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The amygdala is a nucleus located in the mesiotemporal lobe bilaterally with an approximate volume of 1700 mm 3 . It is composed of multiple sub-nuclei including the lateral nucleus, the basal nucleus, and the central nucleus. The basal nucleus can be further subdivided into a basomedial, a basolateral, and a basoventral division. The lateral nucleus is the main sensory input to the amygdala; it possesses dense reciprocal connections to higher-level sensory cortical regions. The central nucleus is the main output from the amygdala for the physiological expression of emotions. Therefore, the central nucleus has multiple connections with the hypothalamus and the brainstem. The basal nucleus receives multiple connections from the lateral nucleus and sends out efferents to the central nucleus, thus acting as a relay nucleus within the amygdala. The basal nucleus forms a connectivity loop with the medial prefrontal cortex (mPFC). This reciprocal connection is thought to be important for the cortical (i.e. top-down) control of the amygdala . The function of the amygdala is to link sensory inputs with psychological and physiological processes. For instance, the sight of palatable food raises the blood pressure of primates, a response that disappears after destructive lesions to the amygdala. The amygdala also plays a critical role in fear conditioning where it links innocuous stimuli with aversive ones through initial pairing of the stimuli. By linking specific autonomic and psychological processes to sensory stimuli, the amygdala establishes the basis of emotional responses to events and situations. In essence, the amygdala helps assigning positive or negative emotions to a given context. In turn, the emotional response improves the subject's readiness to the situation. Because of its basic function, the amygdala influences a vast repertoire of human behaviors and experiences. This influence is carried out through a network of interconnections with critical neural circuits including the memory system, the motivational system, the sympathetic and parasympathetic systems, and higher-order sensory cortices.
Langevin. (2012). The amygdala as a target for behavior surgery. Surgical Neurology International Stereotactic, 3(40). langevin2012.pdf
=Mai Atlas and Amygdala=
Comparison of histological photographs from Mai atlas (Mai et al., 1997) with MR images (380 μm in-plane voxel size) and tracings on one young subject at different levels, from most rostral (row i) to most caudal (row vii) boundaries. Columns show A) histological images; B) MRI slices; C) whole amygdala tracings in yellow; D) amygdalar subregion tracings following the protocol illustrated in idealized terms in the next figure: amygdaloid cortical complex (ACo sROI) is blue; basolateral complex (BL sROI) is purple; basomedial complex (BM sROI) is green; centromedial complex (CM sROI) is red. Arrows and arrowheads illustrate specific points described in the Methods section detailing the protocol. Post-mortem histological sections are shown to provide a standard set of reference images to illustrate the landmarks in our protocol. Note that there are multiple differences between the two types of images in contrast properties.
Illustration of idealized boundaries manually drawn on Mai atlas figures (Mai et al., 1997), from most rostral (1) to most caudal (9). Medial boundaries are in blue; dorsal and dorso-lateral boundaries are in red; ventral and ventro lateral boundaries are in yellow. Red arrows are shown to indicate direction of dorsal boundary toward anterior commissure; arrows are not part of the tracing protocol. See Box 1 for abbreviations.
Entis, J. J. et al. (2012). A reliable protocol for the manual segmentation of the human amygdala and its subregions using ultra-high resolution MRI. Neuroimage, 60(1), 1226–1235. entis2012neuroimage.pdf
One long-standing idea is the amygdala consists of an evolutionarily primitive division associated with the olfactory system (the cortico-medial region) and an evolutionarily newer division associated with the neocortex (the basolateral region). The cortico-medial region includes the cortical, medial, and central nuclei, while the basolateral region consists of the lateral, basal and accessory basal nuclei. More recently, however, it has been argued that the amygdala is neither a structural nor a functional unit, and instead consists of regions that belong to other regions or systems of the brain.
In this scheme, for example, the lateral and basal amygdala are viewed as nuclear extensions of the cortex — rather than amygdala regions related to the cortex — while the central and medial amygdala are said to be ventral extensions of the striatum. This scheme has merit, but in this Primer I shall focus on the organization and function of the nuclei and subnuclei that are traditionally said to be part of the amygdala since most of the functions of the amygdala are understood in these terms. For example, the lateral nucleus of what is now called the amygdala will continue to be an important region in fear learning even if the overall concept of the amygdala were eliminated.
