The brain stem is the oldest and smallest region in the evolving human brain. It evolved hundreds of millions of years ago and is more like the entire brain of present-day reptiles. For this reason, it is often called the 'reptilian brain'. Various clumps of cells in the brain stem determine the brain's general level of alertness and regulate the vegetative processes of the body such as breathing and heartbeat.

It's similar to the brain possessed by the hardy reptiles that preceded mammals, roughly 200 million years ago. It's 'preverbal', but controls life functions such as autonomic brain, breathing, heart rate and the fight or flight mechanism. Lacking language, its impulses are instinctual and ritualistic. It's concerned with fundamental needs such as survival, physical maintenance, hoarding, dominance, preening and mating. It is also found in lower life forms such as lizards, crocodiles and birds. It is at the base of your skull emerging from your spinal column.

The basic ruling emotions of love, hate, fear, lust, and contentment emanate from this first stage of the brain. Over millions of years of evolution, layers of more sophisticated reasoning have been added upon this foundation.

Our intellectual capacity for complex rational thought which has made us theoretically smarter than the rest of the animal kingdom.

When we are out of control with rage, it is our reptilian brain overriding our rational brain components. If someone says that they reacted with their heart instead of their head. What they really mean is that they conceded to their primitive emotions (the reptilian brain based) as opposed to the calculations of the rational part of the brain. There are almond-shaped groups of neurons located deep within the medial temporal lobes of the brain in complex vertebrates, including humans. Shown in research to perform a primary role in the processing and memory of emotional reactions, the amygdalae are considered part of the limbic system.

Emotional Learning

In complex vertebrates, including humans, the amygdala perform primary roles in the formation and storage of memories associated with emotional events. Research indicates that during fear conditioning, sensory stimuli reach the basolateral complexes of the amygdalae, particularly the lateral nuclei, where they form associations with memories of the stimuli. The association between stimuli and the aversive events they predict may be mediated by long-term potentiation, a lingering potential for affected synapses to react more readily.

Memories of emotional experiences imprinted in reactions of synapses in the lateral nuclei elicit fear behavior through connections with the central nucleus of the amygdalae. The central nuclei are involved in the genesis of many fear responses, including freezing (immobility), tachycardia (rapid heartbeat), increased respiration, and stress-hormone release. Damage to the amygdalae impairs both the acquisition and expression of Pavlovian fear conditioning, a form of classical conditioning of emotional responses.

The amygdalae are also involved in appetitive (positive) conditioning. It seems that distinct neurons respond to positive and negative stimuli, but there is no clustering of these distinct neurons into clear anatomical nuclei.

Different nuclei within the amygdala have different functions in appetitive conditioning.

Memory Modulation

The amygdalae also are involved in the modulation of memory consolidation. Following any learning event, the long-term memory for the event is not instantaneously formed. Rather, information regarding the event is slowly assimilated into long-term storage over time (the duration of long-term memory storage can be infinite), a process referred to as memory consolidation, until it reaches a relatively permanent state.

During the consolidation period, the memory can be modulated. In particular, it appears that emotional arousal following the learning event influences the strength of the subsequent memory for that event. Greater emotional arousal following a learning event enhances a person's retention of that event. Experiments have shown that administration of stress hormones to mice immediately after they learn something enhances their retention when they are tested two days later.

The amygdalae, especially the basolateral nuclei, are involved in mediating the effects of emotional arousal on the strength of the memory for the event, as shown by many laboratories including that of James McGaugh. These laboratories have trained animals on a variety of learning tasks and found that drugs injected into the amygdala after training affect the animals' subsequent retention of the task. These tasks include basic classical conditioning tasks such as inhibitory avoidance, where a rat learns to associate a mild footshock with a particular compartment of an apparatus, and more complex tasks such as spatial or cued water maze, where a rat learns to swim to a platform to escape the water. If a drug that activates the amygdalae is injected into the amygdalae, the animals had better memory for the training in the task. If a drug that inactivates the amygdalae is injected, the animals had impaired memory for the task.

Despite the importance of the amygdalae in modulating memory consolidation, however, learning can occur without it, though such learning appears to be impaired, as in fear conditioning impairments following amygdalar damage.

Evidence from work with humans indicates that the amygdala plays a similar role. Amygdala activity at the time of encoding information correlates with retention for that information. However, this correlation depends on the relative "emotionalness" of the information. More emotionally-arousing information increases amygdalar activity, and that activity correlates with retention.

Neuropsychological correlates of amygdala activity

Early research on primates provided explanations as to the functions of the amygdala, as well as a basis for further research. As early as 1888, rhesus monkeys with a lesioned temporal cortex (including the amygdala) were observed to have significant social and emotional deficits. Heinrich Kluver and Paul Bucy later expanded upon this same observation by showing that large lesions to the anterior temporal lobe produced noticeable changes, including overreaction to all objects, hypoemotionality, loss of fear, hypersexuality, and hyperorality. Some monkeys also displayed an inability to recognize familiar objects and would approach animate and inanimate objects indiscriminately, exhibiting a loss of fear towards the experimenters. This behavioral disorder was later named Klčver-Bucy syndrome accordingly.

Later studies served to focus on the amygdala specifically, as the temporal cortex encompasses a broad set of brain structures, making it difficult to find which ones specifically may have correlated with certain symptoms. Monkey mothers who had amygdala damage showed a reduction in maternal behaviors towards their infants, oftentimes physically abusing or neglecting them.

