We will be provided with an authorization token (please note: passwords are not shared with us) and will sync your accounts for you. The amygdala is an almond-like structure that is located within the temporal lobe of the brain, adjacent to the ventral hippocampus.
Despite these well-defined amygdala circuits and connections, it has not been well-understood yet how fear memories are stored, processed, and extinguished particularly at the circuit level.
Fear conditioning is a behavioral paradigm that has been widely used to probe associative fear learning. Sensory information pertinent to the CS and the US is initially integrated and processed in LA. Following association and processing of CS and US signals in LA, the newly integrated information is transferred to BA, and then CEA.
The vast majority of published studies have focused on synaptic changes and plasticity of excitatory connections in the amygdala during fear conditioning in order to elucidate the neuronal substrates of emotional learning and memory. Inhibitory circuits are not only involved in tuning excitatory transmission, but are also active components of intra-amygdala fear pathways necessary for acquisition and extinction of fear memories. Besides adjusting strength of excitatory connections, inhibitory circuits are actively involved in acquisition of fear memories. When learned fear is repeatedly retrieved without presentation of US, the fear responses to CS rapidly decrease. Recent studies revealed that BA neurons also participate in acquisition of fear extinction memories.
Inhibitory connections and their strength are controlled in a temporal fashion by regulators such as biogenic amines and neuropeptides. Serotonin (5-HT), another major biogenic amine, is intimately involved in controlling fear memories. Norepinephrine is also important for processing sensory information related with fear memories. During fear conditioning, the conditioned stimulus (CS) and unconditioned stimulus (US) are relayed to the lateral nucleus of the amygdala (LA) from thalamic and cortical regions of the auditory and somatosensory systems, respectively.
Whereas Little Albert learned to fear white rats in the 1920s, rats learned to fear a simple noise more than 80 years later.
Fear extinction involves creating a conditioned response that counters the conditioned fear response. According to the National Institute of Mental Health, 19 million people in the United States alone suffer from mental illnesses that involve irrational fear responses.
The amygdala is a central structure of the limbic system of the brain that is involved in producing appropriate emotional responses. The purpose of the upper cortical route to the amygdala is to determine whether the stimulus is truly life threatening. The amygdala also has a role to play in the degree to which a threat or trigger gains a person’s attention.
Washington, Jan 28 : The link between amygdala and fear, especially a fear of others unlike us, has gone too far not only in pop culture but also in psychological science, a new study has claimed. The amygdala are almond-shaped groups of nuclei located deep within the medial temporal lobes of the brain in complex vertebrates, including humans. Instead, the amygdala seems to be doing something more subtle - processing events that are related to what a person cares about at the moment.
A lot of the time, people really don't know, or won't say, what they're thinking, and it would be nice to be able to look at a picture of their brain and know the answer. This means that you will not need to remember your user name and password in the future and you will be able to login with the account you choose to sync, with the click of a button. This page doesn't support Internet Explorer 6, 7 and 8.Please upgrade your browser or activate Google Chrome Frame to improve your experience. A number of studies for amygdala neural circuits that underlie fear conditioning have elucidated specific cellular and molecular mechanisms of emotional memory. The neural circuits of the amygdala and its connected brain areas are thought to be critically important for emotional learning, especially the formation and storage of fear memories (LeDoux, 2003). This lack of understanding was mainly due to the absence of methodologies that allow temporal and spatial manipulations of select circuit components.
During fear conditioning, an unconditioned stimulus (US), such as an electrical foot shock, is simultaneously presented with a neutral conditioned stimulus (CS), such as a tone or a light, to subjects. Thus, LA functions as the synaptic interface of the amygdala, receiving sensory signals from various sources such as thalamic and cortical inputs. However, emerging evidence indicates that inhibitory circuits containing interneurons are critical components of neural networks that control neuronal activity and animal behavior. More specifically, inhibitory circuits control fear behavior during acquisition and expression of fear memories and construct new suppressive memories during fear extinction. The reduction of fear responses is attributable to formation of new suppressive memories, a process known as fear extinction (Herry et al., 2010). Although we cannot fully exclude the possibility that this decreased LA neuronal activity may be due to depotentiation of thalamo-amygdala synapses by extinction training (Kim et al., 2007), it would result from actions of inhibitory circuits that are newly recruited by the context signals.
Thus, the inhibitory components of amygdala circuits serve as an interface for modulation by these regulators, which would define the dynamic features of inhibitory circuits for processing sensory information.
Dopamine (DA) is a well-known biogenic amine that controls inhibitory circuits and fear responses.