It is easy to be confused by the terminology used to describe the amygdala nuclei, as different sets of terms are used. This problem is especially acute with regard to the basolateral region of the amygdala. One popular scheme refers to the basolateral region as consisting of the lateral, basal and accessory basal nuclei. Another scheme uses the terms basolateral and basomedial nuclei to refer to the regions that are named as the basal and accessory basal nuclei in the first scheme. Particularly confusing is the use of the term basolateral to refer to both a specific nucleus (the basal or basolateral nucleus) and to the larger region that includes the lateral, basal and accessory basal nuclei (the basolateral complex).
Each of the nuclei can be further partitioned into subnuclei. For example, the lateral nucleus has three major divisions: dorsal, ventrolateral and medial. Further division is also possible: the dorsal subdivision has a superior and an inferior region. That such fine distinctions are relevant is illustrated by the fact that, as described below, cells in the superior and inferior parts of the dorsal subarea of the lateral nucleus have been shown to be involved in different aspects of fear memory (the superior part in learning and the inferior part in long-term storage).
LeDoux, J. (2007). The amygdala. Current Biology, 17(20), R868-R874. ledoux2007amygdalacurrentbiology.pdf =Amygdala in rats and human= The amygdala consists of a number of different regions. Those of most relevance to the pathways of fear conditioning are the lateral (LA), basal (B), accessory basal (AB), and central (CE) nuclei. The piriform cortex (PIR) lies lateral to the amygdala, and the caudate-putamen (CPU) is just dorsal to it. Comparison of the Nissl-stained section (upper left) and an adjacent section stained for acetylcholinesterase (upper right) helps identify the different nuclei. The major pathways connecting LA, B, AB, and CE are shown (lower left panel). (Lower right) A blowup of the LA, emphasizing the fact that each nucleus can be divided into subnuclei. Although anatomical studies have shown that the pathways are organized at the level of the subnuclei, rather than the nuclei (see Pitka¨nen et al 1997), the nuclear connections (lower left panel) provide a sufficiently detailed approximation of the connections for the purposes of considering how the fear conditioning system is, in general, organized. ledoux2000emotioncircuitannualreviewneuroscience.pdf LeDoux, J. E. (2000). Emotion circuits in the brain. Annual Review of Neuroscience, 23, 155-184.
Over the past several years, there has been an explosion of interest in the role of the human amygdala in fear. Deficits in the perception of the emotional meaning of faces, especially fearful faces, have been found in patients with amygdala damage (Adolphs et al 1995, Calder et al 1996). Similar results were reported for detection of the emotional tone of voices (Scott et al 1997). Furthermore, damge to the amygdala (Bechara et al 1995) or areas of temporal lobe including the amygdala (LaBar et al 1995) produced deficits in fear conditioning in humans. Functional imaging studies have shown that the amygdala is activated more strongly in the presence of fearful and angry faces than of happy ones (Breiter et al 1996) and that subliminal presentations of such stimuli lead to stronger activations than do freely seen ones (Whalen et al 1998). Fear conditioning also leads to increases in amygdala activity, as measured by functional magnetic resonance imaging (LaBar et al 1998, Buchel et al 1998), and these effects also occur to subliminal stimuli (Morris et al 1998). Additionally, when the activity of the amygdala during fear conditioning is cross correlated with the activity in other regions of the brain, the strongest relations are seen with subcortical (thalamic and collicular) rather than cortical areas, further emphasizing the importance of the direct thalamao-amygdala pathway in the human brain (Morris et al 1999). Other aspects of emotion and the human brain area are reviewed by Davidson & Irwin (1999), Phelps & Anderson (1997), Cahill & McGaugh (1998).
