summary: A new study identifies beta frequency neural activity in the anterior cingulate cortex (ACC) as important for shaping reward perception and behavior, and suggests that this neural signature is altered in patients with depression, and may serve as a biomarker of anhedonia and a potential therapeutic target.
This research sheds light on how brain activity encodes reward cues and influences future choices. These findings may lead to innovative treatments for psychiatric disorders involving deficits in reward processing.
Key Facts:
- ACC Beta Activities: A key neural signature for recognizing reward and shaping behavior.
- Depression changes: Beta activity is reduced and delayed in patients with treatment-resistant depression.
- Potential biomarkers: Identifying beta activity may improve the diagnosis and treatment of anhedonia.
sauce: Texas Children’s Hospital
As any parent, teacher, or pet owner can attest, rewards play a major role in shaping human and animal behavior. Whether it’s food, a gift, words of appreciation or praise, prestige, or monetary gain, rewards act as positive reinforcement for the associated behavior.
Although the correlation between reward and future choice has been an established paradigm in neuroscience research for over a century, little is known about its underlying neural processes – how the brain encodes, remembers, and translates reward cues into future desired behaviors.
Recent research led by Dr. Samir Sheth, professor and vice chair of research in the Department of Neurosurgery at Baylor College of Medicine, director of the Gordon and Mary Cain Foundation Institute for Pediatric Neurological Research, and investigator at the Jean and Dan Duncan Neurological Institute (DuncanNRI) at Texas Children’s Hospital, has found that beta frequency neural activity in the brain’s anterior cingulate cortex (ACC) is a key neural signature underlying processes related to reward recognition, subsequent choice decisions, and ultimately shaping future behavior.
moreover, Nature Communicationsreported that this neural signature is altered in patients with depression, opening up the exciting possibility of using these neural signals as novel biomarkers and innovative avenues of treatment.
Anhedonia is a presenting symptom of depression and other psychiatric disorders.
Humans derive pleasure from a variety of physical or mental activities, sensory experiences, and interactions with family and friends.
However, people with depression often experience long-term feelings of hopelessness, sadness, or despair due to apathy and anhedonia (a medical term that means the inability to find pleasure or satisfaction in activities or things that were once found enjoyable), all of which can have a significant negative impact on quality of life.
Anhedonia is also associated with other psychiatric and neurological disorders, such as schizophrenia, bipolar disorder, substance abuse disorders, anxiety disorders, and Parkinson’s disease.
Traditional antidepressants and standard medical treatments often do not adequately address the symptoms of people with severe, treatment-resistant depression and other conditions.
A better understanding of anhedonia could lead to the development of more targeted and effective treatments for depression and related conditions.
Reward-biased responses are controlled by beta activity in the frontal lobe
To identify the neural basis underlying anhedonia, Sheth and his team recorded and analyzed neural activity in four brain regions of 15 patients with drug-resistant epilepsy who were undergoing invasive monitoring to identify the origins of seizures.
While their brain activity was monitored, these patients performed a perceptual discrimination task called the Probability Reward Task (PRT), a well-validated behavioral task that objectively measures anhedonia by observing subtle changes in reward-related behavior.
“We found that the unequal allocation of rewards between the two correct answers in this task led to a response bias toward the more frequently rewarded stimulus,” said lead author Jiayan Xiao, PhD, who conducted the research as a graduate student in Sheth’s lab.
“We found that based on the feedback, most people revised their subsequent answers to make choices that were more likely to earn them a reward, regardless of the accuracy of their answers.”
Furthermore, the researchers found that specific signals (neural oscillations in the beta frequency range) emanating from the anterior cingulate cortex (ACC) in the brain’s frontal lobe consistently showed a strong positive correlation with reward-biased behavior and were closely related to reward receipt and its value.
Furthermore, the researchers found that this particular brain region is involved in the evaluation of both reward stimuli and outcomes, and may function as a key node with a common mechanism for reward evaluation.
“Our study addresses a long-standing fundamental question in neuroscience: which specific brain regions and signals control classic reward-biased responses, the famous example of which is Pavlovian conditioning, in which dogs learn to associate the sound of a bell with food,” said co-senior author Benjamin Hayden, PhD, professor of neurosurgery at Baylor University.
Reward-biased responding is altered in patients with treatment-resistant depression
Sheth and his team then administered PRT to four patients with severe, treatment-resistant depression and found that reward processing in the ACC was altered in this group: These patients did not display the typical behavioral response of favoring choices that offered more frequent rewards.
This observation suggests that reward-oriented prediction is lacking and that their choices are less influenced by reward feedback. Consistent with this change in reward-biased behavior, these individuals had reduced and delayed beta activity in the ACC region.
“In this study, we identify ACC beta activity as a potential biomarker for anhedonia,” said Sheth, a McNair Scholar and Cullen Foundation Professor at Baylor University.
“Such biomarkers could have many potential benefits, including improved diagnosis and symptom monitoring in patients with severe depression and other anhedonia-related psychiatric disorders.”
“Furthermore, our findings raise the exciting possibility that modulating ACC beta activity may be an effective treatment for anhedonia, a hypothesis that we plan to test in upcoming clinical trials.”
Neurotechnological advances in this research are occurring at a pace never before possible, thanks in part to funding from the National Institutes of Health’s Advancing Innovative Neurotechnologies in Brain Research Initiative (BRAIN Initiative).
“This study illustrates how BRAIN-funded research is already impacting clinical practice today,” said John Ngai, PhD, director of the NIH BRAIN initiative.
“The innovations in data collection and personalized deep brain stimulation demonstrated in this study may enable a new generation of precision treatments.”
Funding: Research reported in this press release was supported by the National Institutes of Health (grant numbers UH3 NS103549, K01 MH116364, R21 NS104953, UH3 NS100549, and R01 MH114854) and the McNair Medical Research Institute of the Robert and Janice McNair Foundation.
The researchers would also like to thank the Cullen Foundation, the Jean and Dan Duncan Neurological Institute, and the Gordon and Mary Cain Child Neurological Research Foundation Institute at Texas Children’s Hospital.
About this depression research news
author: Rajalakshmi Natarajan
sauce: Texas Children’s Hospital
contact: Rajalakshmi Natarajan – Texas Children’s Hospital
image: Image courtesy of Neuroscience News
Original Research: Open access.
“Beta activity in the human anterior cingulate cortex mediates reward biasSameer Sheth et al. Nature Communications
Abstract
Beta activity in the human anterior cingulate cortex mediates reward bias
The rewards we derive from our choices and actions can have a profound effect on our future behavior.
Understanding how reward bias is implemented in the brain is important for many reasons, including the fact that reduced reward bias is a hallmark of clinical depression.
We hypothesized that reward bias is mediated by the anterior cingulate cortex (ACC), a central cortical region implicated in the integration of reward and executive control and in the pathogenesis of depression.
To test this hypothesis, we recorded neural activity during a biased judgment task in patients undergoing intracranial monitoring for epilepsy or major depressive disorder.
We found that beta (12–30 Hz) oscillations in the ACC predicted both the associated reward and the magnitude of choice bias, and tracking reward receipt predicted bias in future trials.
We found that the magnitude of the bias was reduced in depressed patients, with a corresponding reduction in the beta-specific effect.
Our findings suggest that ACC beta oscillations may modulate the learning of reward information to guide adaptive selection and, more broadly, suggest a potential biomarker of anhedonia and suggest future development of interventions to enhance the impact of reward for therapeutic efficacy.