BLA receives dense serotonergic projections from the dorsal raphe nucleus and also expresses multiple subtypes of 5-HT receptors (Sadikot and Parent, 1990; Figure 3B). Most of us aren't too keen on the prospect of going at our amygdala with an ice pick, though. Scientist Mark Barad of UCLA performed an experiment in which he and his team combined a noise with an electric shock. While studies situate the amygdala as the location of fear memories formed by conditioning, scientists theorize that fear-extinction memories form in the amygdala but then are transferred to the medial prefrontal cortex (mPFC) for storage. For instance, therapy for a person with a fear of snakes might involve visiting a snake farm repeatedly and taking small steps toward touching one. These disorders include generalized anxiety disorder, panic disorder and post-traumatic stress disorder. If it is not, then it dampens the influence on the amygdala arising from the unconscious lower route stimulus.
For PTSD sufferers certain triggers lead to immediate attention so increasing the stimulus’ threat value. 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. But it also activates at other times, for example in response to pleasant photographs and happy faces.
A lot of people came to the amygdala from the study of fear, says Wil Cunningham of Ohio State University, who co-wrote the new paper with Tobias Brosch of New York University. Recent technical advances such as optogenetic approaches have not only confirmed the importance of excitatory circuits in fear conditioning, but have also shed new light for a direct role of inhibitory circuits in both the acquisition and extinction of fear memory in addition to their role in fine tuning of excitatory neural circuitry. BA can be further divided into the basolateral nucleus (BL) and the basomedial nucleus (BM; Figure 1).

However, the recent advent of optogenetics provides valuable tools for researchers to address these circuit level questions with unprecedented temporal and spatial specificities. The subjects learn to predict aversive events and exhibit fear responses not just to the US, but also to the CS. After successful fear extinction, CS cues that previously induced fear responses will no longer cause alterations in neural activity at the circuit level. Hence, the newly recruited inhibitory circuits could then suppress fear-related physiological changes and behavior (Figure 2B). Therefore, burst firing of IL neurons during extinction learning and innervations to BA extinction neurons may contribute to retention and expression of extinction memories. In situ hybridizations for various regulatory receptors expressed in the amygdala (Allen Institute for Brain Science, 2012). In fact, various subtypes of adrenergic receptors are present in BLA (Figure 3C), and infusion of norepinephrine into BLA promotes consolidation of fear memories (LaLumiere et al., 2003). 3, the CS inputs enter the dorsal subregion of the LA, where interactions with the US induce plasticity in two functional cell types (so-called 'trigger' and 'storage' cells). They would play the tone and then immediately apply a shock to the metal floor of the rats' cage.
The new memory created by fear extinction resides in the mPFC and attempts to override the fear memory triggered in the amygdala. First, the person might get within 10 feet of the snake and see that nothing terrible happens. Two other brain structures are involved in these modules, namely the hypothalamus and the pituitary gland. In the case of PTSD the lower unconscious route dominates and the route through the cortex is incapable of dampening sufficiently the response that has already taken place in the ‘low road’ route. Cunningham also thinks many scientists have gotten too attached to a rigid definition of emotions-anger, fear, sadness, happiness, and so on. As a result, the circuits in amygdala could be drawn more elaborately, and it led us to understand how fear or extinction memories are formed in the detailed circuit level, and various neuromodulators affect these circuit activities, inducing subtle behavioral changes.
Therefore, the behavioral features and signaling mechanisms of fear memories are highly conserved across the animal realm. Cortex-like subnuclei (blue) are located laterally, while striatum-like subnuclei (yellow) are located medially. By combining optogenetic tools with other experimental paradigms, such as in vitro and in vivo recordings, recent studies have confirmed and further substantiated that excitatory amygdala connections and dynamic changes in the synaptic strength can modulate various phases of fear memories. Mechanically, sensory information encoding the CS and the US converges in LA, which results in long-term potentiation (LTP) at LA excitatory synapses (Rogan et al., 1997).
Although thalamic and cortical inputs are thought to convey different aspects of sensory information (unprocessed or processed, respectively), they reach same components in LA (Szinyei et al., 2000).
The inhibitory elements in the amygdala circuits were initially thought to control neural activity simply by inhibiting excitatory transmission. Solid and dashed lines indicate strengthened and weakened connections, respectively, during the learning processes. Intriguingly, extinction of fear memories displays several characteristics that differ from those of fear acquisition and expression. Importantly, extinction training does not quantitatively fully normalize the neuronal activity to the levels observed prior to fear conditioning. The two classes of neurons display largely distinct spiking activity in response to a CS, and therefore may discriminate between extinguished and non-extinguished stimuli.
As mentioned above, inactivation of either BA or IL during extinction training session impaired the formation of extinction memories, which represents the interplay between two regions necessary for fear extinction.
