By Ernie Hood
Why, oh why, did you say, “Hit Me!” when you already had 17 in your blackjack hand?
If you’ve ever made a choice under stress that you later regretted (and who among us hasn’t?), you may be able to chalk up that unfortunate decision to the anxiety you experienced during the process.
Results of an experiment with an animal model of anxiety suggest that anxiety disengages a specific set of neurons in the brain’s prefrontal cortex (PFC)—a group of cells specifically associated with choice. Rats given a small dose of an anxiety producing drug were more likely than controls that were given a placebo to be distracted in the experimental setting and less likely to make the appropriate choice to gain a reward.
The study by a group of University of Pittsburgh researchers led by professor of neuroscience and psychiatry Dr. Bita Moghaddam was published in early 2016 in the Journal of Neuroscience. It showed that the anxious rats experienced a phenomenon called hypofrontality, where anxiety disrupted the ability of the critical PFC neurons to engage in flexible decision making, or shifting between behavioral strategies.
“A brain locus of vulnerability for these anxiety-induced mistakes was a group of cells in the PFC that specifically coded for choice. Anxiety weakened the coding power of these neurons,” said Moghaddam.
She noted that the results seen in the rat experiments were relevant to the human experience because human imaging studies have shown that similar hypofrontality, or reduced PFC engagement, is seen in anxious people.
It’s all about the neurons
“I am interested in the neuronal basis of anxiety,” said Moghaddam. “Its relevance to mental health disorders extends well beyond anxiety disorders. Anxiety is a debilitating symptom of many psychiatric disorders, including PTSD, major depression, autism, schizophrenia and addiction. It is, therefore, a serious public health problem.”
She emphasized that the neural effects of anxiety are not the same as those brought on by fear. “Fear is a different construct than anxiety,” she explained. “The imminence of threat associated with fear versus the uncertain probability of potential harm associated with anxiety is unlikely to be associated with identical activation or inactivation of brain systems.”
Previous animal studies of anxiety have mostly focused on response to fear, instead of zeroing in specifically on anxiety itself and where it resides in the function of brain cells.
Of course, the distinction between anxiety and fear has profound implications for both the study and treatment of anxiety, which have heretofore been characterized by a simplistic approach, according to Moghaddam. “We have equated anxiety with fear and have assumed that it over-engages entire brain circuits,” she said. “This study shows that anxiety disengages brain cells in a highly specialized manner.”
In fact, Moghaddam and her co-authors maintain that their findings have considerable implications. “Understanding how anxiety affects PFC encoding of cognitive events is of great clinical and evolutionary significance,” they wrote in the Journal of Neuroscience paper.
Moghaddam noted that the study’s findings, along with her group’s ongoing research program, could represent an important step toward improving treatment. “This can potentially help with improving cognitive behavioral therapy approaches,” she said. “Also, mechanistic models can provide long-term help with development and testing of novel treatments.”
Ongoing research on neurons and psychiatric disorders
Moghaddam and her laboratory colleagues are continuing to pursue this line of research, by recording PFC signals from multiple regions and by using other models of anxiety.
In addition to anxiety, they study the neuronal mechanisms that have been implicated in symptoms of schizophrenia, ADHD, and addictive disorders. Her group’s work has led to fundamentally new thinking about the pathophysiology of schizophrenia, and has identified novel pharmacological approaches for treatment of that devastating brain disease.
One of their new directions is working to characterize the development of neuronal systems during adolescence. With the onset of symptoms for most psychiatric disorders coming during adolescence, understanding what goes wrong in that developmental window is critical for defining the neuronal basis of the disease process and designing strategies to prevent the onset of symptoms.
My neurons made me do it
So the next time you get flustered and do something dumb, you can conveniently blame it on your pesky, misbehaving neurons. Tell your friends and family who look upon your foolish actions with amazement that you’re suffering from hypofrontality, and maybe they’ll cut you some slack.
Better yet, take a deep breath and stop to consider your actions. If your hand is a “hard 17,” that is, 17 without an ace, you should definitely stand pat. If it’s a “soft 17,” with an ace serving as an 11 or a 1, then your properly functioning prefrontal cortex would probably lead you to choose to go for it and take one or more cards. Either way, a non-anxious PFC is your friend—good luck!