Since Pavlov (1927), it has been known that an initially neutral stimulus [a conditioned stimulus (CS)] can acquire affective properties on repeated temporal pairings with a biologically significant event [the unconditioned stimulus (US)]. As the CS-US relation is learned, innate physiological and behavioral responses come under the control of the CS. For example, if a rat is given a tone CS followed by an electric shock US, after a few tone-shock pairings (one is often sufficient), defensive responses (responses that typically occur in the presence of danger) will be elicited by the tone. Examples of species-typical defensive responses that are brought under the control of the CS include defensive behaviors (such as freezing) and autonomic (e.g. heart rate, blood pressure) and endocrine (hormone release) responses, as well as alterations in pain sensitivity (analgesia) and reflex expression (fear-potentiated startle and eyeblink responses). This form of conditioning works throughout the phyla, having been observed in flies, worms, snails, fish, pigeons, rabbits, rats, cats, dogs, monkeys, and humans.
Conditioning to a tone [conditioned stimulus (CS)] involves projections from the auditory system to the lateral nucleus of the amygdala (LA) and from LA to the central nucleus of the amygdala (CE). In contrast, conditioning to the apparatus and other contextual cues present when the CS and unconditioned stimulus are paired involves the representation of the context by the hippocampus and the communication between the hippocampus and the basal (B) and accessory basal (B) nuclei of the amygdala, which in turn project to CE. As for tone conditioning, CE controls the expression of the responses. =Pain Pathways=
“There are two primary ascending nociceptive pathways. These are the spinoparabrachial pathway (red), which originates from the superficial dorsal horn and feeds areas of the brain that are concerned with affect, and the spinothalamic pathway (blue), which probably distributes nociceptive information to areas of the cortex that are concerned with both discrimination and affect. Many more less prominent pathways could be added2, 5, 6, 68-72. (A, adrenergic nucleus; bc, brachium conjunctivum; cc, corpus callosum; Ce, central nucleus of the amygdala; Hip, hippocampus; ic, internal capsule; LC, locus coeruleus; PB, parabrachial area; Po, posterior group of thalamic nuclei; Py, pyramidal tract; RVM, rostroventral medulla; V, ventricle; VMH, ventral medial nucleus of the hypothalamus; VPL, ventral posteriolateral nucleus of the thalamus; VPM; ventral posteriomedial nucleus of the thalamus.)”
Hunt, S. P. (2001). The molecular dynamics of pain control. Nature Reviews Neuroscience, 2.
=Pain and Amygdala=
It is clear now that the amygdala is also part of the pain system. Highly processed, affective and cognitive, polymodal information reaches the amygdala from the thalamus and cortical areas (Shi and Davis 1999; LeDoux 2000; Stefanacci and Amaral 2000; Price 2003) through connections with the LA and the basolateral nucleus of the amygdala (BLA), which then project to the CeA. These inputs from the LA and BLA to the CeA are part of the fear- and anxiety-related circuitry (LeDoux 2000). Through extensions of the spinohypothalamic and spinothalamic pain pathways, the LABLA-CeA circuitry also receives pain-related information from the thalamus (midline and posterior nuclei), granular and dysgranular insular cortex, and anterior cingulate cortex (Augustine 1996; Millan 1999; Shi and Davis 1999; LeDoux 2000; Price 2000; Stefanacci and Amaral 2000).
Neugebauer, V. et al. (2004). The Amygdala and Persistent Pain. The Neuroscientist, 10, 221-234. neugebauer2004theamygdalaandpersistentpainneuroscientist.pdf
=FDG-PET correlation with Pain scales=
A covariation of the FDG-PET signal and the subjective pain perception (VAS) and disability scores (PDI) in different subregions of the amygdala (P\0.001). The brain metabolism in the laterobasal amygdaloid group (LB) was correlated with the VAS pain ratings, whereas a correlation with the PDI scores was found in the superﬁcial group (SF) of the amygdala (Figs. 1, 2). The sites of covariation within the amygdala were lateralized (contralateral to the side of the cluster headache) for the VAS pain scores, but bilateral for the PDI scores. When lowering the signiﬁcance level (P\0.005), an additional trend of covariation (VAS scores) was observed in the ipsilateral amygdala.
