This is part four of our four-part introduction to neuroscience series. For a review of the motor systems at work in the brain, please see our previous article. A review of the foundational concepts in neuroscience and the neuroscience of the five senses may also serve to enhance the reader’s understanding of the forthcoming article. We have included a review of the anatomical terms of location below to assist readers unfamiliar with anatomical terminology.
Anatomical Terms of Location
A quick note regarding neuroanatomical nomenclature: the adjective anterior indicates that a structure is towards the front (face side) of the brain, while posterior indicates that the structure is towards the back. Superior indicates that a structure is towards the top (crown) of the head, while inferior means that the structure is towards the bottom of the brain. In the brain, dorsal can be considered synonymous with superior (like a dorsal fin), and ventral is synonymous with inferior. Medial suggests that a structure is towards the middle of the brain, while lateral indicates that a structure is towards the outside of the brain. A final word of clarification: these descriptors are often used to describe a structure’s relationship to another structure. For example, the brain is superior to the spinal cord.
Emotions and the Limbic System
The limbic system participates in the formation of our emotions and drives. It is made up of a wide array of neurological structures within the brain; however, for our purposes we will examine the amygdala/emoter, hypothalamus/cruise control, hippocampus/memorizer, cingulate gyrus, VTA/motivator, and nucleus accumbens.2 The limbic system can be subdivided into the Aversion Center with the amygdala/emoter serving as its core structure, and the Gratification Center with the nucleus accumbens acting as its core structure.2
The amygdala/emoter generates the sensation of fear when it is activated by the excitatory neurotransmitter glutamate.2 The nucleus accumbens produces the emotional sensation of pleasure when it is stimulated by the neurotransmitter DA/motivation released from axonal projections of neuronal cell bodies located in the VTA/motivator.2 There is much more overlap and less dichotomization in the limbic system than this simplistic subdivision suggests, but for the sake of clarity, our simplistic version of the limbic system will suffice.
The functional connection between the amygdala/emoter and the higher level cortical areas generates our conscious experience of emotion; while connections between the amygdala/emoter and the hypothalamus/cruise control generates the physiological response to emotion.3 A fearful stimulus triggers the release of glutamate and activates the amygdala/emoter, which then signals the hypothalamus/cruise control to increase the SNS/gas drive to the body, thus preparing the body for the fight-flight-or-freeze response.3 At the same time, the amygdala/emoter extends its raw emotional substrate to the ventromedial prefrontal cortex and the insula/internal sensor.3 We will discuss the specifics of the prefrontal cortex towards the end of the article. For now, it is important only that one is aware that these subcortical-cortical connections produce the conscious experience of emotion.1
The final component of the limbic system that we have to discuss is the hippocampus/memorizer. The hippocampus/memorizer gives us our ability to form long-term memories and then to subsequently retrieve them.1 The hippocampus/memorizer and the amygdala/emoter have an intimate relationship in memory formation. Not only are memories formed by the hippocampus/memorizer filled with rich sensory information courtesy of a wide array of sensory association areas, but our memories also have a strong emotional component instilled in them by the amygdala/emoter.1
Let’s look at an example to make sure that we understand the limbic system. Let’s imagine that we received a particularly painful and fear-provoking hypodermic needle vaccination as a child. The initial painful stimulus triggered our amygdala/emoter to generate the emotional substrate of fear. The amygdala/emoter splashed swaths of red fear onto the black and white memory outline of the doctor’s office and the surrounding environment formed by our hippocampus/memorizer with input from our sensory faculties (e.g. sight, sound, smell, taste, and touch).
Flash forward 20 years and maybe we have developed a phobia of shots and the associated doctor’s office. Unfortunately for us, we never age out of needing a tetanus booster, and so we overcome our fear and schedule an appointment. When we arrive at the appointment, our hippocampus/memorizer brings the now hazy and fear-laden childhood memory into conscious awareness. At the same time our amygdala/emoter reproduces a facsimile of the same fearful emotional state. It is at this time that our prefrontal cortex has the opportunity to intervene, but the mechanisms involved in the conscious mediation of fear and anxiety are complex and best left for a later discussion. For now, we will have to suspend our imaginary situation at this unfortunate fearful juncture.
The Physiology of Fear
Let’s return to the hypothalamus/cruise control for a moment before we complete our review of the limbic system. The hypothalamus/cruise control regulates the SNS/gas and PSNS/brake through its connections to the brainstem/CPU.2 The hypothalamus/cruise control receives its marching orders from the cortex and the amygdala/emoter.2 The hypothalamus/cruise control also has connections to the neuroendocrine structure known as the pituitary gland. The pituitary gland regulates growth, metabolic rate, stress level, reproduction, and many other basic functions through the release of hormones.2
For an example of how the hypothalamus/cruise control and pituitary gland work together, let’s examine the stress hormone cortisol. Our adrenal glands sit atop our kidneys within our abdominal cavity and are responsible for releasing cortisol. One of the many functions of cortisol in the body is to render us more reactive to the SNS/gas.4 But how does cortisol know when to make its way out of the adrenals and into the bloodstream?
