Do women experience negative emotions differently than men?

Date:September 23, 2015

Source:Université de Montréal

Summary:Women react differently to negative images compared to men, which may be explained by subtle differences in brain function. This neurobiological explanation for women’s apparent greater sensitivity has been demonstrated by researchers in a new study.

“Not everyone’s equal when it comes to mental illness,” said Adrianna Mendrek, a researcher at the Institut universitaire en santé mentale de Montréal and lead author of the study. “Greater emotional reactivity in women may explain many things, such as their being twice as likely to suffer from depression and anxiety disorders compared to men,” Mendrek added, who is also an associate professor at the University of Montreal’s Department of Psychiatry.

In their research, Mendrek and her colleagues observed that certain areas of the brains of women and men, especially those of the limbic system, react differently when exposed to negative images. They therefore investigated whether women’s brains work differently than men’s and whether this difference is modulated by psychological (male or female traits) or endocrinological (hormonal variations) factors.

For the study, 46 healthy participants — including 25 women — viewed images and said whether these evoked positive, negative, or neutral emotions. At the same time, their brain activity was measured by brain imaging. Blood samples were taken beforehand to determine hormonal levels (e.g., estrogen, testosterone) in each participant.

The researchers found that subjective ratings of negative images were higher in women compared to men. Higher testosterone levels were linked to lower sensitivity, while higher feminine traits (regardless of sex of tested participants) were linked to higher sensitivity. Furthermore, while, the dorsomedial prefrontal cortex (dmPFC) and amygdala of the right hemisphere were activated in both men and women at the time of viewing, the connection between the amygdala and dmPFC was stronger in men than in women, and the more these two areas interacted, the less sensitivity to the images was reported. “This last point is the most significant observation and the most original of our study,” said Stéphane Potvin, a researcher at the Institut universitaire en santé mentale and co-author of the study.

The amygdala is a region of the brain known to act as a threat detector and activates when an individual is exposed to images of fear or sadness, while the dmPFC is involved in cognitive processes (e.g., perception, emotions, reasoning) associated with social interactions. “A stronger connection between these areas in men suggests they have a more analytical than emotional approach when dealing with negative emotions,” added Potvin, who is also an associate professor at the University of Montreal’s Department of Psychiatry. “It is possible that women tend to focus more on the feelings generated by these stimuli, while men remain somewhat ‘passive’ toward negative emotions, trying to analyse the stimuli and their impact.”

This connection between the limbic system and the prefrontal cortex appeared to be modulated by testosterone — the male hormone — which tends to reinforce this connection, as well as by an individual’s gender (as measured be the level of femininity and masculinity). “So there are both biological and cultural factors that modulate our sensitivity to negative situations in terms of emotions,” Mendrek explained. “We will now look at how the brains of men and women react depending on the type of negative emotion (e.g., fear, sadness, anger) and the role of the menstrual cycle in this reaction.”


Story Source:

The above post is reprinted from materials provided by Université de Montréal. Note: Materials may be edited for content and length.


Journal Reference:

  1. Ovidiu Lungu, Stéphane Potvin, Andràs Tikàsz, Adrianna Mendrek. Sex differences in effective fronto-limbic connectivity during negative emotion processing. Psychoneuroendocrinology, 2015; 62: 180 DOI: 10.1016/j.psyneuen.2015.08.012

Human Brain Is Divided On Fear and Panic: Different Areas of Brain Responsible for External, Internal Threats

Feb. 4, 2013 — When doctors at the University of Iowa prepared a patient to inhale a panic-inducing dose of carbon dioxide, she was fearless. But within seconds of breathing in the mixture, she cried for help, overwhelmed by the sensation that she was suffocating.


The patient, a woman in her 40s known as SM, has an extremely rare condition called Urbach-Wiethe disease that has caused extensive damage to the amygdala, an almond-shaped area in the brain long known for its role in fear. She had not felt terror since getting the disease when she was an adolescent.

In a paper published online Feb. 3 in the journal Nature Neuroscience, the UI team provides proof that the amygdala is not the only gatekeeper of fear in the human mind. Other regions — such as the brainstem, diencephalon, or insular cortex — could sense the body’s most primal inner signals of danger when basic survival is threatened.

