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I am a PhD student studying the circuitry of fear and anxiety in the rodent and human brain.


Your brain controls when you feel afraid. Understanding it is not as scary as you think.

Why do we feel afraid?

The circuit: There is a circuit in your brain, led by the amygdala, that super charges your body to feel what we, as humans, perceive as fear.

The amygdala is responsible for my fear of clowns?: Well, in part. Studies in rodents have shown that the amygdala plays a major role in the fear response. The reaction of freezing, wanting to run away, and having your heart beat of out your chest is spear-headed by the amygdala (Read more) .

But you can't ask a rodent if it feels afraid! You are right, but of the same behaviors elicited by humans, when they feel afraid, are also shown in rodents (see the paper).

So what's this amygdala thing anyway?

I'm glad you asked! The amygdala (named from the Greek word for almond) is an almond-shaped area found in almost all mammalian brains (See the different shapes of the amygdala here).

It connects to many of your sensory and cognitive inputs, so what you see, feel in the environment, and even think about passes through the amygdala.

Even more fascinating, the amygdala can form and retain memories! Rodent studies have shown that fear memories are believed to be stored, at first, within amygdala cells (See the paper).

So why is this important? Well, scientists have discovered that if you find where memories are formed, you can potentially erase memories. Regarding the amygdala, researchers have been able to erase a fear memory (See the paper).

That sounds like science fiction. Believe it or not, rodent and human studies have shown that fear memories can be erased. This has huge potential!

Why? Many people suffer from psychiatric disorders that revolve around traumatic fearful memories. Erasing, or modulating, a fear memory can be a potential way to alleviate debilitating symptoms of fear.

So the next time you feel afraid, you can partially blame your amygdala.


Using Neuroscience to Help Understand Fear and Anxiety: A Two-System Framework.

Abstract: Tremendous progress has been made in basic neuroscience in recent decades. One area that has been especially successful is research on how the brain detects and responds to threats. Such studies have demonstrated comparable patterns of brain-behavior relationships underlying threat processing across a range of mammalian species, including humans. This would seem to be an ideal body of information for advancing our understanding of disorders in which altered threat processing is a key factor, namely, fear and anxiety disorders. But research on threat processing has not led to significant improvements in clinical practice. The authors propose that in order to take advantage of this progress for clinical gain, a conceptual reframing is needed. Key to this conceptual change is recognition of a distinction between circuits underlying two classes of responses elicited by threats: 1) behavioral responses and accompanying physiological changes in the brain and body and 2) conscious feeling states reflected in self-reports of fear and anxiety. This distinction leads to a "two systems" view of fear and anxiety. The authors argue that failure to recognize and consistently emphasize this distinction has impeded progress in understanding fear and anxiety disorders and hindered attempts to develop more effective pharmaceutical and psychological treatments. The two-system view suggests a new way forward.

Pub.: 10 Sep '16, Pinned: 22 Apr '17

Optogenetic activation of presynaptic inputs in lateral amygdala forms associative fear memory.

Abstract: In Pavlovian fear conditioning, the lateral amygdala (LA) has been highlighted as a key brain site for association between sensory cues and aversive stimuli. However, learning-related changes are also found in upstream sensory regions such as thalamus and cortex. To isolate the essential neural circuit components for fear memory association, we tested whether direct activation of presynaptic sensory inputs in LA, without the participation of upstream activity, is sufficient to form fear memory in mice. Photostimulation of axonal projections from the two main auditory brain regions, the medial geniculate nucleus of the thalamus and the secondary auditory cortex, was paired with aversive footshock. Twenty-four hours later the same photostimulation induced robust conditioned freezing and this fear memory formation was disrupted when glutamatergic synaptic transmission was locally blocked in the LA. Therefore, our results prove for the first time that synapses between sensory input areas and the LA, previously implicated as a crucial brain site for fear memory formation, actually are sufficient to serve as a conditioned stimulus. Our results strongly support the idea that the LA may be sufficient to encode and store associations between neutral cue and aversive stimuli during natural fear conditioning as a critical part of a broad fear memory engram.

Pub.: 18 Oct '14, Pinned: 22 Apr '17

From fear to safety and back: reversal of fear in the human brain.

Abstract: Fear learning is a rapid and persistent process that promotes defense against threats and reduces the need to relearn about danger. However, it is also important to flexibly readjust fear behavior when circumstances change. Indeed, a failure to adjust to changing conditions may contribute to anxiety disorders. A central, yet neglected aspect of fear modulation is the ability to flexibly shift fear responses from one stimulus to another if a once-threatening stimulus becomes safe or a once-safe stimulus becomes threatening. In these situations, the inhibition of fear and the development of fear reactions co-occur but are directed at different targets, requiring accurate responding under continuous stress. To date, research on fear modulation has focused mainly on the shift from fear to safety by using paradigms such as extinction, resulting in a reduction of fear. The aim of the present study was to track the dynamic shifts from fear to safety and from safety to fear when these transitions occur simultaneously. We used functional neuroimaging in conjunction with a fear-conditioning reversal paradigm. Our results reveal a unique dissociation within the ventromedial prefrontal cortex between a safe stimulus that previously predicted danger and a "naive" safe stimulus. We show that amygdala and striatal responses tracked the fear-predictive stimuli, flexibly flipping their responses from one predictive stimulus to another. Moreover, prediction errors associated with reversal learning correlated with striatal activation. These results elucidate how fear is readjusted to appropriately track environmental changes, and the brain mechanisms underlying the flexible control of fear.

Pub.: 07 Nov '08, Pinned: 22 Apr '17