Stress causes the cortex and amygdala/emoter to signal the hypothalamus/cruise control to release a hormone known as corticotropin-releasing hormone (CRH). CRH is released into the local blood supply and travels to the pituitary gland where it causes the release of adrenocorticotropic hormone (ACTH). ACTH is released into the general circulation and when it arrives at the adrenal glands, it triggers the release of cortisol.4 The other hypothalamus/cruise control hormones also traverse a similarly winding path to produce their oftentimes distant effects.
Let’s switch gears and discuss language. Language is perhaps one of the most complex representational operations of the brain. The proceeding paragraphs will provide a very basic outline of the neuroanatomy of language. At a very basic level, the perisylvian association cortices, on either side of the brain, are largely isolated from limbic and general sensory input.3 The perisylvian structures are highly specialized for the processing and generation of language. Depending on the handedness of an individual, language processing will be more focused on one side of the brain or the other. 98% of right-hand dominant individuals rely on their left hemisphere for language processing.2 Of non-right hand dominant individuals (left hand dominant or ambidextrous), 65% rely on their left hemisphere, 20% on their right hemisphere, and 15% show a co-dominant distribution of language specialization.1
The three areas of the perisylvian association network that have been the subject of the most research over the years are Broca’s area, located in the inferior frontal gyrus; Wernicke’s area, in the superior temporal gyrus; and the inferior parietal lobule (angular and supramarginal gyri). Recall that the primary auditory cortex (A1, also known as “Heschl’s gyrus”) provides the raw sound perception required to begin the language comprehension process.1
Broca’s area is known as a unimodal motor association cortex and is responsible for the motor aspect of speech production and planning.1 Wernicke’s area is a unimodal auditory association cortex that is involved in the translation of sounds from A1 into representational words.1 Finally, the inferior parietal lobule is a multimodal association cortex that provides meaning to word sounds by associating the sounds of a given word with the perceptions of the actual object (physical or metaphysical).1
Broca’s area, Wernicke’s area, and the inferior parietal lobule are all interconnected with one another and with the dorsolateral prefrontal cortex and lateral inferior temporal lobe.1 Recent evidence has suggested that language can be split into dorsal and ventral pathways analogous to the way the visual system is divided.
The ventral pathway is largely unconscious and consists of Wernicke’s area and areas in the posterior middle temporal gyrus.1 The ventral pathway is activated automatically during language processing. As information progresses more anteriorly along the inferior temporal lobe bilaterally, its meaning is further elaborated with greater and greater comprehensive complexity. This pathway is analogous to the visual What Pathway.
The dorsal pathway is conscious and transmits sound-language representations from Wernicke’s area to a temporoparietal sensorimotor interface area known as “Area Spt (sylvian-parieto-temporal).” Area Spt integrates the sensory information into a motor program that is projected to Broca’s area for physical (speech) or metaphysical expression.1
Numbers seem to be somewhat neurologically distinct from language. The inferior parietal sulcus generates our ability to conceptualize and subsequently manipulate numbers using our prefrontal cortex.1
Consciousness, Abstraction, and Cognitive Control
The prefrontal cortex integrates all of the various neurological systems we have discussed to generate a coherent experience of our internal and external world. We will split the prefrontal cortex into medial and lateral aspects. But before we do that, we need to examine the concepts of counterfactual reasoning and structured event complexes.
Counterfactual reasoning refers to the cognitive ability to mentally reason and imagine scenarios that are not actually occurring, or in other words, scenarios that are counter to our immediate “factual” experience.9 Counterfactual reasoning provides us with the ability to plan for imagined futures or study remembered pasts. Counterfactual reasoning gives us the ability to learn from past mistakes to improve future actions.10
Structured event complexes (SECs) describe the analytic manipulation of information generated by counterfactual reasoning. SECs analyze the agents (doers), objects, actions, mental states, and settings of past and future counterfactual events.7 In other words, SECs involve hypothesizing what would happen if a certain agent, object, action, mental state, or setting were substituted for another. An example might be using the SEC construct to ask, “What if instead of raising my voice to my coworker, I responded calmly?”
When we utilize our counterfactual- and SEC-generating abilities, we are no longer constrained by reality, but only by our imaginative capacity. With this foundation in place let’s turn to the medial prefrontal cortex.
