Understanding Consciousness

Why does a relentless stream of subjective experiences normally fill your mind? Maybe that’s just one of those mysteries that will always elude us. 

Yet, research from Northwestern University suggests that consciousness lies well within the realm of scientific inquiry — as impossible as that may currently seem. Although scientists have yet to agree on an objective measure to index consciousness, progress has been made with this agenda in several labs around the world.

“The debate about the neural basis of consciousness rages because there is no widely accepted theory about what happens in the brain to make consciousness possible,” said Ken Paller, professor of psychology in the Weinberg College of Arts and Sciences and director of the Cognitive Neuroscience Program at Northwestern.

“Scientists and others acknowledge that damage to the brain can lead to systematic changes in consciousness. Yet, we don’t know exactly what differentiates brain activity associated with conscious experience from brain activity that is instead associated with mental activity that remains unconscious,” he said.

In a new article, Paller and Satoru Suzuki, also professor of psychology at Northwestern, point out flawed assumptions about consciousness to suggest that a wide range of scientific perspectives can offer useful clues about consciousness.

“It’s normal to think that if you attentively inspect something you must be aware of it and that analyzing it to a high level would necessitate consciousness,” Suzuki noted. “Results from experiments on perception belie these assumptions.

“Likewise, it feels like we can freely decide at a precise moment, when actually the process of deciding begins earlier, via neurocognitive processing that does not enter awareness,” he said. 

The authors write that unconscious processing can influence our conscious decisions in ways we never suspect.

If these and other similar assumptions are incorrect, the researchers state in their article, then mistaken reasoning might be behind arguments for taking the science of consciousness off the table. 

“Neuroscientists sometimes argue that we must focus on understanding other aspects of brain function, because consciousness is never going to be understood,” Paller said. “On the other hand, many neuroscientists are actively engaged in probing the neural basis of consciousness, and, in many ways, this is less of a taboo area of research than it used to be.”

Experimental evidence has supported some theories about consciousness that appeal to specific types of neural communication, which can be described in neural terms or more abstractly in computational terms. Further theoretical advances can be expected if specific measures of neural activity can be brought to bear on these ideas.

Paller and Suzuki both conduct research that touches on consciousness. Suzuki studies perception, and Paller studies memory. They said it was important for them to write the article to counter the view that it is hopeless to ever make progress through scientific research on this topic.

They outlined recent advances that provide reason to be optimistic about future scientific inquiries into consciousness and about the benefits that this knowledge could bring for society.

“For example, continuing research on the brain basis of consciousness could inform our concerns about human rights, help us explain and treat diseases that impinge on consciousness, and help us perpetuate environments and technologies that optimally contribute to the well being of individuals and of our society,” the authors wrote.

They conclude that research on human consciousness belongs within the purview of science, despite philosophical or religious arguments to the contrary.

Their paper, “The Source of Consciousness,” has been published online in the journal Trends in Cognitive Sciences.

(Image: Shutterstock)

New research: teaching the brain to reduce pain

People can be conditioned to feel less pain when they hear a neutral sound, new research from the University of Luxembourg has found. This lends weight to the idea that we can learn to use mind-over-matter to beat pain. The scientific article was published recently in the online journal “PLOS One”.

Scientists have known for many years that on-going pain in one part of the body is reduced when a new pain is inflicted to another part of the body. This pain blocking is a physiological reaction by the nervous system to help the body deal with a potentially more relevant novel threat.

To explore this “pain inhibits pain” phenomenon, painful electric pulses were first administered to a subject’s foot (first pain) and the resulting pain intensity was then measured. Then the subject was asked to put their hand in a bucket of ice water (novel stimulus causing pain reduction), and as they did so, a telephone ringtone sounded in headphones. After this procedure had been repeated several times, it was observed that the pain felt from the electrical stimulation was reduced simply when the ring tone sounded.

The brain had been conditioned to the ringtone being a signal to trigger the body’s physical pain blocking mechanism. The people being tested not only felt significantly less pain, but there were also fewer objective signs of pain, such as activity in the muscles used in the facial expression of pain (frowning). In total, 32 people were tested.