Seifert, C. L. et al. (2011). Neurometabolic correlates of depression and disability in episodic cluster headache. Journal of Neurology, 258(1), 123-131. seifert2011headachejneurol.pdf
The linkage of pain and its affective (autonomic) substrates in the brain was not a viable research target until functional imaging allowed conscious reporting by human subjects to be related to changes in the brain during noxious stimulation. Imaging psychophysics allows brain changes to be correlated with sensory stimulation parameters. In terms of pain, this means that modulating the level of unpleasantness might provide insight into the substrate of affect. One of two views guide investigators in their analysis of the cerebral mechanisms of pain and emotion. The global model posits that most of the cerebral cortex is involved, in some way, in emotion, and that perceptions that are associated with emotional experiences are an emergent property of the brain. Although many parts of the brain contribute to emotion, each area does not necessarily make an equal contribution. The alternative view is that some areas store memories with positive or negative valences and drive asso ciated autonomic outputs, whereas other areas provide sensory and short-term memory substrates that are not specific to emotion, and cannot access autonomic outputs. Systems involved in all short-term memory, including, for example, emotional memory, are not emotion-specific processors. Although the circuits that engage the cingulate cortex in pain processing have long been known, we are only now in a position to link specific aspects of pain perception with its localized emotional substrates, which was not possible without human functional imaging.
Vogt, B. A. (2005). Pain and emotion interactions in subregions of the cingulate gyrus. Nature Reviews Neuroscience, 6(7), 533-544. vogt2005painemotionnaturereviewsneuroscience.pdf
A wealth of animal data implicates the amygdala in aspects of emotional processing. In recent years, functional neuroimaging and neuropsychological studies have begun to refine our understanding of the functions of the amygdala in humans. This literature offers insights into the types of stimuli that engage the amygdala and the functional consequences that result from this engagement. Specific conclusions and hypotheses include: (1) the amygdala activates during exposure to aversive stimuli from multiple sensory modalities; (2) the amygdala responds to positively valenced stimuli, but these responses are less consistent than those induced by aversive stimuli; (3) amygdala responses are modulated by the arousal level, hedonic strength or current motivational value of stimuli; (4) amygdala responses are subject to rapid habituation; (5) the temporal characteristics of amygdala responses vary across stimulus categories and subject populations; (6) emotionally valenced stimuli need not reach conscious awareness to engage amygdala processing; (7) conscious hedonic appraisals do not require amygdala activation; (8) activation of the amygdala is associated with modulation of motor readiness, autonomic functions, and cognitive processes including attention and memory; (9) amygdala activations do not conform to traditional models of the lateralization of emotion; and (10) the extent and laterality of amygdala activations are related to factors including psychiatric status, gender and personality. The strengths and weakness of these hypotheses and conclusions are discussed with reference to the animal literature.
Zald, D. H. (2003). The human amygdala and the emotional evaluation of sensory stimuli. Brain Research Reviews, 41(1), 88-123. zald2003amygdalaemotionevaluationbrainresearchreviews.pdf
Each nucleus of the amygdala has unique inputs and outputs. The lateral amygdala is generally viewed as the gatekeeper of the amygdala. It is the major site receiving inputs from sensory systems — the visual, auditory, somatosensory (including pain), olfactory, and taste systems all have inputs to this region (olfactory and taste information is also transmitted to other nuclei as well). Other amygdala regions receive inputs from other brain areas, allowing diverse kinds of information to be processed by the amygdala.
(B, basal nucleus; Ce, central nucleus; itc, intercalated cells; La, lateral nucleus; M, medial nucleus. Sensory abbreviations: aud, auditory; vis, visual; somato, somatosensory; gust, gustatory (taste)
The auditory input connections of the lateral amygdala have been studied most thoroughly. Auditory inputs reach the lateral amygdala from the auditory thalamus and auditory cortex. The thalamic inputs are from extralemniscal areas that weakly encode frequency properties of the auditory stimulus. These provide a rapid but imprecise auditory signal to the amygdala. Cortical inputs from the auditory and other sensory systems arise from the association areas, rather than from the primary cortical regions. These provide the amygdala with a more elaborate representation than could come from the thalamic inputs. However, because additional synaptic connections are involved, transmission is slower.
