Effect of total amygdalectomy upon regulation of salt intake in rats

Cox, Jacci R.; Cruz, Carlos Eduardo Braga; Ruger, Jeffrey

doi:10.1016/0361-9230(78)90071-0

Cited by 17 publications

(10 citation statements)

References 14 publications

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“…Consistent with the possibility that one or more of the sites discussed perform this integration, sodium appetite is substantially reduced after lesions in the PB (Flynn et al,1991; Scalera et al,1995), BST (Reilly et al,1994; Zardetto‐Smith et al,1994), CeA (Cox et al,1978; Schulkin et al,1989; Galaverna et al,1992; Zardetto‐Smith et al,1994; Johnson et al,1999), and LHA (Wolf,1964a). Critical contributions from any of the aforementioned subcortical sites, driven by input from the HSD2 neurons, would also be consistent with prior evidence that the brain circuitry underlying sodium appetite requires intact connections between the brainstem and forebrain (Grill et al,1986), but not the gustatory thalamus (Scalera et al,1997) or sensory cortex (Wolf et al,1970; Wirsig and Grill,1982).…”

Section: Discussionmentioning

confidence: 71%

“…Indirect inputs from the HSD2 neurons to the CeA may provide a neuroanatomical basis for the established role of the amygdala in modulating salt intake (Cox et al,1978; Johnson et al,1999). For example, the salt ingestion produced by mineralocorticoid administration is abolished by lesions in the amygdala (Schulkin et al,1989; Galaverna et al,1992).…”

Section: Discussionmentioning

confidence: 99%

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Aldosterone-sensitive neurons in the nucleus of the solitary tract: Efferent projections

2006

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The nucleus of the solitary tract (NTS) contains a subpopulation of neurons that express the enzyme 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2), which makes them uniquely sensitive to aldosterone. These neurons may drive sodium appetite, which is enhanced by aldosterone. Anterograde and retrograde neural tracing techniques were used to reveal the efferent projections of the HSD2 neurons in the rat. First, the anterograde tracer Phaseolus vulgaris leucoagglutinin was used to label axonal projections from the medial NTS. Then, NTS-innervated brain regions were injected with a retrograde tracer, cholera toxin beta subunit, to determine which sites are innervated by the HSD2 neurons. The HSD2 neurons project mainly to the ventrolateral bed nucleus of the stria terminalis (BSTvl), the pre-locus coeruleus (pre-LC), and the inner division of the external lateral parabrachial nucleus (PBel). They also send minor axonal projections to the midbrain ventral tegmental area, lateral and paraventricular hypothalamic nuclei, central nucleus of the amygdala, and periaqueductal gray matter. The HSD2 neurons do not innervate the ventrolateral medulla, a key brainstem autonomic site. Additionally, our tracing experiments confirmed that the BSTvl receives direct axonal projections from the neighboring A2 noradrenergic neurons in the NTS, and from the same pontine sites that receive major inputs from the HSD2 neurons (PBel and pre-LC). The efferent projections of the HSD2 neurons may provide new insights into the brain circuitry responsible for sodium appetite.

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Section: Discussionmentioning

confidence: 71%

Section: Discussionmentioning

confidence: 99%

Aldosterone-sensitive neurons in the nucleus of the solitary tract: Efferent projections

2006

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“…It is notable that the amygdala is not necessary for sodium appetite. In the experiments described above, and in later studies with more restricted lesions, rats continued to drink a significantly increased volume of saline (albeit less than unlesioned controls) in response to sodium depletion (Cox et al,1978; Zolovick et al,1980). Thus, the basic input and output sites responsible for sodium appetite lie outside the amygdala.…”

Section: Discussionmentioning

confidence: 95%

“…Total destruction of the amygdala (massive bilateral electrolytic lesions extending rostrocaudally from the level of the optic chiasm to the hippocampus and laterally from the optic tract out to the external capsule) depressed baseline fluid intake (both water and saline) and reduced the increase in saline ingestion that occurs in response to sodium depletion and mineralocorticoid administration (Cox et al,1978). A similar reduction in sodium appetite was produced by large injections of colchicine into the amygdala, which then reversed after recovery from this pharmacological inactivation (Zolovick et al,1980).…”