“This research says panic, or intense fear, is induced somewhere outside of the amygdala,” says John Wemmie, associate professor of psychiatry at the UI and senior author on the paper. “This could be a fundamental part of explaining why people have panic attacks.

If true, the newly discovered pathways could become targets for treating panic attacks, post-traumatic stress syndrome, and other anxiety-related conditions caused by a swirl of internal emotional triggers.

“Our findings can shed light on how a normal response can lead to a disorder, and also on potential treatment mechanisms,” says Daniel Tranel, professor of neurology and psychology at the UI and a corresponding author on the paper.

Decades of research have shown the amygdala plays a central role in generating fear in response to external threats. Indeed, UI researchers have worked for years with SM, and noted her absence of fear when she was confronted with snakes, spiders, horror movies, haunted houses, and other external threats, including an incident where she was held up at knife point. But her response to internal threats had never been explored.

The UI team decided to test SM and two other amygdala-damaged patients with a well-known internally generated threat. In this case, they asked the participants, all females, to inhale a gas mixture containing 35 percent carbon dioxide, one of the most commonly used experiments in the laboratory for inducing a brief bout of panic that lasts for about 30 seconds to a minute. The patients took one deep breath of the gas, and quickly had the classic panic-stricken response expected from those without brain damage: They gasped for air, their heart rate shot up, they became distressed, and they tried to rip off their inhalation masks. Afterward, they recounted sensations that to them were completely novel, describing them as “panic.”

“They were scared for their lives,” says first author Justin Feinstein, a clinical neuropsychologist who earned his doctorate at the UI last year.

Wemmie had looked at how mice responded to fear, publishing a paper in the journal Cell in 2009 showing that the amygdala can directly detect carbon dioxide to produce fear. He expected to find the same pattern with humans.

“We were completely surprised when the patients had a panic attack,” says Wemmie, also a faculty member in the Iowa Neuroscience Graduate Program.

By contrast, only three of 12 healthy participants panicked — a rate similar to adults with no history of panic attacks. Notably, none of the three patients with amygdala damage has a history of panic attacks. The higher rate of carbon dioxide-induced panic in the patients suggests that an intact amygdala may normally inhibit panic.

Interestingly, the amygdala-damaged patients had no fear leading up to the test, unlike the healthy participants, many who began sweating and whose heart rates rose just before inhaling the carbon dioxide. That, of course, was consistent with the notion that the amygdala detects danger in the external environment and physiologically prepares the organism to confront the threat.

“Information from the outside world gets filtered through the amygdala in order to generate fear,” Feinstein says. “On the other hand, signs of danger arising from inside the body can provoke a very primal form of fear, even in the absence of a functioning amygdala.”

Contributing authors include Colin Buzza, Robin Follmer, and William Coryell, from the UI Department of Psychiatry; Rene Hurlemann, from the University of Bonn Department of Psychiatry; Nader Dahdaleh, of the UI Department of Neurosurgery; and Michael Welsh, UI professor of internal medicine and molecular physiology and biophysics and a Howard Hughes Medical Institute investigator. Buzza and Hurlemann are co-first authors on the paper.


Story Source:

The above story is reprinted from materials provided byUniversity of Iowa. The original article was written by John Riehl.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal References:

  1. Justin S Feinstein, Colin Buzza, Rene Hurlemann, Robin L Follmer, Nader S Dahdaleh, William H Coryell, Michael J Welsh, Daniel Tranel, John A Wemmie. Fear and panic in humans with bilateral amygdala damageNature Neuroscience, 2013; DOI: 10.1038/nn.3323
  2. Adam E. Ziemann, Jason E. Allen, Nader S. Dahdaleh, Iuliia I. Drebot, Matthew W. Coryell, Amanda M. Wunsch, Cynthia M. Lynch, Frank M. Faraci, Matthew A. Howard, Michael J. Welsh, John A. Wemmie. The Amygdala Is a Chemosensor that Detects Carbon Dioxide and Acidosis to Elicit Fear BehaviorCell, 2009; 139 (5): 1012 DOI: 10.1016/j.cell.2009.10.029
University of Iowa (2013, February 4). Human brain is divided on fear and panic: Different areas of brain responsible for external, internal threats. ScienceDaily. Retrieved February 5, 2013, from http://www.sciencedaily.com/releases/2013/02/130204130106.htm

