A blog dedicated to important updates and imagery in the fields of psychology and neuroscience. Submissions and discussions are welcome. Come to expand your mind.
The moderator of Isocortex, an avid science nut with a MS.c. in Clinical Neuropsychology, believes that research should be accessible and understandable to everyone with an interest in it.

Free Online Psychology-Related Courses

I’ve compiled a list of various courses available right now for FREE that are related to the fields of psychology, neuroscience, and behavioral medicine. Enjoy, learn, and please share!

Humanities & Social Sciences

Introduction to Sociology by Harvey Molotch, NYU

Literature and Psychoanalysis by John Fletcher, University of Warwick

Philosophy and the Science of Human Nature by Tamar Gendler, Yale

Philosophy of Mind by John Searle, UC Berkeley

The Nature of Mind by John Joseph Campbell, UC Berkeley

Sciences

Adolescent Health and Development by Robert Blum, Johns Hopkins

Animal Behavior by Gerald Schneider, MIT

AI - Natural Language Processing by Christopher Manning, Stanford

Autism and Related Disorders by Frank Volkmar, Yale

Brain Structure and Its Origins by Prof. Gerald Schneider, MIT

Clinical Psychology by Ann Kring, UC Berkeley

Cognitive Neuroscience by Richard Ivry, UC Berkeley

Developmental Psychology by Alison Gopnik, UC Berkeley

Developmental Psychopathology by Stephen Hinshaw, UC Berkeley

Enhancing Humane Science - Improving Animal Research by Alan M. Goldberg & James Owiny, Johns Hopkins

How to Think Like a Psychologist by Multiple Staff, Standford

Human Behavioral Biology by Robert Sapolsky, Stanford

Human-Computer Interaction Seminar by Multiple Staff, Stanford

Human Emotion by Dacher Keltner, UC Berkeley

Introduction to Psychology by Paul Bloom, Yale

Introduction to Psychology by John Gabrieli, MIT

Introduction to Statistics and Data Analysis by Brenda Gunderson, University of Michigan

Issues in Mental Health Research in Developing Countries by Judith Bass, Johns Hopkins

Neural Networks and Biological Modeling by Wolfram Gerstner, École Polytechnique Fédérale de Lausanne

Neuroscience and Behavior by Gerald Schneider, MIT

Psychology of Perception by UW-Madison

Research and Data Analysis in Psychology by Frederic Theunissen, UC Berkeley

Scientific Approaches to Consciousness by John F. Kihlstrom, UC Berkeley

Social Psychology: Self and Society by Robb Willer, UC Berkeley

Statistics for Behavioral Science by Elizabeth Bauer, NYU

Statistical Reasoning I and II by John McGready, Johns Hopkins

The New Psychology of Depression by Mark Williams and Danny Penman, Oxford

Protein Regulator for Cerebral Folding Found

During fetal development of the mammalian brain, the cerebral cortex undergoes a marked expansion in surface area in some species which is accommodated by folding of the tissue in species with most expanded neuron numbers and surface area. Researchers in Germany have now identified and shared a key regulator of this crucial process in Cell.

The greater the degree of folding in the cortex and the more furrows present, the larger the surface area available for reception and processing of neural information. In humans, the exterior of the developing brain remains smooth until about the sixth month of gestation. Only then do superficial folds begin to appear and ultimately dominate the entire brain in humans. Conversely mice, for example, have a much smaller and smooth cerebral cortex.

The mechanisms that control the expansion and folding of the brain during fetal development have so far been mysterious, but now a major player involved in the molecular process that drives cortical expansion in the mouse has been pinpointed. The new study shows that a novel nuclear protein called Trnp1 triggers the enormous increase in the numbers of nerve cells which forces the cortex to undergo a complex series of folds. Indeed, although the normal mouse brain has a smooth appearance, dynamic regulation of Trnp1 results in activating all necessary processes for the formation of a much enlarged and folded cerebral cortex.

The findings are particularly striking because they imply that the same molecule – Trnp1 – controls both the expansion and the folding of the cerebral cortex and is even sufficient to induce folding in a normally smooth cerebral cortex. Trnp1 therefore serves as an ideal starting point from which to dissect the complex network of cellular and molecular interactions that underpin the whole process. I, for one, am a little worried where science might take this one… 

Reblogged from bpod-mrc  33 notes
bpod-mrc:

Recoating Damaged Nerves
Nerve cells in our brains and bodies have long thin protrusions called axons, which transmit electrical signals both to other nerve cells and to body tissues. Wrapped around these axons are multiple thin layers of a substance called myelin, which not only protects the axons but also speeds up their signal transmission. Myelin is itself a type of cell called a Schwann cell and, if myelin becomes damaged by physical injury or disease – such as multiple sclerosis – the Schwann cells attempt to re-myelinate the axons. But the process is often insufficient and the damaged nerves might never fully regain their function. Researchers would thus like to enhance the natural re-myelination process to help damaged cells recapture their lost potential. A new technique that allows re-myelinating Schwann cells (stained green) to be distinguished from undamaged myelin (stained red) should help researchers understand the process and ultimately design treatments to improve it.

