Behave: The Biology of Humans at Our Best and Worst

by Robert M. Sapolsky

Frontal cortical neurons are generalists, with broad patterns of projections, which makes for more work.

Pertinent to this is the concept of “cognitive load.” Make the frontal cortex work hard—a tough working-memory task, regulating social behavior, or making numerous decisions while shopping. Immediately afterward performance on a different frontally dependent task declines.

And that’s when doing the trill is transferred from the frontal cortex to more reflexive brain regions (e.g., the cerebellum). This transition to automaticity also happens when you get good at a sport, when metaphorically your body knows what to do without your thinking about it.

Is resisting lying a demanding task for your frontal cortex, or is it effortless habit? As we’ll see, honesty often comes more easily thanks to automaticity.

Often the neurobiology of automaticity mediates doing the hardest moral acts, while the neurobiology of the frontal cortex mediates working hard on a term paper about the subject.

Logically, primates from fission-fusion species (chimps, bonobos, orangutans, spider monkeys) have better frontocortical inhibitory control over behavior than do non-fission-fusion primates (gorillas, capuchins, macaques).

social complexity expands the frontal cortex.

What are people with FTD like? They exhibit behavioral disinhibition and socially inappropriate behaviors. There’s also an apathy and lack of initiating behavior that reflects the fact that the “decider” is being destroyed.fn32

You’re dreaming. During REM sleep, when dreaming occurs, the frontal cortex goes off-line, and dream scriptwriters run wild.

criminal psychopaths have decreased activity in the frontal cortex and less coupling of the PFC to other brain regions (compared with nonpsychopathic criminals and noncriminal controls). Moreover, a shockingly large percentage of people incarcerated for violent crimes have a history of concussive trauma to the frontal cortex.

First there is the dorsal part of the PFC, especially the dorsolateral PFC (dlPFC)—

The dlPFC is the decider of deciders, the most rational, cognitive, utilitarian, unsentimental part of the PFC.

In contrast to the dlPFC, there’s the ventral part of the PFC, particularly the ventromedial PFC (vmPFC).

Logically, the vmPFC is all about the impact of emotion on decision making.

The functions of the cognitive dlPFC are the essence of doing the harder thing.

Monkeys with dlPFC lesions can’t switch strategies in a task when the rewards given for each strategy shift—they perseverate with the strategy offering the most immediate reward.

The differences appear when it comes to making social/emotional decisions—vmPFC patients just can’t decide.fn37

Briefly, the frontal cortex runs “as if” experiments of gut feelings—“How would I feel if this outcome occurred?”—and makes choices with the answer in mind.

Moreover, eventual decisions are highly utilitarian. vmPFC patients are atypically willing to sacrifice one person, including a family member, to save five strangers.62 They’re more interested in outcomes than in their underlying emotional motives, punishing someone who accidentally kills but not one who tried to kill but failed, because, after all, no one died in the second case.

People with vmPFC damage not only have trouble making decisions but also make bad ones.63 They show poor judgment in choosing friends and partners and don’t shift behavior based on negative feedback.

The more amygdaloid activation and the more negative emotions the participant reported in deciding, the less likely they were to push.

The tegmentum sends projections to the accumbens and (other) limbic areas such as the amygdala and hippocampus. This is collectively called the “mesolimbic dopamine pathway.”

A monkey has learned that when he presses a lever ten times, he gets a raisin as a reward. That’s just happened, and as a result, ten units of dopamine are released in the accumbens. Now—surprise!—the monkey presses the lever ten times and gets two raisins. Whoa: twenty units of dopamine are released. And as the monkey continues to get paychecks of two raisins, the size of the dopamine response returns to ten units. Now reward the monkey with only a single raisin, and dopamine levels decline.

These studies show that the dopamine system is bidirectional.88 It responds with scale-free increases for unexpected good news and decreases for bad.

But our frequent human tragedy is that the more we consume, the hungrier we get. More and faster and stronger. What was an unexpected pleasure yesterday is what we feel entitled to today, and what won’t be enough tomorrow.

In other words, the pleasure is in the anticipation of reward, and the reward itself is nearly an afterthought

Because nothing fuels dopamine release like the “maybe” of intermittent reinforcement.

Logically, gambling shouldn’t evoke much anticipatory dopamine, given the astronomical odds against winning. But the behavioral engineering—the 24-7 activity and lack of time cues, the cheap alcohol pickling fronto-cortical judgment, the manipulations to make you feel like today is your lucky day—distorts and shifts the perception of the odds into a range where dopamine pours out and, oh, why not, let’s try again.

dopamine “binds” the value of a reward to the resulting work.

In other words, dopamine is not about the happiness of reward. It’s about the happiness of pursuit of reward that has a decent chance of occurring.fn50,99

We don’t like waiting.

we delay gratification for insanely long times.

Basically, it’s unknown how we humans do this. We may merely be a type of animal, mammal, primate, and ape, but we’re a profoundly unique one.

How does serotonin do this? Nearly all serotonin is synthesized in one brain region,fn51 which projects to the usual suspects—the tegmentum, accumbens, PFC, and amygdala, where serotonin enhances dopamine’s effects on goal-directed behavior.109

So when a neuron has gotten a hugely excitatory message from the previous neuron in line, its insides can become positively charged relative to the extracellular space around it.

Instead of the “I have nothing to say” state being one of charge neutrality, the inside of the neuron is negatively charged relative to the outside.

I have nothing to say = inside of the neuron is negatively charged. I have something to say = inside is positive.

“resting potential.”

“action pote...

Not true.

Kako je on humoristican..

And out of this comes a rule: the more neurons that neuron A projects to, by definition, the more neurons it can influence; however, the more neurons it projects to, the smaller its average influence will be at each of those target neurons.

This doesn’t matter in the spinal cord, where one neuron typically sends all its projections to the next one in line.

The brain is wired in networks of divergent and convergent signaling.

a type of glial cell wraps around an axon, forming a layer of insulation called a myelin sheath; this “myelination” causes the action potential to shoot down the axon faster.

You can see how that has just made things more complicated—a neuron with its ten thousand dendritic spines is getting excitatory inputs of differing magnitudes from various neurons, getting inhibitory ones from other neurons, and integrating all of this at the axon hillock.

Thus there are lots of different classes of neurotransmitters, each binding to a unique receptor site that is complementary to its shape.

an action potential releases the same type of neurotransmitter from all of the axon terminals of a neuron. Therefore there will be a distinctive neurochemical profile to a particular neuron—“Oh, that neuron is a neurotransmitter A–type neuron. And what that also means is that the neurons that it talks to have neurotransmitter A receptors on their dendritic spines.”

There are dozens of neurotransmitters that have been identified. Some of the most renowned: serotonin, norepinephrine, dopamine, acetylcholine, glutamate (the most excitatory neurotransmitter in the brain), and GABA (the most inhibitory).

Serotonin and dopamine, for example, are made from the dietary amino acids tryptophan and tyrosine, respectively.

Given that, you do not want your neurotransmitters to be huge, complex, ornate molecules, each of which requires generations of stonemasons to construct. Instead they are all made in a small number of steps from their precursors. They’re cheap and easy to make. For example, it takes only two simple synthetic steps to turn tyrosine into dopamine.