural protein in the mouse model also had visible implications: Animals with the mutated gene are hyperactive and demonstrate compulsive repetitions of particular features — like grooming, for example. In behavioral experiments, peculiarities in social and communicative interaction also become distinct. In the brains of the mice, researchers found noticeable mutations of synaptic junctions — specifically in excitatory synapses. When glutamate transmitters bind to glutamate receptors located at these junctions, the nerve cells become excitatory. If the mouse is lacking this structural protein, the transmitters increasingly find a related structural protein on the excitatory synapses, the ProSAP2/Shank3. This protein has also been implicated in the development of autism. At the same time, the composition of glutamate receptors mutates.

But what happens when this related structural protein in the mice is switched off? This is also examined in the study presented. The conclusion is that, in this case as well, mutations of the excitatory synapses occur. Obviously, both structural molecules alternate in fulfilling regular functions. “The study illustrates the significant role glutamatergic systems play in autism and thus contributes to understanding better synaptic changes in autism,” reports Stephanie Wegener, one of the participating scientists at Charité Berlin. The study is therefore an important part of the essential scientific foundation needed to develop possible therapies for autism.

Source: Science Daily

ScienceDaily (May 3, 2012) — The problems of living with bipolar have been well documented, but a new study by Lancaster University has captured the views of those who also report highly-valued, positive experiences of living with the condition.

Researchers at Lancaster’s Spectrum Centre, which is dedicated to the study of bipolar disorder, interviewed and recorded their views of ten people with a bipolar diagnosis, aged between 24 and 57. Participants in the study reported a number of perceived benefits to the condition ranging from to sharper senses to increased productivity.

The research was designed to explore growing evidence that some people with bipolar value their experiences and in some cases would prefer not to be without the condition.

Participants described a wide range of experiences and internal states that they believed they felt to a far greater intensity than those without the condition. These included increased perceptual sensitivity, creativity, focus and clarity of thought.

Some held (or had previously held) high functioning professional jobs or had been studying for higher level qualifications. They described in detail how they experienced times when tasks that are usually quite difficult or time consuming, would feel incredibly easy and the ability to achieve at a high level during these times was clearly immensely rewarding.

Others expressed the view that they felt ‘lucky’ or even ‘blessed’ to have the condition.

Alan, (not his real name) one of the interviewees, said: “It’s almost as if it opens up something in the brain that isn’t otherwise there, and I see colour much more vividly than I used to……So I think that my access to music and art are something for which I’m grateful to bipolar for enhancing. It’s almost as if it’s a magnifying glass that sits between that and myself.”

Researchers even found some people with bipolar reaped positive experiences from their lows such as greater empathy with the suffering of others.

Dr Fiona Lobban, who led the study, said: “Bipolar Disorder is generally seen as a severe and enduring mental illness with serious negative consequences for the people with this diagnosis and their friends and family. For some people this is very much the case. Research shows that long term unemployment rates are high, relationships are marred by high levels of burden on family and friends and quality of life is often poor. High rates of drug and alcohol misuse are reported for people with this diagnosis and suicide rates are twenty times that of the general population.

"However, despite all these factors researchers and clinicians are aware that that some aspects of bipolar experiences are also highly valued by some people. We wanted to find out what these positive experiences were.

"People were very keen to take part in this study and express views which some felt had to be hidden from the medical profession.

"It is really important that we learn more about the positives of bipolar as focusing only on negative aspects paints a very biased picture that perpetuates the view of bipolar as a wholly negative experience. If we fail to explore the positives of bipolar we also fail to understand the ambivalence of some people towards treatment."

Rita Long from Stockport was not part of the study but can identify with its findings. She was 40 when she was diagnosed with the condition but from her school days she was aware that she experienced the world differently to her twin sister.

"We were making Christmas cakes at school and I was so interested and excited by it and my sister says she remembers watching me and thinking, ‘I really wish I could get that excited about making a Christmas cake’. I noticed things, experienced them with a different level of intensity, we’d be on a walk and I’d be saying look at the colour of this, and my sister would be saying, ‘It’s just a berry’. Socially too, people with bipolar can be quite quick witted, humorous. Until much later in life I just presumed those things were part of my personality.

"I don’t want to underestimate how difficult the bad times can be that some people go through with bipolar but at the same time I feel very passionate about the positives. If we are going to move on as a society — in academia, in business, in entertainment — we need people who will push boundaries. People with bipolar can do that."

Source: Science Daily

ScienceDaily (May 3, 2012) — A team led by scientists at The Scripps Research Institute has shown that an extra copy of a brain-development gene, which appeared in our ancestors’ genomes about 2.4 million years ago, allowed maturing neurons to migrate farther and develop more connections.

