A recent study published in Toxicology found that mice exposed to high levels of BPA showed impaired learning, impaired memory, and a blunted response to nicotine. To read an article in response to the study, go here.
My wife has recently been hard at work on an article summarizing the toxic effects and widespread prevalence of BPA within many items of modern day American life, so I've had BPA on the brain (hopefully not literally). BPA isn't just in your old Nalgene bottle. We've actually been scared off to the point that we're planning to no longer eat canned foods.
With the relatively recent expanded use of polycarbonates, other plastics, and a host of other environmental toxins that we use every day without knowing about it, it seems to me that there is potentially a strong link between them and neurodevelopmental disorders in humans. Certainly, the evidence from animal studies suggests a stronger association than, say vaccines.
Friday, December 2, 2011
Friday, November 18, 2011
Assessing the Vegetative State with EEG
Today, Garrett will speak on a recently published paper in the Lancet, in which the researchers applied EEG to patients with traumatic and non-traumatic brain injury.
Thursday, September 22, 2011
Tuesday, September 13, 2011
Fun with Flash
I've been experimenting with making Flash videos for the purposes of condensing portions of my research presentations. I didn't realize that the video capture software I used was also capturing audio, so I apologize for the audible breathing throughout the video. Maybe I'll make another with commentary throughout.
Friday, August 19, 2011
Thursday, August 18, 2011
EEG Primer
If anyone's interested in a background in signal processing as it pertains to EEG signals, the following article is pretty good.
A Primer for EEG Processing in Anesthesia
A Primer for EEG Processing in Anesthesia
Monday, August 15, 2011
Cod Genome Reveals Stunning Gap in Immune System - ScienceNOW
Cod Genome Reveals Stunning Gap in Immune System - ScienceNOW
Not a neuro discovery per se, but still fascinating. An (viable) absence of MHCII and CD4 proteins flies in the face of immunological dogma.
Not a neuro discovery per se, but still fascinating. An (viable) absence of MHCII and CD4 proteins flies in the face of immunological dogma.
Monday, July 25, 2011
New way to reduce the effects of cocaine
Source: http://www.abc.net.au/science/articles/2011/07/25/3275847.htm#artBookmarks
A new target for the treatment of drug addiction has been identified by US and Chinese scientists.
Research led by Dr Zheng-Xiong Xi of the National Institute on Drug Abuse in the USA has found that activation of receptors in the brains of mice can counteract the behavioural and rewarding effects of cocaine.
There are two major cannabinoid receptor types: CB1 and CB2.
CB1 receptors, which are found in large numbers in the brain activated by drugs such as marijuana. They are known to stimulate the brain's reward system, which is why they have been the focus of addiction research.
CB2 receptors are primarily located on the body's immune cells. They are also known to be involved in pain perception.
Until recently, it was thought that CB2 receptors were not present in the brain or that, if they were, it was in such low density that they were not involved in drug addiction.
"Due to the limitations of the technology we weren't able to detect low levels of CB2 receptors," says Xi.
But, six years ago, CB2 receptors were found to be present and active in the brainstem. They were subsequently detected in neurons in the brain.
"This prompted us to re-examine the role of CB2 receptors in drug reward and addiction," says Xi.
"Our research suggests that, even though the levels of CB2 receptors [in the brain] are very low, they are critically involved in cocaine's actions."
The results are published online today in Nature Neuroscience.
Rewarding behaviour
In their study, Xi and colleagues trained mice to self-administer cocaine intravenously. The researchers found that activating CB2 receptors with two different 'agonists' reduced drug-induced behaviour such as hyperactivity.
In addition, the CB2 receptor agonists reduced the bouts and amount of drug intake in normal (wild type) mice and mice who lacked the CB1 receptors, but not those that lacked CB2 receptors.
Further experiments showed the observed effects were mediated by the brain's CB2 receptors and that the rewarding effects of cocaine were blocked.
"Taken all together, the present findings, for the first time suggest that brain CB2 receptors functionally modulate the acute rewarding and locomotor-stimulating effects of cocaine in mice," says Xi.
