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Neurotransmitters, Brain Architecture, and Their Role in Mental Health
Abnormal Psychology · Chapter 3: Biological Underpinnings of Psychological DisordersSection 3.2 · lesson 10 of 9718 min · free with a free account
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In this lesson
How the synapse works, what the systems actually do, and why "chemical imbalance" fails.
- Describe synaptic transmission from end to end, in order
- Name the major transmitter systems and what each is associated with
- State precisely where the chemical imbalance account misleads
- Locate the principal structures and say what each contributes
Transcript
Everything said in the video, section by section (2,466 words). Read along, or search it.
Biological Underpinnings of Psychological Disorders
Neurotransmitters and Brain Architecture
This is the section where the biology gets concrete. How one neuron actually talks to the next, step by step. That sequence is worth learning properly, because almost every biological treatment acts on one of its steps. Then the six transmitter systems that recur through the course. And a correction. You have heard that conditions are caused by a chemical imbalance. We will look at where that idea came from, and exactly where it fails. Then the architecture. What sits below the cortex, and what the cortex does. Two popular claims get corrected along the way. Nobody is left-brained or right-brained. And the brain is better described in circuits than in centers.
Before You Begin
There Is No Happiness Chemical
Two notes before we begin. This material is educational, and not a basis for any decision about medication. No individual medication is named anywhere in this section. Mechanisms are described by drug class only. The second note concerns language, and it matters here more than usual. You will have encountered the idea that conditions are caused by a chemical imbalance. And that particular chemicals are responsible for particular feelings. That account is examined and corrected in this section. So nothing here should be read as saying a transmitter is the happiness chemical. Or the reward chemical. No such description is accurate.
The Synapse
The Most Useful Sequence in the Course
Communication within a neuron is electrical. Communication between neurons is chemical. The conversion between the two happens at the synapse. A brief electrical signal traveling along the axon from the cell body to the terminal. It is all-or-nothing. The cell either fires, or it does not. A stronger input produces more frequent firing, rather than a bigger signal. When the action potential reaches the terminal, vesicles move to the membrane. Vesicles are small membrane-bound packages holding neurotransmitter. They fuse with the terminal membrane and release their contents. A neurotransmitter is a chemical messenger released by one neuron to influence another. The molecules diffuse across the synaptic cleft, which is the gap between the cells. And they bind to receptors. Protein structures shaped so only particular molecules fit. Binding produces the postsynaptic effect. A change in the receiving cell's readiness to fire. Excitatory makes firing more likely. Inhibitory makes it less likely. And a receiving neuron is taking thousands of these inputs at once, and adding them up. Finally the signal has to be ended, or the receiving cell would respond indefinitely. Reuptake transports the transmitter back into the sending cell for reuse. Enzymatic breakdown dismantles the molecules inside the cleft. Both matter clinically, because both are points at which a drug can act.
Where Drugs Act
Four Ways to Change What Happens There
Drugs acting on the brain do not create new processes. They alter the steps we just described. Four ways cover most of this course. An agonist increases the activity of a neurotransmitter system. By mimicking the transmitter at its receptor, by increasing its release. The direction of effect is toward more signaling. An antagonist decreases the activity of a system. Most often by occupying a receptor without activating it, so the transmitter cannot bind. Reuptake inhibition blocks the transporter that returns transmitter to the sending cell. The transmitter stays in the cleft longer and continues to act. Notice that this is a form of agonist action, even though nothing extra was released. Enzyme inhibition blocks the enzymes that break transmitter down in the cleft. One qualification on the lock-and-key comparison, and it matters. A single transmitter typically fits several different receptor subtypes. The effect depends on which subtype it binds, not only on which transmitter it is.
The Response Lag
The Timescale That Settles the Argument
Receptor sensitivity is how strongly receptors respond to a given amount of transmitter. When a system is persistently overstimulated, the receiving cell responds with downregulation. Reducing the number, or the responsiveness, of its receptors. When persistently understimulated, it makes the opposite adjustment. These changes take days to weeks. That timescale matters more than any other single fact in this section. A drug's immediate action at the synapse begins within hours. The clinical change in symptoms, for several classes, takes weeks. Follow that. If the immediate synaptic action were the therapeutic mechanism. Then relief should arrive with it. It does not. That is direct evidence that the therapeutic effect involves slower downstream adaptation. Receptor changes, and plasticity, rather than the immediate chemical change itself. It is also the strongest single argument against the simple deficiency account. People reasonably conclude in week two that a treatment is not working. So it is explained in advance. Early change may be in sleep or appetite rather than mood. The main effect is assessed over weeks. And unwanted effects often arrive before wanted ones. A person who expects that sequence is more likely to still be taking it when it works.