At the cellular level, iontophoresis of 5-HT into LA inhibits excitation of LA projection neurons (Stutzmann et al., 1998). CS information is then transmitted through further stations in the LA to the central nucleus of the amygdala (CE). It was classical conditioning, and it didn't take long for the rats to brace themselves for the shock as soon as they heard the sound. It is these two structures that control the hormones that produce physical reactions associated with particular emotions. Furthermore, there is a connection from the amagydala to the cortex and back from the cortex to the amygdala, the first connection is stronger than the second. The neuronal engrams that permit storage of learned fear are formed almost immediately upon exposure of the subject to threats, and are represented by apparent changes in behavioral patterns.
Furthermore, a number of studies provide evidence that inhibitory elements of amygdala circuits play major roles in defining and processing of fear engrams and fear memories.
This LTP enables the CS alone to elicit fear responses (freezing behavior) normally observed only when subjects confront threats (LeDoux, 2000).
However, the precise roles of the inhibitory circuits are much more complex and instructive than previously thought. First, the extinguished fear memories tend to recover spontaneously over time (Rescorla, 2004). In support of this notion, the extinction neurons have extra-amygdala connectivity that differs from the fear neurons. Moreover, IL sends projections to multiple subnuclei of the amygdala including BLA, CEA, and ITC.
Interactions between the lateral and central amygdala are more complex than illustrated, and involve local-circuit connections (see main text). At that point, their amygdalas paired the sound with the shock, and the sound created a fear response. When nothing terrible happens within 5 feet of the snake, he might get close enough to touch it.
This means fearful feelings affect our conscious thoughts more easily than our thoughts can dampen them. Thus, this perspicuity of fear responses provides opportunities to investigate both the physiological functions of amygdala circuits and the molecular and cellular mechanisms that underlie long-lasting memories. CEA is further divided into lateral (CEl) and medial (CEm) parts, which serve different functions and have distinct connectivity (Ciocchi et al., 2010). Herein, we provide an overview of these new findings that suggest the functional importance of amygdala inhibitory circuits in acquisition, expression, and extinction of fear memories. However, when the CS is presented repeatedly without the US, the ability to elicit fear responses is diminished. Both thalamic and cortical inputs form feedforward inhibition onto pyramidal neurons through local inhibitory neurons (Ehrlich et al., 2009). A subregion of medial prefrontal cortex (mPFC), the prelimbic cortex (PL), is also critical for expression of fear-related behavior (Corcoran and Quirk, 2007). As the major input station for the amygdala, LA receives synaptic inputs from a number of brain regions.
Interestingly, two distinct groups of CEl neurons exhibit opposite responses to CS presentations, especially after fear conditioning. Collectively, reductions in LA neuronal activity alone do not seem to be sufficient for expression of fear extinction memories.

In the thalamic pathway, DA reduces feedforward inhibition from local interneurons to LA projection neurons via activation of dopamine D2 receptors (D2Rs), which eventually allows for LTP induction at thalamo-amygdala synapses (Bissiere et al., 2003).
The LA also communicates with the CE by way of connections with other amygdala regions (not shown), but the direct pathway seems to be sufficient to mediate fear conditioning. The researchers then began the process of fear-extinction training, in which they made the sound but did not apply the shock. It is the amygdala that instantly assesses incoming information and determines the appropriate emotional response.
It is in part due to this that psychotherapies dealing with some emotional problems, like PTSD, fail. In addition, the amygdala contains multiple intercalated cell masses (ITCs), which are thought to regulate the interconnectivity between the distinct amygdala subnuclei and also between the amygdala and extra-amygdala structures.
Interestingly, cortical inputs are innervated to lITCs residing in the external capsule and in turn, lITC also provides feedforward inhibition onto LA pyramidal neurons (Marowsky et al., 2005).
CS-evoked unit activity in PL increases both during and following fear conditioning, but subsequently decreases after fear extinction (Burgos-Robles et al., 2009).
In LA, there is disinhibition of local inhibitory circuits due to the effects of several biogenic amines. Finally, fear responses to a CS can be reinstated simply by re-exposure to the US alone (Rescorla and Heth, 1975). Decreases in LA neuronal activity may be consequence of extinction-induced activation of inhibitory circuits that project to and affect a select subset of LA neurons.
Taken together, two populations of BA neurons seem to belong to different circuits, but this observation merits further investigation to elucidate exact intra-amygdala circuitry containing input or output connections of these two types of BA neurons. A recent study indicated that ITCv neurons directly inhibit the neural activity of CEm neurons, which is consistent with the staining experiment showing enhanced neural activity in ITCv neurons after extinction training (Busti et al., 2011).
LA projection neurons also receive potent feedforward inhibition by lITC when cortical inputs are stimulated (Marowsky et al., 2005).
On determining the appropriate response it sends signals to other brain structures to carry out suitable action; typically signals to the hypothalamus that triggers hormonal changes that alter muscle contraction and influence the heart rate.