The sensory inputs to the lateral amygdala terminate most extensively in the dorsal subnucleus. The dorsal subregion then communicates with the ventrolateral and medial areas, which then connect with other amygdala areas.
Just as the lateral nucleus is the sensory gateway into the amygdala, the central nucleus is believed to be an important output region, at least for the expression of innate emotional responses and associated physiological responses. The expression of these responses involves connections from the medial subdivision of the central nucleus to brainstem areas that control specific behaviors and physiological responses.
Another important set of output connections of the amygdala arise from the basal nucleus. In addition to connecting with the central nucleus, it also connects with striatal areas involved in the control of instrumental behaviors. Thus, while the output connections of central amydgala to the brainstem are involved in controlling emotional reactions, like freezing in the presence of a predator, connections from the basal amygdala to the striatum are involved in controlling actions, like running to safety.
(B, basal nucleus; Ce, central nucleus; itc, intercalated cells; La, lateral nucleus. Modulatory arousal system abbreviations: NE, norepinephrine; DA, dopamine; ACh, acetylcholine; 5HT, serotonin). Other abbreviations: parasym ns, parasympathetic nervous system; symp ns, sympathetic nervous system.)
In order for sensory information received by the lateral amygdala to influence behavior the information must be routed through intramygdala connections. There are some direct connections from the lateral nucleus to the central nucleus but these are relatively sparse. The main channels of communication between the lateral and the central nucleus are thus thought to involve connections from the medial part of the lateral nucleus to other amygdala nuclei that then connect with the central nucleus. For example, the lateral nucleus projects to the basal nucleus which projects to the central nucleus. In addition, both the lateral and basal nuclei project to the intercalated cells which then connect with the central nucleus.
LeDoux, J. (2007). The amygdala. Current Biology, 17(20), R868-R874. ledoux2007amygdalacurrentbiology.pdf
Nitric oxide correlates amygdalar function
When we examine nitric oxide (NO) signaling, we notice two constitutive enzymatic components, the constitutive NO synthase (cNOS), including endothelial (eNOS) and neuronal (nNOS) isoforms. cNOS, as the name implies, is always expressed. When cNOS is stimulated, NO release occurs for a short period of time, but this level of NO can exert profound physiological actions for a long period of time. NO not only is an immune, vascular, and neural autoregulatory signaling molecule, but also performs vital physiological activities via its constitutive expression. Both the amygdala and the hippocampus contain numerous receptors for varying neurotransmitters. The central nucleus of the amygdala is most strongly modulated by dopamine, norepinephrine (NE), epinephrine, and serotonin. The basal nuclei receive moderately high inputs of dopamine, NE, and serotonin, each of which has been demonstrated to exert their desired effect via NO. Taken together, we surmise that NE initially promotes a slight vasoconstriction of the artery during the amygdalar compensatory response, which is defined as the limbic system’s inherent mechanism to maintain homeostasis and lower stress levels. This mechanism is indicated by a slight enhancement of sympathetic activity on stimulation (ie, emotional), and is immediately followed by the release of NO from the peripheral nitroxidergic nerve, which mediates a concentration-dependent vasodilation. In primates, the cerebral arterial diameter, under resting conditions, is maintained by tonic release of NO from the nerve (10%–20%), or from the nerve and endothelium (30%). This observation is supported by other data from our laboratory because of the fact that basal NO is cNOSderived and keeps particular types of cells in a state of inhibition. Endogenous superoxide dismutase in the cerebral artery appears to protect the relaxation induced by NO from perivascular nerves from the NO scavenger action of superoxide anions. This NO then produces the longer-lived phenomenon of smooth muscle relaxation. In another report, it was found that NE vascular hyperresponsiveness in hypertension was dependent on an impairment of NO activity that was realized through NE-induced oxygen free radical production, providing an important contribution to the understanding of this regulatory process.