Philip Horner
Published in PNAS 110(10): 4075-4080 

bpod-mrc:

Recoating Damaged Nerves

Nerve cells in our brains and bodies have long thin protrusions called axons, which transmit electrical signals both to other nerve cells and to body tissues. Wrapped around these axons are multiple thin layers of a substance called myelin, which not only protects the axons but also speeds up their signal transmission. Myelin is itself a type of cell called a Schwann cell and, if myelin becomes damaged by physical injury or disease – such as multiple sclerosis – the Schwann cells attempt to re-myelinate the axons. But the process is often insufficient and the damaged nerves might never fully regain their function. Researchers would thus like to enhance the natural re-myelination process to help damaged cells recapture their lost potential. A new technique that allows re-myelinating Schwann cells (stained green) to be distinguished from undamaged myelin (stained red) should help researchers understand the process and ultimately design treatments to improve it.

Electronic Implant Proposed to Restore Memory

A maverick neuroscientist and biomedical engineer believes he has deciphered the code by which the brain forms long-term memories.Theodore Berger envisions a day in the not too distant future when a patient with severe memory loss can get help from an electronic implant. For more than two decades, Berger has designed silicon chips to mimic the signal processing that neurons devoted to memory do when they’re functioning properly—the work that allows us to recall experiences and knowledge for more than a minute. Ultimately, Berger wants to restore the ability to create long-term memories by implanting chips like these in the brain.

The idea is so audacious and so far outside the mainstream of neuroscience that many of his colleagues think of him as being crazy, but given the success of recent experiments carried out by his group and several close collaborators, Berger is shedding the loony label and increasingly taking on the role of a visionary pioneer. Although yet to conduct human tests of their neural prostheses, their experiments show how a silicon chip externally connected to rat and monkey brains by electrodes can process information just like actual neurons.

The chips are not designed to put individual memories back into the brain, but to allow the brain the capacity to generate memories once again. Berger has spent much of the past 35 years trying to understand fundamental questions about the behavior of neurons in the hippocampus. It’s very clear the hippocampus makes short-term memories into long-term memories, but what is not clear is how the hippocampus accomplishes this complicated feat. Berger has developed mathematical theorems that describe how electrical signals move through the neurons of the hippocampus to form a long-term memory, and he has proved that his equations match reality.

Within the next two years, Berger and his colleagues hope to implant an actual memory prosthesis in animals. They also want to show that their hippocampal chips can form long-term memories in many different behavioral situations, since it’s possible that the code so far is not capable of generalizing. The distant goal is to jump onto human clinical projects in the hopes to improve the quality of life for somebody who has a severe memory deficit. Even if it can only give patients the ability to form new long-term memories for half the conditions that most people live in we’ll have already made huge bounds.  

Dr. Karl Deisseroth and colleagues at Stanford University have developed a technique called CLARITY that uses hydrogel to make the brain look like it is made of Jell-O. They have successfully applied this technique to a whole mouse brain as well as part of a human brain. Using CLARITY, they are able to observe neuronal networks three dimensionally while still maintaining the biochemistry of the brain. This allows researchers to observe recent activity by staining specific pathways and structures with dyes attached to antibodies that recognize specific proteins. The hope is to use CLARITY to understand mental health disorders. Considering this technique also reportedly works well with other tissues (livers, heart, etc), it may revolutionize tissue imaging.

Neurocorrelates for Psychopathic Lack of Empathy Investigated

It has long been understood that people with psychopathy have a marked lack of empathy – one of the behavioral characteristics associated with high repetitive and violent crime rates. However, the neural processes correlated with empathic processing have yet to be directly examined in individuals with psychopathy, especially in response to the perception of other people’s pain or distress, until now. A study conducted by the University of Chicago and the University of New Mexico published in JAMA Psychiatry has confirmed that prisoners who are psychopathic lack the basic neurophysiological “hardwiring” that enables them to care for others.

Participants were shown a series of scenarios depicting people being intentionally hurt while having their brain scanned in an fMRI machine. They were also tested on their responses to seeing short videos of facial expressions showing pain. Those in the high psychopathy group exhibited less activation in areas of the brain important for monitoring ongoing behavior, estimating consequences and incorporating emotional learning into moral decision-making thought to play a fundamental role in empathic concern. However, the unexpected finding was that those in the high psychopathy group also showed more activation compared to controls in an area of the brain associated with emotion and somatic resonance.

The results of the study could help clinical psychologists design better treatment programs for psychopaths, although full rehabilitation is still a pipe dream that is currently unlikely to be achieved. 