“We have shown that just as the physiological reaction of saliva secretion was provoked in Pavlov’s dogs by the ringing of a bell, an analogous effect occurs regarding the ability to mask pain in humans,” said Fernand Anton, Professor of Biological Psychology at the University of Luxembourg. “Conversely, similar learning effects may be involved in the enhancement and maintenance of pain in some patients,” added Raymonde Scheuren, lead researcher in this study.

Chimp Intelligence “Runs In Families,” Environment Less Important

A chimpanzee’s intelligence is largely determined by its genes, while environmental factors may be less important than scientists previously thought, according to a Georgia State University research study.

The study found that some, but not all, cognitive, or mental, abilities, in chimpanzees depend significantly on the genes they inherit. The findings are reported in the latest issue of Current Biology.

“Intelligence runs in families,” said Dr. William Hopkins, professor in the Center for Behavioral Neuroscience at Georgia State and research scientist in the Yerkes National Primate Research Center at Emory University. “The suggestion here is that genes play a really important role in their performance on tasks while non-genetic factors didn’t seem to explain a lot. So that’s new.”

The role of genes in human intelligence or IQ has been studied for years, but Hopkins’ study is among the first to address heritability in cognitive abilities in nonhuman primates. Studies have shown that human intelligence is inherited through genes, but social and environmental factors, such as formal education and socioeconomic status, also play a role and are somewhat confounded with genetic factors. Chimpanzees, which are highly intelligent and genetically similar to humans, do not have these additional socio-cultural influences.

“Chimps offer a really simple way of thinking about how genes might influence intelligence without, in essence, the baggage of these other mechanisms that are confounded with genes in research on human intelligence,” Hopkins said.

The study involved 99 chimpanzees, ranging in age from 9 to 54, who completed 13 cognitive tasks designed to test a variety of abilities. Hopkins used quantitative genetics analysis to link the degree of relatedness between the chimpanzees to their similarities or differences in performance on the various cognitive measures to determine whether cognitive performance is inherited in chimpanzees.

Genes were found to play a role in overall cognitive abilities, as well as the performance on tasks in several categories.

Traditionally, researchers studying animal intelligence or animal learning have shared the view that environment and how previous behavior is reinforced affect how animals perform on a particular task.

“In our case, at least, it suggests that purely environmental explanations don’t really seem to tell the whole story,” Hopkins said. “Genes matter as well.”

Hopkins also studied the structure of chimpanzee intelligence to determine whether there were any similarities to the structure of human intelligence.

“We wanted to see if we gave a sample of chimpanzees a large array of tasks,” he said, “would we find essentially some organization in their abilities that made sense. The bottom line is that chimp intelligence looks somewhat like the structure of human intelligence.”

In the future, Hopkins wants to continue the study with an expanded sample size. He would also like to pursue studies to determine which genes are involved in intelligence and various cognitive abilities as well as how genes are linked to variation in the organization of the brain.

Hopkins also would like to determine which genes changed in human evolution that allowed humans to have such advanced intelligence.

(Image: Anup Shah / Nature Picture Library)

Cinnamon May Be Used to Halt the Progression of Parkinson’s disease

Neurological scientists at Rush University Medical Center have found that using cinnamon, a common food spice and flavoring material, can reverse the biomechanical, cellular and anatomical changes that occur in the brains of mice with Parkinson’s disease (PD). The results of the study were recently published in the June 20 issue of the Journal of Neuroimmune Pharmacology.

“Cinnamon has been used widely as a spice throughout the world for centuries,” said Kalipada Pahan, PhD, study lead researcher and the Floyd A. Davis professor of neurology at Rush. “This could potentially be one of the safest approaches to halt disease progression in Parkinson’s patients.”

“Cinnamon is metabolized in the liver to sodium benzoate, which is an FDA-approved drug used in the treatment for hepatic metabolic defects associated with hyperammonemia,” said Pahan. It is also widely used as a food preservative due to its microbiocidal effect.

Chinese cinnamon (Cinnamonum cassia) and original Ceylon cinnamon (Cinnamonum verum) are two major types of cinnamon that are available in the US.

