Dorsolateral prefrontal cortex
Dorsolateral prefrontal cortex | |
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Details | |
Identifiers | |
Latin | cortex praefrontalis dorsolateralis |
MeSH | D000087643 |
FMA | 276189 |
Anatomical terms of neuroanatomy |
The dorsolateral prefrontal cortex (DLPFC or DL-PFC) is an area in the prefrontal cortex of the primate brain. It is one of the most recently derived parts of the human brain. It undergoes a prolonged period of maturation which lasts into adulthood.[1] The DLPFC is not an anatomical structure, but rather a functional one. It lies in the middle frontal gyrus of humans (i.e., lateral part of Brodmann's area (BA) 9 and 46[2]). In macaque monkeys, it is around the principal sulcus (i.e., in Brodmann's area 46[3][4][5]). Other sources consider that DLPFC is attributed anatomically to BA 9 and 46[6] and BA 8, 9 and 10.[1]
The DLPFC has connections with the orbitofrontal cortex, as well as the thalamus, parts of the basal ganglia (specifically, the dorsal caudate nucleus), the hippocampus, and primary and secondary association areas of neocortex (including posterior temporal, parietal, and occipital areas).[7][8] The DLPFC is also the end point for the dorsal pathway (stream),[9] which is concerned with how to interact with stimuli.
An important function of the DLPFC is the executive functions, such as working memory, cognitive flexibility,[10] planning, inhibition, and abstract reasoning.[11] However, the DLPFC is not exclusively responsible for executive functions. All complex mental activity requires the additional cortical and subcortical circuits with which the DLPFC is connected.[12] The DLPFC is also the highest cortical area that is involved in motor planning, organization and regulation.[12]
Structure
As the DLPFC is composed of spatial selective
Function
Primary functions
The DLPFC is known for its involvement in the executive functions, which is an umbrella term for the management of
DLPFC is not required for the memory of a single item. Thus, damage to the dorsolateral prefrontal cortex does not impair recognition memory.[17] Nevertheless, if two items must be compared from memory, the involvement of DLPFC is required. People with damaged DLPFC are not able to identify a picture they had seen, after some time, when given the opportunity to choose from two pictures.[17] Moreover, these subjects also failed in Wisconsin Card-Sorting Test as they lose track of the currently correct rule and persistently organize their cards in the previously correct rule.[18] In addition, as DLPFC deals with waking thought and reality testing, it is not active when one is asleep.[18] Likewise, DLPFC is most frequently related to the dysfunction of drive, attention and motivation.[19] Patients with minor DLPFC damage display disinterest in their surroundings and are deprived of spontaneity in language as well as behavior.[19] Patients may also be less alert than normal to people and events they know.[19] Damage to this region in a person also leads to the lack of motivation to do things for themselves and/or for others.[19]
Decision making
The DLPFC is involved in both risky and moral
Working memory
Working memory is the system that actively holds multiple pieces of transitory information in the mind, where they can be manipulated. The DLPFC is important for working memory;[23] reduced activity in this area correlates to poor performance on working memory tasks.[24] However, other areas of the brain are involved in working memory as well.[25]
There is an ongoing discussion if the DLPFC is specialized in a certain type of working memory, namely computational mechanisms for monitoring and manipulating items, or if it has a certain content, namely visuospatial information, which makes it possible to mentally represent coordinates within the spatial domain.[23]
There have also been some suggestions that the function of the DLPFC in verbal and spatial working memory is lateralised into the left and right hemisphere, respectively. Smith, Jonides and Koeppe (1996)[26] observed a lateralisation of DLPFC activations during verbal and visual working memory. Verbal working memory tasks mainly activated the left DLPFC and visual working memory tasks mainly activated the right DLPFC. Murphy et al. (1998)[27] also found that verbal working memory tasks activated the right and left DLPFC, whereas spatial working memory tasks predominantly activated the left DLPFC. Reuter-Lorenz et al. (2000)[28] found that activations of the DLPFC showed prominent lateralisation of verbal and spatial working memory in young adults, whereas in older adults this lateralisation was less noticeable. It was proposed that this reduction in lateralisation could be due to recruitment of neurons from the opposite hemisphere to compensate for neuronal decline with ageing. Overall, the DLPFC is complex and yet not fully understood.
Secondary functions
The DLPFC may also be involved in the act of deception and lying,
Additionally, supporting evidence suggests that the DLPFC may also play a role in conflict-induced behavioral adjustment, for instance when an individual decides what to do when faced with conflicting rules.
