The role of the amygdala and prefrontal cortex in aggression | UA Library
Major connections to the the amygdala also come from the medial prefrontal cortex. These connections appear to be involved in the process of extinction. Scientists detected changes in the brain architecture of 18 year-olds whose parents had reported being under chronic stress when those same adolescents were. When this prefrontal-amygdala connection is weak, excessive anxiety “The prefrontal cortex is supposed to keep areas like the amygdala in.
Participants practiced keeping still in the mock scanner, and were given feedback paused video if they moved their heads. This sequence was optimized for participants with high motion Tisdall et al. The first four volumes of each scan were automatically discarded to allow time for scanner magnetization to reach equilibrium.
Participants looked at a fixation cross throughout the scan.
THE BRAIN FROM TOP TO BOTTOM
Structural analyses Structural data were used in registration see belowto identify a bilateral amygdala seed, and to calculate bilateral amygdala volume. Scan quality was included as a covariate in structural analyses, and controlled for in whole-brain resting-state analyses. Cortical reconstruction and volumetric segmentation of the structural images were performed using the standard FreeSurfer processing stream Dale et al. The surfaces were visually inspected for errors and manually edited by researchers who were blind to participant information.
Cortical reconstructions were checked for accuracy after editing, and were deemed accurate by blinded researchers for all participants included in the functional connectivity analyses. The amygdala segmentations were also visually inspected for quality, and were found to be accurate for all participants. Resting-state analyses The functional imaging data were preprocessed using Nipype, a Python-based framework for flexibly integrating neuroimaging analysis tools Gorgolewski et al.
Simultaneous realignment and slice timing correction was conducted using an algorithm implemented in Nipy Roche, The following confounds were regressed out of the functional data: They further proposed that connections between the mPFC and amygdala normally allow the organism to adjust its emotional behavior when environmental circumstances change, and that some alteration in this circuitry, causing a loss of prefrontal control of the amygdala, might underlie the inability of persons with anxiety disorders to regulate their emotions.
Over the past decade, considerable research has been conducted on the role of the mPFC and the amygdala, and their interactions in fear extinction. In this article, we review the original impetus for pursing the role of the mPFC, and survey some of the findings that have come since.
We also review parallel research on the role of the amygdala in extinction, and present some new findings regarding amygdala-mPFC interactions.
Previous Section Next Section Prefrontal Cortex Contributions to Fear Extinction To assess the prefrontal cortex contributions to fear extinction, we first briefly review its general anatomical organization in mammals. Next, we return to the original findings that motivated interest in the role of the mPFC in extinction of conditioned fear, and then we consider the evidence that has subsequently accumulated, which has both confirmed and refined our understanding of mPFC involvement in the regulation of fear.
Anatomical Organization of the Prefrontal Cortex in Mammals The prefrontal cortex consists of several functionally distinct subregions Posner ; Seamans et al. In humans and other primates, these include the lateral prefrontal cortex, orbital frontal cortex, and mPFC.
The lateral prefrontal cortex, especially the dorsolateral region, is involved in working memory and executive control functions Goldman-Rakic ; Owen et al. The orbital frontal cortex is involved in reward, motivation, and emotional decision making Damasio ; Robbins ; Rolls; Rogers et al. The mPFC itself has several divisions, including the anterior cingulate cortex and several more ventral areas that include the infralimbic IL and prelimbic PL cortices, and the medial frontal gyrus.
The anterior cingulate is divided into two parts, a dorsal part involved in attention and cognitive control and a more ventral part involved in emotional regulation Bush et al. In non-primate species, the prefrontal cortex is poorly developed.
Indeed, it is generally accepted that the lateral prefrontal cortex is a unique primate specialization Povinelli and Preuss ; Preuss However, the orbital frontal cortex and various other mPFC regions anterior cingulate, IL, PL are present in rodents and other non-primate mammals Uylings et al. The role of the mPFC areas in extinction of fear has been examined, and is reviewed below. Evidence Implicating the mPFC in Fear Extinction Research on the neural basis of fear extinction was stimulated by two studies in the late s showing that damage to sensory processing regions of the cortex auditory or visual leads to increased resistance to extinction LeDoux et al.