Section: Discussionmentioning

confidence: 99%

Aldosterone‐sensitive neurons in the nucleus of the solitary tract: Bidirectional connections with the central nucleus of the amygdala

Geerling

Loewy

2006

J of Comparative Neurology

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The HSD2 (11-β-hydroxysteroid dehydrogenase type 2-expressing) neurons in the nucleus of the solitary tract (NTS) of the rat are aldosterone-sensitive and have been implicated in sodium appetite (Geerling et al., 2006a;Geerling et al., 2006b). The central nucleus of the amygdala (CeA) has been shown to modulate salt intake in response to aldosterone, so we investigated the connections between these two sites. A prior retrograde tracing study only revealed a minor projection from the HSD2 neurons directly to the CeA, but these experiments suggested that a more substantial projection may be relayed through the parabrachial nucleus. Small injections of cholera toxin beta subunit (CTb) into the external lateral parabrachial subnucleus (PBel) produced both retrograde cell body labeling in the HSD2 neurons and anterograde axonal labeling in the lateral subdivision of the CeA. Also, injections of either CTb or Phaseolus vulgaris leucoagglutinin into the medial subdivision of the CeA labeled a descending projection from the amygdala to the medial NTS. Axons from the medial CeA formed numerous varicosities and terminals enveloping the HSD2 neurons. Complementary CTb injections, centered in the HSD2 subregion of the NTS, retrogradely labeled neurons in the medial CeA. These bidirectional projections could form a functional circuit between the HSD2 neurons and the CeA. The HSD2 neurons may represent one of the functional inputs to the lateral CeA, and their activity may be modulated by a return projection from the medial CeA. This circuit could provide a neuroanatomical basis for the modulation of salt intake by the CeA. Keywords11 beta hydroxysteroid dehydrogenase type 2; HSD2; 11HSD2; aldosterone; mineralocorticoid; nucleus of the solitary tract; nucleus tractus solitarius; NTS; sodium appetite; salt appetite; salt ingestion; ingestive behavior; central nucleus of the amygdala

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“…In light of the need for integrating multiple somatic and visceral sensory inputs necessary for the generation of salt appetite, the ExA becomes a primary subcortical candidate for this function. Earlier studies investigating the amygdala in salt appetite showed that extensive damage to large parts of the amygdala 50,51 or transection of the ventral amygdalofungal pathway 52 decreased experimentally induced sodium intake. More recent studies have been directed at a more precise determination of the nuclei or components of the ExA that are necessary for full expression of salt appetite.…”

Section: The Implication Of Components Of the Extended Amygdala (Exa)mentioning

confidence: 99%

The Extended Amygdala and Salt Appetite

Johnson

Olmos

Pastuskovas

et al. 1999

Annals of the New York Academy of Sciences

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Both chemo- and mechanosensitive receptors are involved in detecting changes in the signals that reflect the status of body fluids and of blood pressure. These receptors are located in the systemic circulatory system and in the sensory circumventricular organs of the brain. Under conditions of body fluid deficit or of marked changes in fluid distribution, multiple inputs derived from these humoral and neural receptors converge on key areas of the brain where the information is integrated. The result of this central processing is the mobilization of homeostatic behaviors (thirst and salt appetite), hormone release, autonomic changes, and cardiovascular adjustments. This review discusses the current understanding of the nature and role of the central and systemic receptors involved in the facilitation and inhibition of thirst and salt appetite and on particular components of the central neural network that receive and process input derived from fluid- and cardiovascular-related sensory systems. Special attention is paid to the structures of the lamina terminalis, the area postrema, the lateral parabrachial nucleus, and their association with the central nucleus of the amygdala and the bed nucleus of the stria terminalis in controlling the behaviors that participate in maintaining body fluid and cardiovascular homeostasis.

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Effect of total amygdalectomy upon regulation of salt intake in rats

Cited by 17 publications

References 14 publications

Aldosterone-sensitive neurons in the nucleus of the solitary tract: Efferent projections

Aldosterone-sensitive neurons in the nucleus of the solitary tract: Efferent projections

Aldosterone‐sensitive neurons in the nucleus of the solitary tract: Bidirectional connections with the central nucleus of the amygdala

The Extended Amygdala and Salt Appetite

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