Salamon, E., Esch, T., & Stefano, G. B. (2005). Role of amygdala in mediating sexual and emotional behavior via coupled nitric oxide release1. Acta Pharmacologica Sinica, 26(4), 389-395. salamon2005amygdalaemotionsexnoactapharmacologicasinica.pdf
The central nucleus of the amygdala (Ce) is the terminal area of a spino(trigemino)-parabrachio-amygdaloid nociceptive pathway that originates in lamina I of the spinal and medullary dorsal horn and relays in the parabrachial (PB) area (Bernard et al., 1989; Bernard & Besson, 1990; Jasmin et al., 1997). The involvement of this pathway in pain processes was demonstrated by electrophysiological, anatomical and c-fos experiments. The electrophysiological data indicate that lamina I spino(trigemino)-parabrachial (Hylden et al., 1985; 1986; Hayashi & Tabata, 1989; Light et al., 1993; Bester et al. 2000) as well as parabrachio-amygdaloid (Bernard & Besson, 1988; Bernard & Besson, 1990; Huang et al., 1993a; Bernard et al., 1994) neurons are primarily driven by noxious stimuli.
=Nociceptive Amygdala= there are direct nociceptive inputs to the laterocapsular part of the CeA, which is now defined as the “nociceptive amygdala” because of its high content of nociceptive neurons (Bourgeais and others 2001; Neugebauer and Li 2002, 2003; Li and Neugebauer 2003). The term nociception refers to the neuronal processes resulting in a stimulus being perceived as painful. The latero-capsular CeA receives nociceptivespecific information from the spinal cord and brainstem through the spino-parabrachio-amygdaloid pain pathway (Gauriau and Bernard 2002) as well as through direct projections from the spinal cord (Burstein and Potrebic 1993; Wang and others 1999). The CeA forms widespread connections with forebrain areas, hypothalamus, and brainstem. to regulate emotional behavior (Davis 1998; LeDoux 2000; Bourgeais and others 2001). Neurons in the laterocapsular part of the CeA project heavily to the substantia innominata dorsalis, which provides connections with the agranular insular cortex, orbital and medial prefrontal cortices, cholinergic basal forebrain nuclei, bed nucleus of the stria terminalis, and medial dorsal thalamus, as well as the hypothalamus and brainstem areas (Bourgeais and others 2001). The latero-capsular CeA also forms direct and indirect (via medial CeA) connections connections with the medial dorsal thalamus through the ventral amygdaloid pathway (VAP), the hypothalamus via the stria terminalis and VAP, and the brainstem either directly through the VAP or indirectly via the hypothalamus (Davis 1998; LeDoux 2000; Price 2003). Brainstem targets include the periaqueductal grey (PAG), parabrachial nucleus (PB), reticular formation, dorsal nucleus of the vagus, solitary tract nucleus, and ventrolateral medulla (Davis 1998; LeDoux 2000; Price 2003). Through these connections with brain areas and systems involved in nociception and pain, fear and anxiety, attention and cognition, autonomic function and stress responses, and endogenous pain control, the CeA is well positioned to play a key role in the emotional-affective pain response and pain modulation (Bernard and others 1996; Heinricher and McGaraughty 1999; Millan 1999; Fields 2000; Rhudy and Meagher 2000; Bourgeais and others 2001; Gauriau and Bernard 2002).
Neugebauer, V. et al. (2004). The Amygdala and Persistent Pain. The Neuroscientist, 10, 221-234. neugebauer2004theamygdalaandpersistentpainneuroscientist.pdf
The central nucleus of the amygdala (CE) is the interface with motor systems. Damage to CE interferes with the expression of conditioned fear responses (Gentile et al., 1986; Hitchcock and Davis, 1986; Iwata et al., 1986; Kapp et al., 1979; Van de Kar et al., 1991), while damage to areas that CE projects to selectively interrupts the expression of individual responses. For example, damage to the lateral hypothalamus affects blood pressure but not freezing responses, and damage to the peraqueductal gray interferes with freezing but not blood pressure responses (LeDoux et al., 1988). Similalry, damage to the bed nucleus of the stria terminalis has no effect on either blood pressure or freezing responses (LeDoux et al., 1988) but disrupts the conditioned release of pituitary-adrenal stress hormones (Van de Kar et al., 1991). Because CE receives inputs from LA, B, and AB (Pitkanen et al., 1997), it is in a position to mediate the expression of conditioned fear responses elicited by both acoustic and contextual CSs.