Battling addiction
Xi adds that several pharmaceutical companies already have CB2 agonists in preclinical trials, but that they have been developed to treat pain.
"Our findings open a new field; CB2 agonists have a very high potential for treating addiction," he says.
Dr Nadia Solowij of the University of Wollongong agrees and speculates that the study will also have relevance for other drug addictions including opiates.
"They found minimal side-effects by specifically targeting these cannabinoid receptors and they showed specific effects on the dopamine [reward] system," she says.
However, Solowij adds that the addiction and reward systems involve interactions between many different receptor and neurochemical systems in the brain and that more research is needed to fully understand the changes that result from CB2 activation.
Xi acknowledges that "these are very early initial studies," and adds that they will now test their compounds in other animal species, starting with the rat.
He and his colleagues are also focussing on finding the mechanism by which activation of CB2 receptors inhibits dopamine release.
Thursday, July 7, 2011
Visualizing Cell Transplants
This is an open-ended methods question for anyone out there. We're at the point in our lab where we're about to implant various cell populations into inbred hosts, with the hope of verifying that these cells are surviving and incorporating into normal tissue. Survival times range from 4 weeks to 26 weeks.
What methods does your lab use to do this? We've considered lentiviral transduction and transfection with GFP/luciferase expressing plasmids.
What methods does your lab use to do this? We've considered lentiviral transduction and transfection with GFP/luciferase expressing plasmids.
Scientists Use ‘Optogenetics’ to Control Reward-Seeking Behavior
From Neuroscience News
The findings suggest that therapeutics targeting the path between two critical brain regions, the amygdala and the nucleus accumbens, represent potential treatments for addiction and other neuropsychiatric diseases.
Using a combination of genetic engineering and laser technology, researchers at the University of North Carolina at Chapel Hill have manipulated brain wiring responsible for reward-seeking behaviors, such as drug addiction. The work, conducted in rodent models, is the first to directly demonstrate the role of these specific connections in controlling behavior.
The UNC study, published online on June 29, 2011, by the journal Nature, uses a cutting-edge technique called “optogenetics” to tweak the microcircuitry of the brain and then assess how those changes impact behavior. The findings suggest that therapeutics targeting the path between two critical brain regions, namely the amygdala and the nucleus accumbens, represent potential treatments for addiction and other neuropsychiatric diseases.
“For most clinical disorders we knew that one region or another in the brain was important, however until now we didn’t have the tools to directly study the connections between those regions,” said senior study author Garret D. Stuber, PhD, assistant professor in the departments of cell and molecular physiology, psychiatry and the Neuroscience Center in UNC School of Medicine. “Our ability to perform this level of sophistication in neural circuit manipulation will likely to lead to the discovery of molecular players perturbed during neuropsychiatric illnesses.”
Because the brain is comprised of diverse regions, cell types and connections in a compact space, pinpointing which entity is responsible for what function can be quite tricky. In the past, researchers have tried to get a glimpse into the inner workings of the brain using electrical stimulation or drugs, but those techniques couldn’t quickly and specifically change only one type of cell or one type of connection. But optogenetics, a technique that emerged six years ago, can.
In the technique, scientists transfer light-sensitive proteins called “opsins” – derived from algae or bacteria that need light to grow – into the mammalian brain cells they wish to study. Then they shine laser beams onto the genetically manipulated brain cells, either exciting or blocking their activity with millisecond precision.
In Stuber’s initial experiments, the target was the nerve cells connecting two separate brain regions associated with reward, the amygdala and the nucleus accumbens. The researchers used light to activate the connections between these regions, essentially “rewarding” the mice with laser stimulations for performing the mundane task of poking their nose into a hole in their cage. They found that the opsin treated mice quickly learned to “nosepoke” in order to receive stimulation of the neural pathway. In comparison, the genetically untouched control mice never caught on to the task.