DLPFC may also be associated with human intelligence. However, even when correlations are found between the DLPFC and human intelligence, that does not mean that all human intelligence is a function of the DLPFC. In other words, this region may be attributed to general intelligence on a broader scale as well as very specific roles, but not all roles. For example, using imaging studies like
The DLPFC may also be involved in threat-induced anxiety.
Social cognition
Among the prefrontal lobes, the DLPFC seems to be the one that has the least direct influence on social behavior, yet it does seem to give clarity and organization to social cognition.[11] The DLPFC seems to contribute to social functions through the operation of its main speciality the executive functions, for instance when handling complex social situations.[11] Social areas in which the role of the DLPFC is investigated are, amongst others, social perspective taking[8] and inferring the intentions of other people,[8] or theory of mind;[11] the suppression of selfish behavior,[8][35] and commitment in a relationship.[36]
Relation to neurotransmitters
As the DLPFC undergoes long maturational changes, one change that has been attributed to the DLPFC for making early cognitive advances is the increasing level of the neurotransmitter dopamine in the DLPFC.[1] In studies where adult macaques' dopamine receptors were blocked, it was seen that the adult macaques had deficits in the A-not-B task, as if the DLPFC was taken out altogether. A similar situation was seen when the macaques were injected with MPTP, which reduces the level of dopamine in the DLPFC.[1] Even though there have been no physiological studies about involvement of cholinergic actions in sub-cortical areas, behavioral studies indicate that the neurotransmitter acetylcholine is essential for working memory function of the DLPFC.[37]
Clinical significance
Schizophrenia
Schizophrenia may be partially attributed to a lack in activity in the frontal lobe.[18] The dorsolateral prefrontal cortex is especially underactive when a person has chronic schizophrenia.[citation needed] Schizophrenia is also related to lack of dopamine neurotransmitter in the frontal lobe.[citation needed][18] The DLPFC dysfunctions are unique among the schizophrenia patients as those that are diagnosed with depression do not tend to have the same abnormal activation in the DLPFC during working memory-related tasks.[24] Working memory is dependent upon the DLPFC's stability and functionality, thus reduced activation of the DLPFC causes schizophrenic patients to perform poorly on tasks involving working memory. The poor performance contributes to the added capacity limitations in working memory that is greater than the limits on normal patients.[38][citation needed] The cognitive processes that deal heavily with the DLPFC, such as memory, attention, and higher order processing, are the functions that once distorted contribute to the illness.[24][page needed]
Depression
Along with regions of the brains such as the limbic system, the dorsolateral prefrontal cortex deals heavily with major depressive disorder (MDD). The DLPFC may contribute to depression due to being involved with the disorder on an emotional level during the suppression stage.[39] While working memory tasks seem to activate the DLPFC normally,[40] its decreased grey matter volume correlates to its decreased activity. The DLPFC may also have ties to the ventromedial prefrontal cortex in their functions with depression.[39] This can be attributed to how the DLPFC's cognitive functions can also involve emotions, and the VMPFC's emotional effects can also involve self-awareness or self-reflection. Damage or lesion to the DLPFC can also lead to increased expression of depression symptoms.[41]
Stress
Exposure to severe
Substance use
Substance use disorders (SUD) may correlate with dorsolateral prefrontal cortex dysfunction.[44] Those who recreationally use drugs have been shown to engage in increased risky behavior, possibly correlating with a dysfunction of the DLPFC. The executive controlling functions of the DLPFC in individuals who recreationally use drugs may have a connection that is lessen from risk factoring areas such as the anterior cingulate cortex and insula.[44] This weakened connection is even shown in healthy subjects, such as a patient who continued to make risky decisions with a disconnect between their DLPFC and insula. Lesions of the DLPFC may result in irresponsibility and freedom from inhibitions,[45] and the use of drugs can invoke the same response of willingness or inspiration to engage in the daring activity.
Alcohol
Alcohol creates deficits on the function of the prefrontal cortex.[46] As the anterior cingulate cortex works to inhibit any inappropriate behaviors through processing information to the executive network of the DLPFC,[46] as noted before this disruption in communication can lead to these actions being made. In a task known as Cambridge risk task, SUD participants have been shown to have a lower activation of their DLPFC. Specifically in a test related to alcoholism, a task called the Wheel of Fortune (WOF) had adolescents with a family history of alcoholism present lower DLPFC activation.[44] Adolescents that have had no family members with a history of alcoholism did not exhibit the same decrease of activity. [citation needed]
See also
- Attention versus memory in prefrontal cortex
- Attentional shift
- Brodmann area 46
- Cognitive control
- Dorsomedial prefrontal cortex
- Mesocortical pathway
- Wisconsin Card Sorting Test
- Frontoparietal network
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