LeDoux, J. E. (2003). The Emotional Brain, Fear, and the Amygdala. Cellular and Molecular Neurobiology, 23(4), 727-738. ledoux2003emotionalbrainfearamygdalacellularmolecularneurobiology.pdf
Implicit Emotional Learning and Memory The lateral nucleus (LA) is typically viewed as the sensory interface of the amygdala and as a key site of plasticity, while the centralnucleus (CE) is viewed as the output region. LA receives inputs from both thalamic and cortical stations in the auditory system, and both are involved in CS transmission. LA projects to CE both directly and indirectly. It is still unclear whether the direct connection from LA to CE is sufficient or whether a link through the basal nuclei and/or the intercalated cell masses might be involved, or even whether direct sensory connections to CE might play a role. As with tone conditioning, the CE is involved in controlling responses, but the input region involves synapses in the basal nucleus.
The Amygdala Facilitates Attention to Salient Stimuli Kapp and colleagues (B.S. Kapp et al., 1996, 1997, Soc. Neurosci., abstract) have shown that cells in CE respond to a CS and that fluctuations in the cortical EEG are correlated with changes in the spontaneous activity of CE cells. Both direct and indirect pathways are proposed for the amygdala's transitory modulation of cortical regions. First, there are reciprocal connections between amygdalanuclei and sensory cortex (Amaral et al., 2003), indicating a means by which the amygdala could influence sensory processes through direct projections. Second, the CE projects to the nucleus basalis of Meynert (NBM), which projects to widespread cortical areas, many of which are sensory-processing regions. Acetycholine, which is released in these cortical areas via the NBM, has been shown to facilitate neuronal responsivity.
Emotional Regulation and Coping Damage to the centralnucleus of the amygdala prevents freezing to the CS (a passive form of coping) but does not interfere with the ability to learn responses that terminate or prevent the CS (active coping).
Phelps, E. A. & LeDoux, J. E. (2005). Contributions of the Amygdala to Emotion Processing: From Animal Models to Human Behavior. Neuron, 48(1), 175-187. phelpsledoux2005neuron.pdf
=Human PET results= Only SSRI and placebo responders exhibited reduced neural activity in the left basomedial/basolateral (BM/BLA) and right ventrolateral (VLA) amygdala subregions, suggesting that these areas are related to anxiety relief. (a) Coronal images displaying decreased cerebral blood flow with treatment (pre–post) in three amygdala clusters, resultant from conjunction analyses. (1) The conjunction of selective serotonin reuptake inhibitor (SSRI) and placebo responders (with nonresponders to SSRIs and placebo as exclusive mask) showed overlapping amygdala deactivations with statistical peaks in the right ventrolateral and left basomedial/basolateral regions, indicating a common anxiolytic effect. (2) The conjunction of SSRI responders and SSRI nonresponders (with placebo responders and nonresponders as exclusive mask) revealed a common deactivation of the left lateral section of the amygdala, indicating a nonanxiolytic pharmacodynamic effect. (3) The conjunction of all groups, ie, SSRI and placebo responders/nonresponders, revealed a common deactivation of the left lateral amygdala, indicating an effect related to repeated testing over time. (b) Corresponding plots of percent change (±SE) in amygdala blood flow in responders and nonresponders in the three amygdala clusters related to (1) common anxiolytic effect of SSRIs and placebo; (2) non-anxiolytic pharmacodynamic effect of SSRIs, and (3) effect related to repeated testing.
