Scientists have found that people with conservative views have brains with larger amygdalas, almond shaped areas in the centre of the brain often associated with anxiety and emotions.
On the otherhand, they have a smaller anterior cingulate, an area at the front of the brain associated with courage and looking on the bright side of life. [...]
The results, which will be published next year, back up a (different) study that showed that some people were born with a “Liberal Gene” that makes people more likely to seek out less conventional political views.
The gene, a neurotransmitter in the brain called DRD4, could even be stimulated by the novelty value of radical opinions, claimed the researchers at the University of California. (via.)
The posterior cingulate cortex (PCC) is activated when normal subjects see faces or hear voices of emotionally significant people in their lives; however, in autism the level of activation is impaired. [...]
The use of selective serotonin reuptake inhibitor (SSRI) medication has been shown to be successful in the treatment of autistic behaviors in some individuals. Serotonin (5-HT) has a role in neuronal development and has been extensively studied in autism with reports of excess 5-HT in the blood (hyperserotonemia) in some people with autism. [...]
The results show that there was a significant decrease in the density of one key type of serotonin receptor, the 5HT2A receptor, in the superficial cortical layers of the PCC in the adult autistic group when compared to age-matched controls. Similar results were found recently in the anterior cingulate cortex, an area involved in social-emotional processing. Evaluated together, these findings suggest that the 5-HT2a serotonin receptor decrease occurs in widespread cortical areas and may play a central role in some of the social deficits observed in autism. (via.)
Just some loosely connected neuro-things I wanted to save somewhere.
- Notably without citation, Wikipedia claims BDNF is also expressed in the retina, the central nervous system, motor neurons, the kidneys, and the prostate (aside from just the hippocampus and cerebral cortex). (via.)
- BDNF knockingout in mice affects coordination, balance, hearing, taste, and breathing. “Knockout mice also exhibit cerebellar abnormalities and an increase in the number of sympathetic neurons.” (via.)
- BDNF is increased by prolonged seizures, and important to GABA pathways. (via.)
- Hypergraphia, a condition which afflicts individuals with a compulsive desire to write, is associated with temporal lobe epilepsy… and quite a few interesting characters have had it. (via.)
- Hyperlexia, the extreme variety of a compulsion to read, may be caused by a “cerebral infarction in the left anterior cingulate cortex and corpus callosum.” (via.)
- Temporal lobe epileptics are often hyposexual. (via.)
Bilateral cingulotomy is a form of psychosurgery, introduced in 1952 as an alternative to lobotomy. Today, it is mainly used as a last resort for the treatment of obsessive-compulsive disorder and chronic pain. The objective of this surgical procedure is the severing of the supracallosal fibres of the cingulum bundle, which pass through the anterior cingulate gyrus. (via.)
First of all… I simply wasn’t aware that this form of surgery existed. Second of all… This page (the bilateral cingulotomy one) is actually, in some ways, more informative on the topic of the anterior cingulate cortex than the actual Wikipedia page on the anterior cingulate cortex.
Oh one other note… I realized while doing searches on this bilateral cingulotomy is often misspelled as bilateral cingulatomy. I’m actually not entirely sure which is the correct spelling, but I think it’s cingulotomy.
As I have mentioned in at least one previous post, choline may have some anxiolytic effects. The reason being for this is that choline, in at least one study was shown to have an inverse relationship with reported anxiety levels in a study’s participants.
Additionally I recently made a post about a study that showed a reduction in choline in the anterior cingulate cortices of people who have been smoking.
“The ACC is involved in mediating conditioned reinforcement, craving and relapsing behavior in addiction,” said study co-author Christian G. Schütz, M.D., M.P.H., from the Department of Psychiatry at the University of Bonn.
So this begs the question… could supplementing choline play at least a small part in a larger scheme to help smokers prevent relapse when they decide to quit?
Using magnetic resonance imaging (MRI) to assess brain function, Coghill and colleagues found that study participants who said that a heat stimulus was intensely painful had pronounced activation of brain regions that are important in pain. In contrast, people who said that the same stimulus was only mildly painful had minimal activation of these same areas.
“One of the most difficult aspects of treating pain has been having confidence in the accuracy of patients’ self-reports of pain,” said Coghill, an assistant professor of neurobiology and anatomy. “These findings confirm that self-reports of pain intensity are highly correlated to brain activation and that self-reports should guide treatment of pain.”
For the research, 17 normal, healthy volunteers (eight women and nine men) had a computer-controlled heat stimulator placed on their leg. While their brains were scanned, this device heated a small patch of their skin to 120° Fahrenheit, a temperature that most people find painful. However, participants reported very different experiences of pain. Using a 10-point scale, the least sensitive person rated the pain around a “one,” while the most sensitive person rated the pain as almost a “nine.”