A team led by Scripps Research Institute scientists has found evidence that, as humans evolved, an extra copy of a brain-development gene allowed neurons to migrate farther and develop more connections. (Credit: Photo courtesy of The Scripps Research Institute)

What genetic changes account for the vast behavioral differences between humans and other primates? Researchers so far have catalogued only a few, but now it seems that they can add a big one to the list. A team led by scientists at The Scripps Research Institute has shown that an extra copy of a brain-development gene, which appeared in our ancestors’ genomes about 2.4 million years ago, allowed maturing neurons to migrate farther and develop more connections.

Surprisingly, the added copy doesn’t augment the function of the original gene, SRGAP2, which makes neurons sprout connections to neighboring cells. Instead it interferes with that original function, effectively giving neurons more time to wire themselves into a bigger brain.

"This appears to be a major example of a genomic innovation that contributed to human evolution," said Franck Polleux, a professor at The Scripps Research Institute. "The finding that a duplicated gene can interact with the original copy also suggests a new way to think about how evolution occurs and might give us clues to human-specific developmental disorders such as autism and schizophrenia."

Read more …

ScienceDaily (May 3, 2012) — UCSF scientists have identified patterns of brain activity in the rat brain that play a role in the formation and recall of memories and decision-making. The discovery, which builds on the team’s previous findings, offers a path for studying learning, decision-making and post-traumatic stress syndrome.

Brain patterns through which the rats see rapid replays of past experiences are fundamental to their ability to make decisions. Disturbing those particular brain patterns impaired the animals’ ability to learn rules based on memories of things that had happened in the past. (Credit: © Oleg Kozlov / Fotolia)

The researchers previously identified patterns of brain activity in the rat hippocampus, a brain region critical for memory storage. The patterns sometimes represented where an animal was in space, and, at other times, represented fast-motion replays of places the animal had been, but no one knew whether these patterns indicated the process of memory formation and recollection.

In the journal Science this week (online May 3, 2012), the UCSF researchers demonstrated that the brain activity is critical for memory formation and recall. Moreover, they showed that the brain patterns through which the rats see rapid replays of past experiences are fundamental to their ability to make decisions. Disturbing those particular brain patterns impaired the animals’ ability to learn rules based on memories of things that had happened in the past.

"We think these memory-replay events are central to understanding how the brain retrieves past experiences and uses them to make decisions," said neuroscientist Loren Frank, PhD, a associate professor of physiology and a member of the Keck Center for Integrative Neuroscience at UCSF, who led the research with Shantanu Jadhav, PhD, a post-doctoral fellow. "They offer insight into how a past experience can have such a profound effect on how we think and feel."

The finding gives scientists a new way to investigate fundamental processes like learning and decision-making in animals and in people. It also may help shed light on memory disorders like post-traumatic stress disorder (PTSD), which is characterized by strong, disturbing and uncontrolled memories.

Without Links to the Past, Rats Face Indecision

Seeking to understand how the recall of specific memories in the brain guides our thinking, Frank and his colleagues built a system for detecting the underlying patterns of neuronal activity in rats. They fitted the animals with electrodes and built a system that enabled them to detect a specific pattern, called a sharp-wave ripple, in the hippocampus. Whenever they detected a ripple, they would send a small amount of electricity into another set of electrodes that would immediately interrupt the ripple event, in effect turning off all memory replay activity without otherwise affecting the brain.

The UCSF researchers knew that these sharp-wave ripples would be activated when the animals had to make choices about which direction to turn as they wended their way toward their reward: a few drops of sweetened condensed milk. These signals seem to be flashes of memory recall, said Frank, a rat’s past knowledge flooding back to inform it on what had happened in the past and where it might go in the future. Squashing the sharp-wave ripples, the UCSF team found, disrupted the recall and subverted the rat’s ability to correctly navigate the maze.

This shows, said Frank, that the sharp-wave ripples are critical for this type of memory recall. Through these brain waves, the rat reprocesses and replays old experiences in a fleeting instant — lessons from the past essential for shaping their perception of the present.

"We think these memory replay events are a fundamental constituent of memory retrieval and play a key role in human perspective and decision-making as well," he said. "These same events have been seen in memory tasks in humans, and now we know they are critical for memory in rats. We think that these fast-forward replays make up the individual elements of our own memories, which jump rapidly from event to event."

Next, the team wants to tease out information about how the rats actually use these memory replay events to make decisions and how amplifying or blocking specific replay events will change the way an animal learns and remembers. They also think that these events could be important for understanding memory problems, as when stressful memories intrude into daily life.

Source: Science Daily