Then Stuber and his colleagues wanted to see whether this brain wiring had a role in more natural behavioral processes. So they trained mice to associate a cue – a light bulb in the cage turning on – to a reward of sugar water. This time the opsin that the researchers transferred into the brains of their rodent subjects was one that would shut down the activity of neural connections in response to light. As they delivered the simple cue to the control mice, they also blocked the neuronal activity in the genetically altered mice. The control mice quickly began responding to the cue by licking the sugar-producing vessel in anticipation, whereas the treated mice did not give the same response.
The researchers are now exploring how changes to this segment of brain wiring can either make an animal sensitized to or oblivious to rewards. Stuber says their approach presents an incredibly useful tool for studying basic brain function, and could one day provide a powerful alternative to electrical stimulation or pharmacotherapy for neuropsychiatric illnesses like Parkinson’s disease.
“For late-stage Parkinson’s disease it has become more routine to use deep brain stimulation, where electrodes are chronically implanted into brain tissue, constantly stimulating the tissue to alleviate some of the disease symptoms,” said Stuber. “From the technical perspective, implanting our optical fibers is not going to be more difficult than that. But there is quite a bit of work to be done before we get to that point.”
The findings suggest that therapeutics targeting the path between two critical brain regions, the amygdala and the nucleus accumbens, represent potential treatments for addiction and other neuropsychiatric diseases.
Using a combination of genetic engineering and laser technology, researchers at the University of North Carolina at Chapel Hill have manipulated brain wiring responsible for reward-seeking behaviors, such as drug addiction. The work, conducted in rodent models, is the first to directly demonstrate the role of these specific connections in controlling behavior.
The UNC study, published online on June 29, 2011, by the journal Nature, uses a cutting-edge technique called “optogenetics” to tweak the microcircuitry of the brain and then assess how those changes impact behavior. The findings suggest that therapeutics targeting the path between two critical brain regions, namely the amygdala and the nucleus accumbens, represent potential treatments for addiction and other neuropsychiatric diseases.
“For most clinical disorders we knew that one region or another in the brain was important, however until now we didn’t have the tools to directly study the connections between those regions,” said senior study author Garret D. Stuber, PhD, assistant professor in the departments of cell and molecular physiology, psychiatry and the Neuroscience Center in UNC School of Medicine. “Our ability to perform this level of sophistication in neural circuit manipulation will likely to lead to the discovery of molecular players perturbed during neuropsychiatric illnesses.”
Because the brain is comprised of diverse regions, cell types and connections in a compact space, pinpointing which entity is responsible for what function can be quite tricky. In the past, researchers have tried to get a glimpse into the inner workings of the brain using electrical stimulation or drugs, but those techniques couldn’t quickly and specifically change only one type of cell or one type of connection. But optogenetics, a technique that emerged six years ago, can.
In the technique, scientists transfer light-sensitive proteins called “opsins” – derived from algae or bacteria that need light to grow – into the mammalian brain cells they wish to study. Then they shine laser beams onto the genetically manipulated brain cells, either exciting or blocking their activity with millisecond precision.
In Stuber’s initial experiments, the target was the nerve cells connecting two separate brain regions associated with reward, the amygdala and the nucleus accumbens. The researchers used light to activate the connections between these regions, essentially “rewarding” the mice with laser stimulations for performing the mundane task of poking their nose into a hole in their cage. They found that the opsin treated mice quickly learned to “nosepoke” in order to receive stimulation of the neural pathway. In comparison, the genetically untouched control mice never caught on to the task.
Then Stuber and his colleagues wanted to see whether this brain wiring had a role in more natural behavioral processes. So they trained mice to associate a cue – a light bulb in the cage turning on – to a reward of sugar water. This time the opsin that the researchers transferred into the brains of their rodent subjects was one that would shut down the activity of neural connections in response to light. As they delivered the simple cue to the control mice, they also blocked the neuronal activity in the genetically altered mice. The control mice quickly began responding to the cue by licking the sugar-producing vessel in anticipation, whereas the treated mice did not give the same response.