People who reported higher levels of pain showed increased activation in areas of the brain important in pain: the primary somatosensory cortex, which contributes to the perception of where a painful stimulus is located on the body and how intense it is, and the anterior cingulate cortex, which is involved in the processing the unpleasant feelings evoked by pain. However, there was little difference between subjects in activation of the thalamus, which is involved in transmitting pain signals from the spinal cord to higher brain regions.
“This difference between cortical and thalamic patterns of activation may help explain pain differences between individuals,” said Coghill. “This finding raises the intriguing possibility that incoming painful information is processed by the spinal cord in a generally similar manner. But, once the brain gets involved, the experience becomes very different from one individual to the next.”
Coghill believes that most individual differences in pain sensitivity are probably due to a combination of cognitive factors, such as past experience with pain, emotional state at the time pain is experienced, and expectations about pain. (via.)
Twenty years ago Rosenfeld found that he could change the pain threshold in mice by training them to alter their brainwave patterns through a process called conditioned learning, where an altered brainwave state was rewarded by direct stimulation of the reward centres in their brains. Since this meant placing an electrode into the brain, however, his team never tried the technique on people.
Now Fumiko Maeda, Christopher deCharms and their colleagues at Stanford University in California have tried showing people real-time feedback from a functional magnetic resonance imaging (fMRI) scanner.
The difference between EEGs and fMRI, says Rosenfeld, is that fMRI allows you to show volunteers how much activity there is in specific areas of their brains. “From scalp recordings, you don’t really know what you are recording,” he says.
The eight volunteers saw the activity of a pain-control region called the rostral anterior cingulate cortex represented on a screen either as a flame that varied in size, or as a simple scrolling bar graph.
This brain region is known to modulate both the intensity and the emotional impact of pain. During the scans the volunteers had to endure painful heat on the palm of their hand. They were asked to try to increase or decrease the signal from the brain scanner and to periodically rate their pain sensations.
It took just three 13-minute sessions in the scanner for the eight volunteers to learn to vary the brain activity level, and thus to develop some control over their pain sensations, the researchers reported at the Cognitive Neuroscience Society meeting in San Francisco last week.
The effect seemed to last beyond the sessions in the scanner, although the researchers have yet to determine how strongly and for how long. The volunteers could not explain how they did it. The researchers ruled out other explanations for the effect through a series of controls. They gave people false feedback data, no feedback at all, or feedback from a part of the brain unrelated to pain control. They also sometimes asked people to pay attention to the pain or distracted their attention away from it. (via.)
The contrasts between disbelief and belief showed increased signal in the anterior insula, a region involved in the sensation of taste, the perception of pain, and the feeling of disgust, indicating that “false propositions might actually disgust us,” the authors state. “Our results appear to make sense of the emotional tone of disbelief, placing it on a continuum with other modes of stimulus appraisal and rejection,” they add.
Uncertainty evoked a positive signal in the anterior cingulate cortex (ACC) and a decreased signal in the caudate, a region of the basal ganglia, which plays a role in motor action. Noting that both belief and disbelief showed an increased signal in the caudate compared to uncertainty, the authors suggest that the basal ganglia may play a role in mediating the cognitive and behavioral differences between decision and indecision.
The study raises the possibility that the differences between belief, disbelief and uncertainty may one day be reliably distinguished by neuroimaging techniques. They conclude: “This would have obvious implications for the detection of deception, for the control of the placebo effect during the process of drug design, and for the study of any higher-cognitive phenomenon in which the differences between belief, disbelief, and uncertainty might be a relevant variable.” (via.)
DYN is the major posttranslational product of the PDYN gene and the presumed endogenous ligand for the KOPr (Chavkin et al., 1982; Corbett et al. 1982). [...] DYN and KOPr are highly expressed in the prefrontal-cortico-striatal loop. PDYN expressing neurons are present throughout the neocortex with highest expression in the medial PFC and anterior cingulate (Alvarez-Bolado et al., 1990; Hurd, 1996). DYN content is low in comparison to other regions. However, immunoreactive cell bodies are found in layers II, III, V and VI. Neurons in layer V are presumed to be corticofugal fibers that innervate the NAc and other subcortical regions. (via.)
DYN = Dynorphin
PDYN = Prodynorphin
KOPr = Kappa opioid receptor
Mayberg, for instance, asks volunteers to recall a sad memory. When they start crying, she uses a PET scan to measure blood flow in the brain. The “hottest” area (the one with the biggest increase in blood flow) turns out to be a small part of the anterior cingulate called area 25, part of the limbic system. While this area gets more active, the prefrontal cortex, or thinking area, turns off.
In healthy people immersed in sad feelings, the brain can quickly shift back toward equilibrium. “The phone rings, the baby cries, the boss calls and you immediately disengage from the sadness and the thinking part of the brain turns back on,” she says. With depressed people, this ability to shift back to equilibrium is altered. (via: dynorphin and depression)