Previously Unknown Mechanism of Memory Formation Discovered

Jan. 30, 2013 — It takes a lot to make a memory. New proteins have to be synthesized, neuron structures altered. While some of these memory-building mechanisms are known, many are not. Some recent studies have indicated that a unique group of molecules called microRNAs, known to control production of proteins in cells, may play a far more important role in memory formation than previously thought.


Now, a new study by scientists on the Florida campus of The Scripps Research Institute has for the first time confirmed a critical role for microRNAs in the development of memory in the part of the brain called the amygdala, which is involved in emotional memory. The new study found that a specific microRNA — miR-182 — was deeply involved in memory formation within this brain structure.

“No one had looked at the role of microRNAs in amygdala memory,” said Courtney Miller, a TSRI assistant professor who led the study. “And it looks as though miR-182 may be promoting local protein synthesis, helping to support the synapse-specificity of memories.”

In the new study, published in theJournal of Neuroscience, the scientists measured the levels of all known microRNAs following an animal model of learning. A microarray analysis, which enables rapid genetic testing on a large scale, showed that more than half of all known microRNAs are expressed in the amygdala. Seven of those microRNAs increased and 32 decreased when learning occurred.

The study found that, of the microRNAs expressed in the brain, miR-182 had one of the lowest levels and these decreased further with learning. Despite these very low levels, its overexpression prevented the formation of memory and led to a decrease in proteins that regulate neuronal plasticity (neurons’ ability to adapt) through changes in structure.

These findings suggest that learning-induced suppression of miR-182 is a main supporting factor in the formation of long-term memory in the amagdala, as well as an underappreciated mechanism for regulating protein synthesis during memory consolidation, Miller said.

Further analysis identified miR-182 as a repressor of proteins that control actin — a major component of the cytoskeleton, the scaffolding that holds cells together.

“We know that memory formation requires changes in dendritic spines on the neurons through regulation of the actin cytoskeleton,” Miller said. “When miR-182 is suppressed through learning it halts, at least in part, repression of actin-regulating proteins, so there’s a good chance that miR-182 exerts important control over the actin cytoskeleton.”

Miller is now interested in whether or not high levels of miR-182 accumulate in the aging brain, something that would help to explain a tendency toward memory loss in the elderly. She also notes that other research has shown that animal models lacking miR-182 had no significant physical or cellular abnormalities, suggesting that miR-182 could be a viable target for drug discovery.


Story Source:

The above story is reprinted from materials provided byThe Scripps Research Institute.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. E. M. Griggs, E. J. Young, G. Rumbaugh, C. A. Miller.MicroRNA-182 Regulates Amygdala-Dependent Memory FormationJournal of Neuroscience, 2013; 33 (4): 1734 DOI: 10.1523/JNEUROSCI.2873-12.2013
The Scripps Research Institute (2013, January 30). Previously unknown mechanism of memory formation discovered. ScienceDaily. Retrieved January 31, 2013, from http://www.sciencedaily.com/releases/2013/01/130130121545.htm

Neuroscientists Pinpoint Location of Fear Memory in Amygdala

Jan. 27, 2013 — A rustle of undergrowth in the outback: it’s a sound that might make an animal or person stop sharply and be still, in the anticipation of a predator. That “freezing” is part of the fear response, a reaction to a stimulus in the environment and part of the brain’s determination of whether to be afraid of it.

An image showing neurons in the lateral subdivision of the central amygdala (CeL). In red are somatostain-positive (SOM+) neurons, which control fear; in green are another set of neurons known as PKC-delta cells. (Credit: Image courtesy of Bo Li)

 

A neuroscience group at Cold Spring Harbor Laboratory (CSHL) led by Assistant Professor Bo Li Ph.D., together with collaborator Professor Z. Josh Huang Ph.D., have just released the results of a new study that examines the how fear responses are learned, controlled, and memorized. They show that a particular class of neurons in a subdivision of the amygdala plays an active role in these processes.