The researchers are now exploring how changes to this segment of brain wiring can either make an animal sensitized to or oblivious to rewards. Stuber says their approach presents an incredibly useful tool for studying basic brain function, and could one day provide a powerful alternative to electrical stimulation or pharmacotherapy for neuropsychiatric illnesses like Parkinson’s disease.
“For late-stage Parkinson’s disease it has become more routine to use deep brain stimulation, where electrodes are chronically implanted into brain tissue, constantly stimulating the tissue to alleviate some of the disease symptoms,” said Stuber. “From the technical perspective, implanting our optical fibers is not going to be more difficult than that. But there is quite a bit of work to be done before we get to that point.”
Wednesday, June 15, 2011
Welcome!
A neuroscience journal club is being started at Upstate, the emphasis of which will be on significant findings in the field of interest du jour. With the sudden burst of enthusiasm and postive energy that went into the journal club's creation, I thought I would take the opportunity to get an online extension of the journal club going--in blog form.
The goal of this blog is three-fold. First, it should provide a running record of the papers we discuss. Second, it should allow students, faculty, and casual internet observes to comment on new findings in a different way. While the live format (to take place on alternating Fridays) is nice, having a chance to craft a written response to somebody's work is good, too. Third, the blog might turn out to be a useful way to communicate and collaborate across the program, outside of the confines of journal club.
So what will go on the blog and who will contribute to it? Anyone scheduled to give a talk will be granted permission to create a new post on the blog. (In fact, if you're interested in posting at all, let me know, and I'll magically grant you priveleges. The one piece of fine print is that you'll need a Google or Blogspot account before you get started.)
My thinking is that each main post will correspond to a journal article slated for review. The main post should outline the major findings of the paper and anything else the presenter thinks is interesting (methods, novel model, shift in paradigm, etc.). The post will then be opened up for comments. Hopefully, this will be the stage where things take off.
As for the running record of papers we are to discuss, labeling your post with various tags is useful. Doing so not only helps with search functions within the blog, but it opens the blog's content up to general Google searches as well. PubMed search terms are probably good to include, but my take is the more, the better. Also, try to use search terms similar to those used in the past (e.g. "motor neuron" instead of "motoneuron" or vice versa). This will enable more returns when someone does search.
Finally, there are the blog features outside of the main posts to think about. This will probably be an evolving project, so if there are any functions you'd like to see (e.g. calendar, links to other sites, etc.) let me know and I will add them or you can add them yourself.
That's it from me. I'm looking forward to Chrissa's talk on June 24!
The goal of this blog is three-fold. First, it should provide a running record of the papers we discuss. Second, it should allow students, faculty, and casual internet observes to comment on new findings in a different way. While the live format (to take place on alternating Fridays) is nice, having a chance to craft a written response to somebody's work is good, too. Third, the blog might turn out to be a useful way to communicate and collaborate across the program, outside of the confines of journal club.
So what will go on the blog and who will contribute to it? Anyone scheduled to give a talk will be granted permission to create a new post on the blog. (In fact, if you're interested in posting at all, let me know, and I'll magically grant you priveleges. The one piece of fine print is that you'll need a Google or Blogspot account before you get started.)
My thinking is that each main post will correspond to a journal article slated for review. The main post should outline the major findings of the paper and anything else the presenter thinks is interesting (methods, novel model, shift in paradigm, etc.). The post will then be opened up for comments. Hopefully, this will be the stage where things take off.
As for the running record of papers we are to discuss, labeling your post with various tags is useful. Doing so not only helps with search functions within the blog, but it opens the blog's content up to general Google searches as well. PubMed search terms are probably good to include, but my take is the more, the better. Also, try to use search terms similar to those used in the past (e.g. "motor neuron" instead of "motoneuron" or vice versa). This will enable more returns when someone does search.
Finally, there are the blog features outside of the main posts to think about. This will probably be an evolving project, so if there are any functions you'd like to see (e.g. calendar, links to other sites, etc.) let me know and I will add them or you can add them yourself.
That's it from me. I'm looking forward to Chrissa's talk on June 24!
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