Possible Mechanisms of Involvement of the Amygdaloid Complex in the Control of Gastric Motor Function

Lyubashina, O. A.

doi:10.1023/b:neab.0000018750.65372.18

Cited by 15 publications

(18 citation statements)

References 20 publications

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“…While the role of the amygdala to modulate gastric motility has not been studied to the same degree, nevertheless it has been known for some time that, in anesthetized animals, stimulation of the CeA alters gastric pressure (increased or decreased depending on the medial-lateral location of the stimulating electrode) in a vagally dependent manner (157, 303, 311). The role of the amygdala in regulation and modulation of GI functions is not restricted to the stomach, however.…”

Section: Cns Regulation Of Sympathetic and Parasympathetic Control Ofmentioning

confidence: 99%

Central Nervous System Control of Gastrointestinal Motility and Secretion and Modulation of Gastrointestinal Functions

Browning

Travagli

2014

Comprehensive Physiology

429

388

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Although the gastrointestinal (GI) tract possesses intrinsic neural plexuses that allow a significant degree of autonomy over GI functions, the central nervous system (CNS) provides extrinsic neural inputs that regulate, modulate, and control these functions. While the intestines are capable of functioning in the absence of extrinsic inputs, the stomach and esophagus are much more dependent upon extrinsic neural inputs, particularly from parasympathetic and sympathetic pathways. The sympathetic nervous system exerts a predominantly inhibitory effect upon GI muscle and provides a tonic inhibitory influence over mucosal secretion while, at the same time, regulates GI blood flow via neurally mediated vasoconstriction. The parasympathetic nervous system, in contrast, exerts both excitatory and inhibitory control over gastric and intestinal tone and motility. Although GI functions are controlled by the autonomic nervous system and occur, by and large, independently of conscious perception, it is clear that the higher CNS centers influence homeostatic control as well as cognitive and behavioral functions. This review will describe the basic neural circuitry of extrinsic inputs to the GI tract as well as the major CNS nuclei that innervate and modulate the activity of these pathways. The role of CNS-centered reflexes in the regulation of GI functions will be discussed as will modulation of these reflexes under both physiological and pathophysiological conditions. Finally, future directions within the field will be discussed in terms of important questions that remain to be resolved and advances in technology that may help provide these answers.

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Section: Cns Regulation Of Sympathetic and Parasympathetic Control Ofmentioning

confidence: 99%

Central Nervous System Control of Gastrointestinal Motility and Secretion and Modulation of Gastrointestinal Functions

Browning

Travagli

2014

Comprehensive Physiology

429

388

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“…CeA lesions also reduce baseline CRF expression in the hypothalamus and stress-induced release of ACTH and CORT (Beaulieu et al, 1986; Prewitt and Herman, 1994). Anatomical studies indicate that the CeA provides major output to autonomic regions that mediate not only fear and anxiety-related behaviors but also enteric processes such as gastric emptying and colonic motility (LeDoux et al, 1988; Lyubashina, 2004; Swanson and Petrovich, 1998). A summary of the anatomical connectivity of the amygdala with projections relevant to the integration of visceral and somatic pain, motor activity of the GI tract, as well as stress and anxiety is displayed in Figure 1.…”

Section: Anxiety and Ibs: What Is The Connection?mentioning

confidence: 99%

“…A summary of the anatomical connectivity of the amygdala with projections relevant to the integration of visceral and somatic pain, motor activity of the GI tract, as well as stress and anxiety is displayed in Figure 1. Although the role of the amygdala in the regulation of GI motor function is an understudied area, electrical stimulation of the CeA can inhibit gastric motility through direct projections from the CeA to the dorsal motor nucleus of the vagus and nucleus of the solitary tract (Krettek and Price, 1978; Lyubashina, 2004; Schwaber et al, 1982). In addition, Figure 2 illustrates the projections from the CeA to the locus coeruleus (LC) and Barrington's nucleus that modify distal colonic motility through manipulation of the sacral parasympathetic nucleus (Sakanaka et al, 1986; Valentino et al, 1999).…”

Section: Anxiety and Ibs: What Is The Connection?mentioning

confidence: 99%

Role of Anxiety in the Pathophysiology of Irritable Bowel Syndrome: Importance of the Amygdala

Myers¹,

Meerveld²

2009

Front. Neurosci.