“Although both types of cinnamon are metabolized into sodium benzoate, by mass spectrometric analysis, we have seen that Ceylon cinnamon is much more pure than Chinese cinnamon as the latter contains coumarin, a hepatotoxic molecule,” said Pahan.

“Understanding how the disease works is important to developing effective drugs that protect the brain and stop the progression of PD,” said Pahan. “It is known that some important proteins like Parkin and DJ-1 decrease in the brain of PD patients.”

The study found that after oral feeding, ground cinnamon is metabolized into sodium benzoate, which then enters into the brain, stops the loss of Parkin and DJ-1, protects neurons, normalizes neurotransmitter levels, and improves motor functions in mice with PD.

This research was supported by grants from National Institutes of Health.

“Now we need to translate this finding to the clinic and test ground cinnamon in patients with PD. If these results are replicated in PD patients, it would be a remarkable advance in the treatment of this devastating neurodegenerative disease,” said Dr. Pahan.

Parkinson’s disease is a slowly progressive disease that affects a small area of cells within the mid-brain known as the substantia nigra. Gradual degeneration of these cells causes a reduction in a vital chemical neurotransmitter, dopamine. The decrease in dopamine results in one or more of the classic signs of Parkinson’s disease that includes: resting tremor on one side of the body; generalized slowness of movement; stiffness of limbs; and gait or balance problems. The cause of the disease is unknown. Both environmental and genetic causes of the disease have been postulated.

Parkinson’s disease affects about 1.2 million patients in the United States and Canada. Although 15 percent of patients are diagnosed before age 50, it is generally considered a disease that targets older adults, affecting one of every 100 persons over the age of 60. This disease appears to be slightly more common in men than women.

Study cracks how the brain processes emotions

Although feelings are personal and subjective, the human brain turns them into a standard code that objectively represents emotions across different senses, situations and even people, reports a new study by Cornell University neuroscientist Adam Anderson.

“We discovered that fine-grained patterns of neural activity within the orbitofrontal cortex, an area of the brain associated with emotional processing, act as a neural code which captures an individual’s subjective feeling,” says Anderson, associate professor of human development in Cornell’s College of Human Ecology and senior author of the study. “Population coding of affect across stimuli, modalities and individuals,” published online in Nature Neuroscience.

Their findings provide insight into how the brain represents our innermost feelings – what Anderson calls the last frontier of neuroscience – and upend the long-held view that emotion is represented in the brain simply by activation in specialized regions for positive or negative feelings, he says.

“If you and I derive similar pleasure from sipping a fine wine or watching the sun set, our results suggest it is because we share similar fine-grained patterns of activity in the orbitofrontal cortex,” Anderson says.

“It appears that the human brain generates a special code for the entire valence spectrum of pleasant-to-unpleasant, good-to-bad feelings, which can be read like a ‘neural valence meter’ in which the leaning of a population of neurons in one direction equals positive feeling and the leaning in the other direction equals negative feeling,” Anderson explains.

For the study, the researchers presented participants with a series of pictures and tastes during functional neuroimaging, then analyzed participants’ ratings of their subjective experiences along with their brain activation patterns.

Anderson’s team found that valence was represented as sensory-specific patterns or codes in areas of the brain associated with vision and taste, as well as sensory-independent codes in the orbitofrontal cortices (OFC), suggesting, the authors say, that representation of our internal subjective experience is not confined to specialized emotional centers, but may be central to perception of sensory experience.

They also discovered that similar subjective feelings – whether evoked from the eye or tongue – resulted in a similar pattern of activity in the OFC, suggesting the brain contains an emotion code common across distinct experiences of pleasure (or displeasure), they say. Furthermore, these OFC activity patterns of positive and negative experiences were partly shared across people.

“Despite how personal our feelings feel, the evidence suggests our brains use a standard code to speak the same emotional language,” Anderson concludes.

Discovery of New Drug Targets for Memory Impairment in Alzheimer’s Disease

We are now a step closer to having a drug that can cure dementia and memory loss. Research team in Korea has discovered that reactive astrocytes, which have been commonly observed in Alzheimer’s patients, aberrantly and abundantly produce the chief inhibitory neurotransmitter GABA and release it through the Best1 channel. The released GABA strongly inhibits neighboring neurons to cause impairment in synaptic transmission, plasticity and memory. This discovery will open a new chapter in the development of new drugs for treating such diseases.