Knowing what the problem is (a cortex to amygdala connection) can be insufficient to correct the problem (an amygdala to cortex connection).
ITCs are composed of GABAergic neurons (Busti et al., 2011) and are located along the borders of the BLA. The GAD67 expression profile indicates that inhibitory neurons are sparsely present in the cortex-like subnuclei and densely present in ITCs and the striatum-like subnuclei. Activity of PL neurons during CS presentation is thought to be originated from activity of BLA because the CS-evoked activity in PL is regulated by BLA (Sotres-Bayon et al., 2012). However, if the organism is exposed to fearful situations, then inhibition is released and the resulting decrease in synaptic inhibition of LA projection neurons permits occurrence of LTP and associative learning (Bissiere et al., 2003). A more successful approach is to work on the first connection: that between the amygdala and the cortex. Depending on the residing loci, ITCs are named as the lateral paracapsular (lITC), the dorsal (ITCd), and the ventral (ITCv) ITC (Figure 1). Therefore, fear extinction is likely to recruit inhibitory circuits to suppress expression of the existing fear memories. Notably, there are marked deficits in expression of extinction memories when ITCv is lesioned (Likhtik et al., 2008).
Thus, reduced feedforward inhibition from local LA interneurons and lITC GABAergic neurons enhances the activity of LA projection neurons and allows occurrence of LTP. Hence, it is conceivable that PL would control fear expression by modulating activity of BA. Furthermore, activated CElon cells appear to suppress CEloff cells that normally lead to tonic inhibition of CEm neurons (Figure 2A).
Augmented activity of fear neurons, mediated through reciprocal connections with PL regions, is necessary to activate CEm output neurons. These suggest that inhibitory neurons in ITCv are required for normal retention and expression of fear extinction memories, possibly through feedforward inhibition of CEA neurons. There are a number of synaptic inputs impinging onto LA projection neurons, and only the salient signals that are above a specific intensity should induce LTP and fear memories. Thus, increased activity of CElon cells in response to a CS results in excitation of CEm neurons through disinhibition (Haubensak et al., 2010). Collectively, it is fairly reasonable to speculate that fear extinction memories require augmented transmission from BA to ITCv and that IL modulates synaptic transmission by regulating both the ITCv and BA extinction neurons (Figure 2B).
Therefore, synaptic plasticity in BLA is gated and adjusted by amygdala inhibitory circuits and DA is critically involved in shaping the firing patterns of BLA neurons by acting on the inhibitory components. The second route to the amygdala arising from an emotional stimulus goes via the cortex where it is consciously evaluated.
On the other hands, DA is able to directly increase the excitability of BLA pyramidal neurons and fast-spiking BLA interneurons, which further amplify salient signals over the specific threshold (Kroner et al., 2005). Tonic suppression derived from local inhibitory neurons helps the circuit to ignore these unimportant signals. Decreased connectivity between extinction-resistant neurons in LA and fear neurons in BA could also contribute to fear extinction.
Therefore, DA released during fear conditioning also enhances the signal-to-noise ratio, which helps amygdala circuits determine meaningful information. Thus, the tonic effects of inhibitory neurons are essential for specific stimulation of LA projection neurons and encoding of precise memories.
LA also sends excitatory signals to ITCd neurons, which in turn inhibit CEl neurons (Pare and Duvarci, 2012).
Furthermore, IL cortex sends glutamatergic projections to ITCv and possibly extinction neurons of BA. Supporting this hypothesis, animals show generalized anxiety phenotypes after foot shock conditioning when activation of dopaminergic neurons in response to aversive stimuli is genetically attenuated (Zweifel et al., 2011).
Several studies have supported active roles of inhibitory circuits by showing that specific fear memories are not formed in the absence of inhibitory components.
These IL projections may participate in suppression of BA fear neurons via local inhibitory circuits. Overall, inhibitory neurons mediate effects of DA on fear memories, including the gating of synaptic plasticity and shaping of cellular firing patterns. For instance, deletion of presynaptic GABAB receptors from glutamatergic inputs projecting onto LA projection neurons facilitates non-associative homosynaptic LTP in the cortical pathway and results in fear generalization that is an important characteristics of anxiety disorders (Shaban et al., 2006). Supporting the inhibitory functionality from ITCd to ITCv, fear conditioning enhances expression of activity markers in ITCd, but not in ITCv (Busti et al., 2011).
Thus, basal inhibitory circuits serve to increase the signal-to-noise ratio for salient inputs during fear conditioning and ultimately to enhance the specificity of neural activity toward the salient events. These various pathways may be necessary for providing modulatory interfaces that confer distinct features to fear responses depending on diverse circumstances.

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