In 1981, researchers found that selective radio frequency lesions of the whole amygdala caused Klčver-Bucy Syndrome.

With advances in neuroimaging technology such as MRI, neuroscientists have made significant findings concerning the amygdala in the human brain. Consensus of data shows the amygdala has a substantial role in mental states, and is related to many psychological disorders. In a 2003 study, subjects with Borderline Personality Disorder showed significantly greater left amygdala activity than normal control subjects. Some borderline patients even had difficulties classifying neutral faces or saw them as threatening.

In 2006, researchers observed hyperactivity in the amygdala when patients were shown threatening faces or confronted with frightening situations. Patients with more severe social phobia showed a correlation with increased response in the amygdala.

Similarly, depressed patients showed exaggerated left amygdala activity when interpreting emotions for all faces, and especially for fearful faces. Interestingly, this hyperactivity was normalized when patients went on antidepressants. By contrast, the amygdala has been observed to relate differently in people with Bipolar Disorder. A 2003 study found that adult and adolescent bipolar patients tended to have considerably smaller amygdala volumes and somewhat smaller hippocampal volumes.

Two preliminary small-scale studies have also linked lower neuron density in the amygdala with autism, though it's unclear whether this is a cause or an effect of the condition.

In the News...

In Our Messy, Reptilian Brains - MSNBC - April 9, 2007

Let others rhapsodize about the elegant design and astounding complexity of the human brain - the most complicated, most sophisticated entity in the known universe, as they say. David Linden, a professor of neuroscience at Johns Hopkins University, doesn't see it that way. To him, the brain is a "cobbled-together mess." Impressive in function, sure.

But in its design the brain is "quirky, inefficient and bizarre ... a weird agglomeration of ad hoc solutions that have accumulated throughout millions of years of evolutionary history," he argues in his new book, "The Accidental Mind," from Harvard University Press. More than another salvo in the battle over whether biological structures are the products of supernatural design or biological evolution (though Linden has no doubt it's the latter), research on our brain's primitive foundation is cracking such puzzles as why we cannot tickle ourselves, why we are driven to spin narratives even in our dreams and why reptilian traits persist in our gray matter.

Just as the mouse brain is a lizard brain "with some extra stuff thrown on top," Linden writes, the human brain is essentially a mouse brain with extra toppings. That's how we wound up with two vision systems. In amphibians, signals from the eye are processed in a region called the midbrain, which, for instance, guides a frog's tongue to insects in midair and enables us to duck as an errant fastball bears down on us.

Our kludgy brain retains this primitive visual structure even though most signals from the eye are processed in the visual cortex, a newer addition. If the latter is damaged, patients typically say they cannot see a thing. Yet if asked to reach for an object, many of them can grab it on the first try. And if asked to judge the emotional expression on a face, they get it right more often than chance would predict - especially if that expression is anger.

They're not lying about being unable to see. In such "blindsight," people who have lost what most of us think of as vision are seeing with the amphibian visual system. But because the midbrain is not connected to higher cognitive regions, they have no conscious awareness of an object's location or a face's expression. Consciously, the world looks inky black. But unconsciously, signals from the midbrain are merrily zipping along to the amygdala (which assesses emotion) and the motor cortex (which makes the arm reach out).

Primitive brains control movement with the cerebellum. Tucked in the back of the brain, this structure also predicts what a movement will feel like, and sends inhibitory signals to the somatosensory cortex, which processes the sense of touch, telling it not to pay attention to expected sensations (such as the feeling of clothes against your skin or the earth beneath your soles). This is why you can't tickle yourself: the reptilian cerebellum has kept the sensation from registering in the feeling part of the brain. Failing to register feelings caused by your own movements claims another victim: your sense of how hard you are hitting someone. Hence, "but Mom, he hit me harder!"

Neurons have hardly changed from those of prehistoric jellyfish. "Slow, leaky, unreliable," as Linden calls them, they tend to drop the ball: at connections between neurons, signals have a 70 percent chance of sputtering out. To make sure enough signals do get through, the brain needs to be massively interconnected, its 100 billion neurons forming an estimated 500 trillion synapses. This interconnectedness is far too great for our paltry 23,000 or so genes to specify. The developing brain therefore finishes its wiring out in the world (if they didn't, a baby's head wouldn't fit through the birth canal). Sensory feedback and experiences choreograph the dance of neurons during our long childhood, which is just another name for the period when the brain matures.

With modern parts atop old ones, the brain is like an iPod built around an eight-track cassette player. One reptilian legacy is that as our eyes sweep across the field of view, they make tiny jumps. At the points between where the eyes alight, what reaches the brain is blurry, so the visual cortex sees the neural equivalent of jump cuts. The brain nevertheless creates a coherent perception out of them, filling in the gaps of the jerky feed. What you see is continuous, smooth. But as often happens with kludges, the old components make their presence felt in newer systems, in this case taking a system that worked well in vision and enlisting it higher-order cognition. Determined to construct a seamless story from jumpy input, for instance, patients with amnesia will, when asked what they did yesterday, construct a story out of memory scraps.

It isn't only amnesiacs whose brains confabulate. There is no good reason why dreams, which consolidate memories, should take a narrative form. If they're filing away memories, we should just experience memory fragments as each is processed. The cortex's narrative drive, however, doesn't turn off during sleep. Like an iPod turning on that cassette player, the fill-in-the-gaps that works so well for jumpy eye movements takes the raw material of memory and weaves it into a coherent, if bizarre, story. The reptilian brain lives on.

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