Locating fear memory in the amygdala

Previous research had indicated that structures inside the amygdalae, a pair of almond-shaped formations that sit deep within the brain and are known to be involved in emotion and reward-based behavior, may be part of the circuit that controls fear learning and memory. In particular, a region called the central amygdala, or CeA, was thought to be a passive relay for the signals relayed within this circuit.

Li’s lab became interested when they observed that neurons in a region of the central amygdala called the lateral subdivision, or CeL, “lit up” in a particular strain of mice while studying this circuit.

“Neuroscientists believed that changes in the strength of the connections onto neurons in the central amygdala must occur for fear memory to be encoded,” Li says, “but nobody had been able to actually show this.”

This led the team to further probe into the role of these neurons in fear responses and furthermore to ask the question: If the central amygdala stores fear memory, how is that memory trace read out and translated into fear responses?

To examine the behavior of mice undergoing a fear test the team first trained them to respond in a Pavlovian manner to an auditory cue. The mice began to “freeze,” a very common fear response, whenever they heard one of the sounds they had been trained to fear.

To study the particular neurons involved, and to understand them in relation to the fear-inducing auditory cue, the CSHL team used a variety of methods. One of these involved delivering a gene that encodes for a light-sensitive protein into the particular neurons Li’s group wanted to look at.

By implanting a very thin fiber-optic cable directly into the area containing the photosensitive neurons, the team was able to shine colored laser light with pinpoint accuracy onto the cells, and in this manner activate them. This is a technique known as optogenetics. Any changes in the behavior of the mice in response to the laser were then monitored.

A subset of neurons in the central amygdala controls fear expression

The ability to probe genetically defined groups of neurons was vital because there are two sets of neurons important in fear-learning and memory processes. The difference between them, the team learned, was in their release of message-carrying neurotransmitters into the spaces called synapses between neurons. In one subset of neurons, neurotransmitter release was enhanced; in another it was diminished. If measurements had been taken across the total cell population in the central amygdala, neurotransmitter levels from these two distinct sets of neurons would have been averaged out, and thus would not have been detected.

Li’s group found that fear conditioning induced experience-dependent changes in the release of neurotransmitters in excitatory synapses that connect with inhibitory neurons — neurons that suppress the activity of other neurons — in the central amygdala. These changes in the strength of neuronal connections are known as synaptic plasticity.

Particularly important in this process, the team discovered, were somatostatin-positive (SOM+) neurons. Somatostatin is a hormone that affects neurotransmitter release. Li and colleagues found that fear-memory formation was impaired when they prevent the activation of SOM+ neurons.

SOM+ neurons are necessary for recall of fear memories, the team also found. Indeed, the activity of these neurons alone proved sufficient to drive fear responses. Thus, instead of being a passive relay for the signals driving fear learning and responses in mice, the team’s work demonstrates that the central amygdala is an active component, and is driven by input from the lateral amygdala, to which it is connected.

“We find that the fear memory in the central amygdala can modify the circuit in a way that translates into action — or what we call the fear response,” explains Li.

In the future Li’s group will try to obtain a better understanding of how these processes may be altered in post-traumatic stress disorder (PTSD) and other disorders involving abnormal fear learning. One important goal is to develop pharmacological interventions for such disorders.

Li says more research is needed, but is hopeful that with the discovery of specific cellular markers and techniques such as optogenetics, a breakthrough can be made.

 

Story Source:

The above story is reprinted from materials provided byCold Spring Harbor Laboratory.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Haohong Li, Mario A Penzo, Hiroki Taniguchi, Charles D Kopec, Z Josh Huang, Bo Li. Experience-dependent modification of a central amygdala fear circuitNature Neuroscience, 2013; DOI: 10.1038/nn.3322
Cold Spring Harbor Laboratory (2013, January 27). Neuroscientists pinpoint location of fear memory in amygdala. ScienceDaily. Retrieved January 30, 2013, from http://www.sciencedaily.com/releases/2013/01/130128104739.htm