Six Systems
No Transmitter Has One Job
Six systems recur in this course. Before the list, hold three cautions in view, because this is the most misquoted material in the field. First, no transmitter has one job. Each participates in many functions, in different regions, through different receptor subtypes. The same molecule can be excitatory at one receptor and inhibitory at another. Second, associated with means associated with. That a system is implicated in a condition does not mean that too little, or too much, causes it. Third, the systems interact. Changing one alters the others. Serotonin participates in mood regulation, sleep, appetite, pain signaling, and impulse control. But lowering it experimentally does not reliably produce a depressive episode. Dopamine participates in motivation, anticipation of reward, movement, and learning from outcomes. It is not a pleasure chemical. It tracks anticipation and salience more than enjoyment. Norepinephrine handles arousal, alertness, attention, and the physical stress response. GABA is the main inhibitory transmitter, reducing neural firing throughout the brain. Glutamate is the main excitatory transmitter, involved in nearly all fast signaling. Acetylcholine handles muscle activation, attention, learning and memory. Many drugs block it incidentally, which is why dry mouth and blurred vision recur as side effects. Several conditions appear beside more than one system, and each system beside more than one condition. A table where every condition had its own transmitter would be easier to learn, and wrong.
Examined
Where the Chemical Imbalance Account Misleads
The chemical imbalance account proposes that conditions are caused by too much or too little. Too much or too little of a particular neurotransmitter. Where did it come from? The reasoning was reasonable, and it ran backwards. In the mid twentieth century, several drugs were noticed to change psychiatric symptoms. Their effects on particular transmitter systems were then identified. From the fact that a drug increases a transmitter and reduces symptoms. It was inferred that the symptoms had been produced by too little of that transmitter. That is an inference from treatment back to cause, and it is not valid. A headache relieved by a painkiller was not caused by a lack of the painkiller. Now what the evidence actually supports. Three statements, each defensible. Neurotransmitter systems are involved in psychological conditions. Drugs acting on those systems change symptoms for a substantial number of people. And differences in these systems are found between groups. None of those three establishes that a deficiency or excess causes any condition. Experimentally lowering a transmitter does not reliably produce the condition in people without it. No measurable level distinguishes people with a condition well enough to be used diagnostically. And the response lag shows the immediate chemical change is not the therapeutic effect. What replaces it is not a different chemical story, but a different kind of story. Circuits, communication between regions, and adaptation over time. With neurotransmitters as the medium of communication, rather than the quantity that is wrong. Describing a conversation as a shortage of sound waves is not false about the medium. It tells you nothing about the argument. One caution against overcorrecting. None of this means medication does not work. It means the mechanism is more complicated than the slogan.
Below The Cortex
Brainstem, Cerebellum, and the Limbic Structures
The structures at the base of the brain are easy to overlook and impossible to do without. The brainstem is the stalk connecting the brain to the spinal cord. It controls breathing, heart rate, blood pressure, and level of arousal. Within it, a network of nuclei regulates sleep and wakefulness. And supplies much of the brain with the transmitter systems we just described. Which is why those systems have effects that are widespread and hard to localize. The cerebellum coordinates movement, balance, and timing. It was long treated as purely motor, and is now implicated in cognitive and emotional processes. Now the limbic structures. Three matter most here. The amygdala detects threatening or otherwise significant stimuli, and initiates a rapid response. It responds faster than conscious appraisal. Which is why a person can be startled before knowing what startled them. Avoid the standard overstatement. It is not the fear center. It responds to significance in general, including positive significance. The hippocampus is essential to forming new memories, and placing them in context. Its contextual role matters clinically. Distinguishing this situation is dangerous from a situation like this was once dangerous. That is contextual work, and difficulty with it features in trauma-related presentations. The hypothalamus regulates sleep, appetite, temperature, and hormone release. It is the principal interface between the nervous and endocrine systems. And it explains a clinical puzzle. Why sleep and appetite disturbance appear so consistently in conditions defined by mood.