The medial prefrontal cortex can actually be split into three distinct structures from top to bottom: the dorsomedial prefrontal cortex (dmPFC), the ventromedial PFC (vmPFC), and the medial orbitofrontal cortex (mOFC).
The dmPFC is involved in deciding whether a particular situation requires action or inaction.11 For example, a quick counterfactual reasoning simulation between shouting at a colleague or restraining this action would be made possible by our dmPFC.
Our vmPFC generates analyses about oneself and others.12 Self-referential thought, inferred emotional states of another, and social awareness are all roles of the vmPFC. For instance, the evaluation of another’s (or one’s own) emotional state for the purposes of generating an SEC is made possible by the vmPFC.
The mOFC gives us the ability to evaluate cost-benefit balances for a given real or hypothetical (counterfactual) situation.13 For example, our mOFC allows us to decide whether the hedonic reward provided by a second piece of cake is worth the cost of the guilt we anticipate experiencing upon finishing said chocolaty goodness.
Now let’s turn to the outside of the brain: the lateral prefrontal cortices.
The lateral PFC can be divided into two structures: the ventrolateral PFC (vlPFC) and the dorsolateral PFC (dlPFC). The vlPFC receives information from all of the different sensory modalities, generates working memory, and retrieves long-term memory stored in the hippocampus/memorizer.1 The dlPFC takes all of the aforementioned information from the vlPFC and manipulates it at a more complex and conscious level.1 The dlPFC is intimately connected with the motor cortices and provides the executive ability to trigger a desired behavior.
Let’s use an example to clarify the relationship between the vlPFC and the dlPFC. If we were given a set of directions and told to memorize them, then our vlPFC would be solely responsible for the direction rehearsal in our working memory. If, however, we were then asked to reverse the directions, then the dlPFC would have to retrieve the information from the vlPFC and undertake the cognitively demanding task of reversing the order of the directions. Thus, we can see that as one moves up from the vlPFC to the dlPFC cognitive complexity increases.1
This completes our four-part introduction to neuroscience series. The material, although dry at times, will serve as a foundation for future articles that address the complexity of various neural subsystems that require a basic knowledge of neuroanatomy to comprehend.
- Squire LR, ed. Fundamental Neuroscience. 4th ed. Amsterdam ; Boston: Elsevier/Academic Press; 2013.
- Haines DE, Ard MD, eds. Fundamental Neuroscience for Basic and Clinical Applications [study Smart with Student Consult]. 4th ed. Philadelphia: Elsevier, Saunders; 2013.
- Vanderah TW, Gould DJ, Nolte J. Nolte’s The Human Brain: An Introduction to Its Functional Anatomy. Seventh edition. Philadelphia, PA: Elsevier; 2016.
- Baynes J, Dominiczak MH. Medical Biochemistry.; 2014. http://www.clinicalkey.com/dura/browse/bookChapter/3-s2.0-C20110076986. Accessed July 9, 2016.
- Bruce C, Desimone R, Gross CG. Visual properties of neurons in a polysensory area in superior temporal sulcus of the macaque. J Neurophysiol. 1981;46(2):369-384.
- Gottfried JA, ed. Neurobiology of Sensation and Reward. Boca Raton, FL: CRC Press; 2011.
- Barbey AK, Krueger F, Grafman J. Structured event complexes in the medial prefrontal cortex support counterfactual representations for future planning. Philos Trans R Soc Lond B Biol Sci. 2009;364(1521):1291-1300. doi:10.1098/rstb.2008.0315.
- Alitto HJ, Usrey WM. Corticothalamic feedback and sensory processing. Curr Opin Neurobiol. 2003;13(4):440-445.
- Kahneman D, Miller DT. Norm theory: Comparing reality to its alternatives. Psychol Rev. 1986;93(2):136-153. doi:10.1037/0033-295X.93.2.136.
- McCrea SM. Self-handicapping, excuse making, and counterfactual thinking: consequences for self-esteem and future motivation. J Pers Soc Psychol. 2008;95(2):274-292. doi:10.1037/0022-35126.96.36.1994.
- Roese NJ, Hur T, Pennington GL. Counterfactual thinking and regulatory focus: implications for action versus inaction and sufficiency versus necessity. J Pers Soc Psychol. 1999;77(6):1109-1120.
- Mandel D. Counterfactuals, emotions, and context. Cogn Emot. 2003;17(1):139-159. doi:10.1080/02699930302275.
- Roese NJ, Olson JM, eds. What Might Have Been: The Social Psychology of Counterfactual Thinking. Mahwah, N.J: Lawrence Erlbaum Associates; 1995.