Alzheimer’s disease, which is the most common cause of dementia, is fatal and currently, there is no cure. In Alzheimer’s disease, brain cells are damaged and destroyed, leading to devastating memory loss. It is reported that 1 in 8 Americans aged 65 or over have Alzheimer’s disease. In 2011, 7,600 elderly people with dementia lost their way back home and became homeless in Korea. However, to date, there has been no clear understanding of the mechanisms underlying dementia in Alzheimer’s disease. So far, neuronal death is the only proposed mechanism available in scientific literature.

The research team discovered that reactive astrocytes in the brains of Alzheimer’s disease model mice produce the inhibitory transmitter GABA by the enzyme Monoamine oxidase B(MAO-B) and release GABA through the Bestrophin-1 channel to suppress normal information flow during synaptic transmission. Based on this discovery, the team was able to reduce the production and release of GABA by inhibiting MAO-B or Bestrophin-1, and successfully ameliorate impairments in neuronal firing, synaptic transmission and memory in Alzheimer’s disease model mice.

In the behavioral test, the team used the fact that mice tend to prefer dark places. If a mouse experiences an electric shock in a dark place, it will remember this event and avoid dark places from then on. However, a mouse with modeled Alzheimer’s disease cannot remember if such shock is related to dark places and keeps going back to dark places. The team demonstrated that treating these mice with a MAO-B inhibitor fully recovered the mice’s memory. The selegiline is currently used in Parkinson’s disease as an adjunct therapy and considered as a one of best promising medicine for MAO-B inhibitor. But it has been previously shown to be less effective in Alzheimer’s disease.

The team proved that selegiline is effective for a short time, but when it is used in long term, it loses its efficacy in Alzheimer’s disease model mice. When treated for 1 week, selegiline brought the neuronal firing to a normal level. But when it was treated for 2 and 4 weeks, neuronal firing came back to the levels of untreated mice. From these results, the team proposed that there is a pressing need for a new drug that has long lasting effects.

Dr. C. Justin Lee said, “From this study, we reveal the novel mechanism of how Alzheimer’s patients might lose their memory. We also propose new therapeutic targets, which include GABA production and release mechanisms in reactive astrocytes for treatment of Alzheimer’s disease. Furthermore, we provide a stepping stone for the development of MAO-B inhibitors with long lasting efficacy.”

Discovery of new means to erase pain

A study published in the scientific journal Nature Neuroscience by Yves De Koninck and Robert Bonin, two researchers at Université Laval, reveals that it is possible to relieve pain hypersensitivity using a new method that involves rekindling pain so that it can subsequently be erased. This discovery could lead to novel means to alleviate chronic pain.

The researchers from the Faculty of Medicine at Université Laval and Institut universitaire en santé mentale de Québec (IUSMQ) were inspired by previous work on memory conducted some fifteen years ago. These studies had revealed that when a memory is reactivated during recall, its neurochemical encoding is temporarily unlocked. Simultaneous administration of a drug that blocks neurochemical reconsolidation of the memory results in its erasure.

The investigators wanted to see whether a similar mechanism was at play during neurochemical encoding of pain sensitization. To this end, they injected capsaicin in the foot of mice. Capsaicin, the pungent chemical in chili pepper, triggers a burning sensation. The procedure, which causes no physical damage, triggers pain hypersensitivity through a process of protein synthesis in the spinal cord. After capsaicin injections, the mechanical pressure at which mice would flinch was about a third of that in the normal situation.

Three hours later, the researchers administered a second dose of capsaicin and, at the same time, a drug that blocks protein synthesis. The hypersensitivity then vanished rapidly. Within less than 2 hours, the pressure tolerated by the mice was back to 70% of normal.

Yves De Koninck explains that “when the protein synthesis inhibitor is administered alone, the hypersensitivity remains. The second injection of capsaicin is necessary to render the sensitivity to pain unstable and be able to interfere with its neurochemical reconsolidation. The challenge now will be to find protein synthesis inhibitors that are nontoxic and cause minimal side effects in humans”.