The Cortex
Four Lobes, and One Relationship That Recurs
The cerebral cortex is the folded outer layer, where the most complex processing happens. It is conventionally divided into four lobes on each side. The occipital lobe, at the back, processes visual information. It is rarely a primary site in psychological conditions. The parietal lobe handles touch, spatial awareness, and integration across the senses. The temporal lobe, at the side, handles hearing and language comprehension. It also contains the hippocampus and the amygdala. And it is implicated in auditory hallucination in psychotic conditions. The frontal lobe handles movement, speech production, planning, and the initiation of action. The front portion of it, the prefrontal cortex, deserves separate treatment. It carries out executive function. The processes that plan, hold information in mind, and inhibit unhelpful responses. Difficulty here appears across a wide range of conditions. It means executive difficulty is worth assessing routinely. And it means finding it tells you very little about which condition a person has. One relationship recurs throughout this course, so learn it now. The prefrontal cortex influences the amygdala. Damping threat responses once a situation has been appraised as safe. Reduced regulation of that kind is described across anxiety and trauma-related presentations. Treat it as a framework supported at group level, not an account of any individual.
Two Corrections
Lateralization, and Circuits Rather Than Centers
Two corrections before we finish the architecture. Lateralization is the tendency for some functions to be handled more by one hemisphere. It is real, and it is narrower than the popular version suggests. Language production and comprehension are more strongly lateralized than most functions. Usually to the left hemisphere in most right-handed people. With considerably more variation than that summary implies. Some aspects of spatial processing show a right-hemisphere tendency. Now the quickest refutation of the popular claim. The corpus callosum is the thick band of fibers connecting the two hemispheres. It carries continuous traffic between them. The hemispheres are not two systems working separately. So the claim that people are left-brained or right-brained is not supported. Individuals do not show a general dominance of one hemisphere. The underlying fact was real, and it was stretched into a personality theory it cannot bear. Second correction. The structure-by-structure presentation is a teaching device. Current explanation is framed in terms of circuits and connectivity. Sets of connected regions working together, and the pattern of communication between them. Three reasons drove that shift. No single structure is sufficient for any complex psychological function. The same structure participates in many functions, depending on what it is connected to. And imaging shows differences in coordination between regions, where within-region differences are small.
How We Know
Every Method Measures Something Else
Nearly all the evidence above comes from imaging. Reading imaging findings well means knowing what each method measures. Structural MRI measures the physical structure of tissue. Size, shape, and volume of regions, with spatial detail around a millimeter. It has no time dimension, and a structural difference does not tell you when it arose. Or whether it followed the condition rather than preceding it. Functional MRI measures blood flow changes, as an indirect index of neural activity. Time is coarse, in seconds. Space is fine, a few millimeters. Note that it measures blood flow, not firing. And group averages conceal wide individual variation. EEG measures electrical activity at the scalp, summed across large populations of neurons. Time resolution is excellent, in milliseconds. Spatial resolution is poor. It cannot localize the source of a signal with confidence. PET measures the distribution of an injected tracer. That allows receptor and metabolic mapping, and it involves a radioactive tracer. Diffusion imaging measures the movement of water along fiber tracts, to infer connections. It infers pathways from water movement, and does not show that a pathway is used. Now read across those methods and notice the trade-off. No method has both fine temporal and fine spatial resolution. And every one of them measures something other than the thing of interest. Group-level differences are reliably found. It does not follow that a scan can diagnose a person.
A Composite Case
A Mapping, and What Kind of Statement It Is
One composite case, constructed for instruction, describing no real person. Yusuf is twenty-seven. He describes persistent tension and difficulty concentrating. And a sense of being permanently on alert. He startles easily, sleeps poorly, and avoids the part of the city where he was assaulted. That was eighteen months ago, and the difficulties began after it. He describes intrusive recollections triggered by sounds resembling those he heard at the time. And he says he knows the current street is safe, while feeling that it is not. Now map that onto the architecture. His heightened startle and constant alert involve threat-detection circuitry. The amygdala, together with the arousal systems of the brainstem. His difficulty distinguishing this street from that street involves the hippocampus. Knowing a place is safe while not feeling safe involves prefrontal regulation. Now read that mapping again, and notice what kind of statement it is. It is a redescription of Yusuf's symptoms in anatomical vocabulary. It is not a demonstration that these structures caused his difficulties. It is not evidence about which structures are atypical in Yusuf specifically. And it is not a scan result. No scan was performed, and none would settle it. Differences in these circuits may follow from sustained arousal rather than precede it. So the mapping earns its place for two narrower reasons. It makes his experience intelligible as a system doing what it evolved to do. Rather than as a personal failure, which is often therapeutic in itself. And it makes a prediction that matters clinically. If the difficulty involves threat detection and its regulation, then practice for the regulator should help.
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