Brain Cell Linked to Unexpected Role in Healing

The production of a certain kind of brain cell that had been considered an impediment to healing may actually be needed to staunch bleeding and promote repair after a stroke or head trauma, researchers at Duke Medicine report in Nature. These cells, known as astrocytes, can be produced from stem cells in the brain after injury. They migrate to the site of damage where they are much more effective in promoting recovery than previously thought. This insight from studies in mice may help researchers develop treatments that foster brain repair.

Once damaged, mature neurons cannot multiply, so most research efforts have focused on inducing brain stem cells to produce more immature neurons to replace them. This strategy has proved difficult, because in addition to making neurons, neural stem cells also produce astrocytes and oligodendrocytes, known as glial cells. Although glial cells are important for maintaining the normal function of neurons in the brain, the increased production of astrocytes from neural stem cell has been considered an unwanted byproduct, causing more harm than good. Proliferating astrocytes secrete proteins that can induce tissue inflammation and undergo gene mutations that can lead to aggressive brain tumors.

In their study of mice, the Duke team found an unexpected insight about the astrocytes produced from stem cells after injury. Stem cells live in a special area or “niche” in the postnatal/adult brain called the subventricular zone, and churn out neurons and glia in the right proportions based on cues from the surrounding tissue.

After an injury, however, the subventricular niche pumps out more astrocytes. Significantly, the current study found they are different from astrocytes produced in most other regions of the brain. These cells make their way to the injured area to help make an organized scar, which stops the bleeding and allows tissue recovery. When the generation of these astrocytes in the subventricular niche was experimentally blocked after a brain injury, hemorrhaging occurred around the injured areas and the region did not heal.

Naturally there is a lot of interest in how new neurons can stimulate functional recovery, but if you make neurons without stopping the bleeding, the neurons don’t even get a chance. The brain somehow knows this, so that could be why it produces these unique astrocytes in response to injury. Since bleeding in the brain after injury is a common and serious problem for patients, further research into this area may lead to effective therapies for accelerated brain recovery.

Permanent Way to Bypass the Blood-Brain Barrier Found

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Neurodegenerative and central nervous system (CNS) diseases represent a major public health issue. Multiple drugs exist to treat and potentially cure these debilitating diseases, but 98 percent of all potential pharmaceutical agents are prevented from reaching the CNS directly due to the blood-brain barrier. Many attempts have been made to deliver drugs across the blood-brain barrier using methods such as osmotic disruption and implantation of catheters into the brain; however these methods are temporary and prone to infection and dislodgement.

Using mucosa, or the lining of the nose, researchers at Boston University have published what may be the first known method to permanently bypass the blood-brain barrier, thus opening the door to new treatment options for those with neurodegenerative and CNS disease. In this study using a mouse model, researchers describe a novel method of creating a semi-permeable window in the blood-brain barrier using purely autologous tissues to allow for higher molecular weight drug delivery to the CNS. They demonstrated for the first time that these membranes are capable of delivering molecules to the brain which are up to 1,000-times larger than those excluded by the blood-brain barrier.

The connection between poor sleep, memory loss and brain deterioration as we grow older has been elusive. But earlier this year, scientists at the University of California, Berkeley, have found a link between these hallmark maladies of old age. Their discovery opens the door to boosting the quality of sleep in elderly people to improve memory.

Human Stem Cell Restores Learning in Mice

A study at UW-Madison published in Nature Biotechnology is the first to show that human embryonic stem cells can successfully implant themselves in the brain and then heal neurological deficits.

Once inside the mouse brain, the implanted stem cells formed two common types of neurons which communicate with the neurotransmitters GABA or acetylcholine. These two cell types are both critical to brain function. Cholinergic neurons are involved in Alzheimer’s and Down syndrome, but GABA neurons are involved in many additional disorders, including schizophrenia, epilepsy, depression and addiction. Being able to reverse or repair these types of conditions is one of the main goals of stem cell transplantation.

The mice in the study had an area of their brain damaged that connects to the hippocampus – a vital memory center – by GABA and cholinergic neurons. The transplanted cells were then placed within the hippocampus, on the other end of the memory circuit from the damage, where in response to chemical directions from the brain they began to specialize and connect to appropriate cells. The process is akin to removing a section of telephone cable. If you can find the correct route, you could wire the replacement from either end.

After the transplant, the mice scored significantly better on common tests of learning and memory. For example, they were more adept in the water maze test which challenged them to remember the location of a hidden platform in a pool. The location, timing and purity of cells were critical to success.

While this type of stem-cell therapy is a promising option for straight forward and controlled neurological damage, it may be much harder to apply to more complex animals and disease patterns. For instance, in many psychiatric disorders we don’t really know which part of the brain has gone wrong. It is more likely that we will see an immediate application of this research in creating models for drug screening and discovery.