Faria, V., Appel, L., Åhs, F., Linnman, C., Pissiota, A., Frans, Ö., et al. (2012). Amygdala Subregions Tied to SSRI and Placebo Response in Patients with Social Anxiety Disorder. Neuropsychopharmacology. faria2012amygdalassriplaceboneuropsychopharmacology.pdf
Subregional assignment within the amygdala. This figure shows the result of the second step of the hierarchical assignment procedure that was used in the present study: after assigning peaks to the ‘core’ region of the amygdala with high anatomical probability (dark blue volume, cf. Fig. 1 and Fig. 2), these peaks were assigned to the amygdala subregions LB (blue squares), SF (green squares), and CM (magenta squares). Peaks outside of the amygdala core area are indicated by grey dots. Only 6 peaks (3.7% of all peaks assigned to the core region of the amygdala) were found in CM. All of them were located in the left CM region. Note that not all of these peaks can be easily seen, some of the CM peaks are (mostly) obscured by other peaks. These results from subregional assignment indicate that in particular the right CM region is, judging from the available evidence in this study, a ‘white spot’ in the functional map of the human amygdala. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of the article.)
Ball, T., Derix, J., Wentlandt, J., Wieckhorst, B., Speck, O., Schulze-Bonhage, A., et al. (2009). Anatomical specificity of functional amygdala imaging of responses to stimuli with positive and negative emotional valence. Journal of Neuroscience Methods, 180(1), 57-70. ball2009amygdalametaanalysisemotionjneurosciencemethods.pdf
Searches so far: (Google Scholar) Amygdala Central Nucleus fMRI Amygdala Central Nucleus fMRI pain Amygdala Central Nucleus fMRI emotion Amygdala Central Nucleus fMRI emotion pain Basolateral Nucleus of the Amygdala fMRI pain emotion Centromedial group of the Amygdala fMRI pain emotion
Ball, T., Derix, J., Wentlandt, J., Wieckhorst, B., Speck, O., Schulze-Bonhage, A., et al. (2009). Anatomical specificity of functional amygdala imaging of responses to stimuli with positive and negative emotional valence. Journal of Neuroscience Methods, 180(1), 57-70.
Entis, J. J. et al. (2012). A reliable protocol for the manual segmentation of the human amygdala and its subregions using ultra-high resolution MRI. Neuroimage, 60(1), 1226–1235.
Faria, V., Appel, L., Åhs, F., Linnman, C., Pissiota, A., Frans, Ö., et al. (2012). Amygdala Subregions Tied to SSRI and Placebo Response in Patients with Social Anxiety Disorder. Neuropsychopharmacology.
Hunt, S. P. (2001). The molecular dynamics of pain control. Nature Reviews Neuroscience, 2.
Langevin. (2012). The amygdala as a target for behavior surgery. Surgical Neurology International Stereotactic, 3(40).
LeDoux, J. E. (2000). Emotion circuits in the brain. Annual Review of Neuroscience, 23, 155-184.
LeDoux, J. E. (2003). The Emotional Brain, Fear, and the Amygdala. Cellular and Molecular Neurobiology, 23(4), 727-738.
LeDoux, J. E. (2007). The amygdala. Current Biology, 17(20), R868-R874.
Neugebauer, V. et al. (2004). The Amygdala and Persistent Pain. The Neuroscientist, 10, 221-234.
Salamon, E., Esch, T., & Stefano, G. B. (2005). Role of amygdala in mediating sexual and emotional behavior via coupled nitric oxide release1. Acta Pharmacologica Sinica, 26(4), 389-395.
Seifert, C. L. et al. (2011). Neurometabolic correlates of depression and disability in episodic cluster headache. Journal of Neurology, 258(1), 123-131.
Phelps, E. A. & LeDoux, J. E. (2005). Contributions of the Amygdala to Emotion Processing: From Animal Models to Human Behavior. Neuron, 48(1), 175-187.
Vogt, B. A. (2005). Pain and emotion interactions in subregions of the cingulate gyrus. Nature Reviews Neuroscience, 6(7), 533-544.
Zald, D. H. (2003). The human amygdala and the emotional evaluation of sensory stimuli. Brain Research Reviews, 41(1), 88-123.