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A common characteristic of irritable bowel syndrome (IBS) is that symptoms, including abdominal pain and abnormal bowel habits, are often triggered or exacerbated during periods of stress and anxiety. However, the impact of anxiety and affective disorders on the gastrointestinal (GI) tract is poorly understood and may in part explain the lack of effective therapeutic approaches to treat IBS. The amygdala is an important structure for regulating anxiety with the central nucleus of the amygdala facilitating the activation of the hypothalamic-pituitary-adrenal axis and the autonomic nervous system in response to stress. Moreover, chronic stress enhances function of the amygdala and promotes neural plasticity throughout the amygdaloid complex. This review outlines the latest findings obtained from human studies and animal models related to the role of the emotional brain in the regulation of enteric function, specifically how increasing the gain of the amygdala to induce anxiety-like behavior using corticosterone or chronic stress increases responsiveness to both visceral and somatic stimuli in rodents. A focus of the review is the relative importance of mineralocorticoid receptor and glucocorticoid receptor-mediated mechanisms within the amygdala in the regulation of anxiety and nociceptive behaviors that are characteristic features of IBS. This review also discusses several outstanding questions important for future research on the role of the amygdala in the generation of abnormal GI function that may lead to potential targets for new therapies to treat functional bowel disorders such as IBS.

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“…The central nucleus of the amygdala (CeA) provides output to autonomic regions that mediate not only anxietyrelated behaviors but also GI processes such as gastric emptying and colonic motility (16,24,25,44,48). Widespread connections to autonomic brain stem nuclei including reciprocal projections with the motor nucleus of the vagus, nucleus of the solitary tract, and locus coeruleus (LC) provide a mechanism for amygdaloid modulation of GI function…”

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confidence: 99%

Divergent effects of amygdala glucocorticoid and mineralocorticoid receptors in the regulation of visceral and somatic pain

Myers

Meerveld

2010

American Journal of Physiology-Gastrointestinal and Liver Physi

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Elevated amygdala activity and increased responsiveness of the hypothalamic-pituitary-adrenal axis have been observed in irritable bowel syndrome (IBS) patients. Recently, we demonstrated that corticosterone (Cort) placed on the amygdala induced anxiety-like behavior coupled with decreased thresholds for visceral and somatic pain in rats. Moreover, these studies suggested that the effects of Cort were dependent on both the glucocorticoid receptor (GR) and mineralocorticoid receptor (MR); however, the specific contributions of these receptors to the interaction between corticosteroids and the amygdala are still unclear. In the present study, we sought to define the distinct roles of amygdaloid GR and MR in anxiety-like behavior, visceral sensitivity, and somatic sensitivity through selective pharmacological activation. Male Fischer 344 rats received bilateral implants on the dorsal margin of the central amygdala containing the GR agonist dexamethasone (Dex), the MR agonist aldosterone (Aldo), or cholesterol as a control. Our results showed that GR or MR activation significantly reduced open arm exploration on the elevated plus maze, a measure of anxiety-like behavior. Aldo increased the number of abdominal muscle contractions in response to all levels of colorectal distension (CRD). In contrast, Dex only increased visceral sensitivity at noxious levels of CRD. Furthermore, GR but not MR activation reduced somatic pain thresholds measured by the mechanical force required to elicit hindlimb withdrawal. In summary, GR and MR mediated-mechanisms induce anxiety and visceral hypersensitivity, whereas somatic sensitivity involves only GR, suggesting that corticosteroids may enhance visceral and somatic sensation via divergent processes originating in the amygdala and involving specific steroid receptor mechanisms. irritable bowel syndrome; hypothalamic-pituitary-adrenal axis; pain sensitivity; aldosterone; dexamethasone IRRITABLE BOWEL SYNDROME (IBS) is a functional gastrointestinal (GI) disorder of unknown etiology characterized by chronic abdominal pain and altered bowel patterns. A prominent feature of IBS symptomatology is altered visceral perception exhibited by hypersensitivity of the colon to luminal distension (5,41,59). IBS patients also demonstrate a twofold higher rate of comorbidity with somatic pain disorders than controls (40,61). Stress is known to play an important role in the onset and exacerbation of symptomatology, which was demonstrated by the statistical relationship between life stress and the subsequent intensity of bowel symptoms (4, 60). Additionally, statistical correlations among mean daily stress, indexes of anxiety and depression, and GI symptoms (abdominal pain and altered bowel patterns) suggest a prominent role for stressrelated processes in the symptomatology of the disorder (20). In fact, IBS patients possess elevated cortisol levels both at baseline and in response to stress (6, 12). Furthermore, functional MRI has revealed that, in response to visceral stimulation, IBS patients displa...

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Possible Mechanisms of Involvement of the Amygdaloid Complex in the Control of Gastric Motor Function

Cited by 15 publications

References 20 publications

Central Nervous System Control of Gastrointestinal Motility and Secretion and Modulation of Gastrointestinal Functions

Central Nervous System Control of Gastrointestinal Motility and Secretion and Modulation of Gastrointestinal Functions

Role of Anxiety in the Pathophysiology of Irritable Bowel Syndrome: Importance of the Amygdala

Divergent effects of amygdala glucocorticoid and mineralocorticoid receptors in the regulation of visceral and somatic pain

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