In their study, LeDoux et al. This hypothesis was based on a variety of disparate findings that implicated the latter two regions in the extinction of one or more behavioral tasks, although at the time little work had been done on the neural basis of extinction using fear-conditioning tasks.
Lesions circumscribed to the vmPFC had no effect on the amount of fear behavior freezing expressed on a given trial but greatly increased the number of CS-alone trials required to extinguish the behavior. Damage to the dorsal mPFC led to an increased resistance to extinction but also resulted in an increased amount of freezing behavior expressed on each trial Morgan and LeDoux With the dorsal mPFC lesions, it was unclear if the effect on extinction was really due to increased resistance to extinction, because the effect could also be explained by the overall increase in the expression of conditioned fear.
In contrast, damage to the vmPFC selectively impaired extinction over days without increasing the expression of fear within trials, and therefore most subsequent research on the role of the mPFC in extinction has focused on the vmPFC.
A later study addressing the role of the vmPFC in extinction failed to replicate Morgan's findings Gewirtz et al. However, this study used fear-potentiated startle, a training and testing paradigm that differs significantly from the task described so far, which we will refer to as simple fear conditioning. Differences between the training task e. Although Gewirtz et al.
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Indeed, studies from several other research groups using similar simple fear-conditioning tasks, rather than potentiated startle, have implicated the mPFC in fear extinction. For example, Morrow et al. Quirk and colleagues Lebron et al.
Furthermore, Quirk and collaborators Quirk et al. Particularly dramatic is the finding that pairing the tone CS with brief IL stimulation reduces freezing in rats, suggesting that IL stimulation is sufficient to simulate extinction learning Milad and Quirk ; Milad et al. Results from electrophysiological and imaging studies in rats and humans provide further support for the view that functional changes in mPFC are associated with the retrieval of extinction training.
Milad and Quirk found that IL neurons respond to CS exposure on the day following extinction training, suggesting that these cells do not respond to the CS during fear conditioning or during extinction training, but instead specifically respond when the memory of extinction training is retrieved. Cannulas were implanted at a 15o angle at the following coordinates relative to bregma: Following cannulation, both cannulas and headstages were fitted onto the skull with dental cement and anchored by skull screws.
The headstages were attached to 4 electrodes; two delivered the unconditioned stimulus US of periorbital stimulation, and two recorded electromyographic EMG activity as a measure of blinks.
The electrodes insulated stainless steel wire with a diameter of 0. The insulation was removed from a section of each electrode in order to make contact with the muscle. Each of the electrode wires was coiled securely in place. Infusions During microinfusions, stylets were replaced with infusion cannulas protruding 1 mm past the guide cannula. The syringe and tubes were filled with water, and a small air bubble separated the water from the vehicle or drug solution.
In experiment 1, the mPFC was either infused with artificial cerebral spinal fluid aCSF vehicle or bilaterally inactivated via infusions of 0.
In experiment 2, the mPFC was bilaterally activated via infusions of 0. All infusions were given at a rate of 0. Stress Procedure At least 7 days after the surgery, rats were acclimated to the conditioning chamber 60 min and spontaneous blinks were recorded. They were then transported to a separate context and infused with aCSF or muscimol.
Half of this group was transferred into another context different from those in which the infusions and training occurred and placed into a dark soundproof chamber. In this chamber, they were loosely restrained and exposed to 30 low intensity 1 mA, 60 Hz, 1 sec stimulations to the tail. In experiment 2, following infusions, unstressed animals were also taken into the context in which stressed animals were exposed to the stressor but were only loosely restrained for 30 minutes in the chambers before being returned to their home cages.