The organization of projections from the central nucleus of the amygdala to brainstem sites involved in central autonomic regulation: A combined retrograde transport-immunohistochemical study

Veening, Jan G.; Swanson, Larry W.; Sawchenko, Paul E.

doi:10.1016/0006-8993(84)91220-4

Cited by 461 publications

(270 citation statements)

References 76 publications

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“…BLA receives multimodal sensory input from the cortex and thalamus, and studies of phenomena as diverse as fear learning and drug reward suggest that the primary function of the BLA is to integrate information from conditioned and unconditioned stimuli and to communicate this information to areas of the brain involved in motivational and emotional responses (21,23,25). A major projection of the BLA is to the CEA, whose primary function is to gate information from the BLA, and from a host of other cortical and subcortical areas, to the limbic-forebrain, hypothalamic, and brainstem regions controlling specific endocrine, autonomic, arousal, and behavioral responses (37)(38)(39)(40). Furthermore, there is considerable evidence that information from the BLA is also transmitted to the hippocampus by means of its projections to the entorhinal cortex and can modulate neural plasticity in the DG (41,42).…”

Section: Discussionmentioning

confidence: 99%

The central and basolateral nuclei of the amygdala exhibit opposite diurnal rhythms of expression of the clock protein Period2

Lamont

Robinson

Stewart

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

216

231

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There is considerable evidence that circadian rhythms in mammals can be modulated by emotional state, but how emotional state modulates specific circadian outputs is poorly understood. We analyzed the expression of the circadian clock protein Period2 (PER2) in three regions of the limbic forebrain known to play key roles in emotional regulation, the central nucleus of the amygdala (CEA), the basolateral amygdala (BLA), and the dentate gyrus (DG). We report here that cells in all three regions exhibit daily rhythms in expression of PER2 that are under the control of the master clock, the suprachiasmatic nucleus (SCN). The rhythm in the CEA and the rhythms in the BLA and DG are diametrically opposite in phase and are differentially affected by adrenalectomy. Adrenalectomy completely abolished the PER2 rhythm in the CEA but had no effect on the PER2 rhythms in the BLA and DG. We previously reported a rhythm in PER2 expression in the oval nucleus of the bed nucleus of the stria terminalis that is identical in phase and sensitivity to adrenalectomy to that found in the CEA. Together, these findings show that key structures of the limbic forebrain exhibit daily oscillations in clock gene expression that are controlled not only by input from the SCN but, importantly, by hormonal and neurochemical changes that normally accompany motivational and emotional states. Thus, cells within these areas are strategically positioned to integrate the inputs from the SCN and emotional states to modulate circadian rhythms downstream from the SCN clock.hippocampus ͉ suprachiasmatic nucleus ͉ oval nucleus ͉ circadian clock I n mammals, the suprachiasmatic nucleus (SCN) of the hypothalamus is recognized as a master clock responsible for the regulation of all behavioral and physiological circadian rhythms (1). The rhythm of the SCN, although sensitive to the daily cycle of light, is relatively invulnerable to environmental challenges and changes in physiology (2, 3). Yet it is recognized that stressors and changes in emotional states can have disruptive effects on behavioral and physiological rhythms (4-8). Furthermore, disruptions of circadian rhythms have negative effects on mood and well being, as observed during jet lag or shift work (9, 10).Although the SCN is the only clock structure required for the generation of circadian rhythmicity, recent studies show that circadian rhythms in expression of clock genes, such as Per1 and Per2, can be found in other brain regions that participate in the control of specific behavioral and physiological outputs. These include, but are not limited to, the striatum, paraventricular hypothalamic nucleus, arcuate nucleus, preoptic area, and olfactory bulbs (11-17). The study of clock genes in these and other functionally defined brain regions may help to determine how the SCN clock controls specific circadian rhythms and, importantly, may contribute to an understanding of how diverse experiences and pathological conditions can affect circadian rhythms downstream from the SCN clock.We found recently th...

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Section: Discussionmentioning

confidence: 99%

The central and basolateral nuclei of the amygdala exhibit opposite diurnal rhythms of expression of the clock protein Period2

Lamont

Robinson

Stewart

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

216

231

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“…The BNST is a primary target of the amygdala (de Olmos et al, 1985;Sun et al, 1991;Alheid et al, 1995), and both the BNST and the amygdala share almost identical brainstem target areas implicated in stress and anxiety responses (Schwaber et al, 1980;Takeuchi et al, 1982Takeuchi et al, , 1983Sofroniew, 1983;Swanson et al, 1984;Veening et al, 1984;Holstege et al, 1985;Magnuson, 1987, 1992;Moga et al, 1989). Interestingly, some of the projections to the amygdala (cf.…”

Section: Implications For a Possible Distinction Between Fear And Anxmentioning

confidence: 99%

Role of the Hippocampus, the Bed Nucleus of the Stria Terminalis, and the Amygdala in the Excitatory Effect of Corticotropin-Releasing Hormone on the Acoustic Startle Reflex

1997

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Previously, we demonstrated that transection of the fimbria/ fornix blocked the excitatory effect of corticotropin-releasing hormone (CRH) on startle (CRH-enhanced startle), suggesting that the hippocampus and its efferent target areas that communicate via the fimbria may be critically involved in CRHenhanced startle. The bed nucleus of the stria terminalis (BNST) receives direct projections from the ventral hippocampus via the fimbria/fornix. Therefore, the role of the ventral hippocampus, the BNST, and the amygdala in CRH-enhanced startle was investigated. NMDA lesions of the BNST completely blocked CRH-enhanced startle, whereas chemical lesions of the ventral hippocampus and the amygdala failed to block CRH-enhanced startle. However, the same amygdala-lesioned animals showed a complete blockade of fear-potentiated startle, a conditioned fear response sensitive to manipulations of the amygdala. In contrast, BNST-lesioned rats had normal fear-potentiated startle. This indicates a double dissociation between the BNST and the amygdala in two different paradigms that enhance startle amplitude. Microinfusions of CRH into the BNST, but not into the ventral hippocampus, mimicked intracerebroventricular CRH effects. Furthermore, infusion of a CRH antagonist into the BNST blocked CRH-enhanced startle in a dose-dependent manner. Control studies showed that this blockade did not result from either leakage of the antagonist into the ventricular system or a local anesthetic effect caused by infusion of the antagonist into the BNST. The present studies strongly suggest that CRH in the CSF can activate the BNST, which could lead to activation of brainstem and hypothalamic BNST target areas involved in anxiety and stress responses. Key words: bed nucleus of the stria terminalis (BNST ); amygdala; hippocampus; corticotropin-releasing hormone (CRH); startle; anxiety; fearIntracerebroventricular inf usion of corticotropin-releasing hormone (CRH) elicits a constellation of behavioral, physiological, and endocrinological changes similar to those produced by natural stressors (cf. Dunn and Berridge, 1990). Thus far, however, the exact anatomical sites responsible for these behavioral and physiological actions of CRH after intracerebroventricular administration have not been identified. As part of an effort to delineate the neural circuitry underlying intracerebroventricular CRH effects, recently we investigated a possible involvement of the septum, using increased acoustic startle amplitude after CRH (CRH-enhanced startle) as a behavioral measure (Lee and Davis, 1997). Electrolytic lesions of the whole septum and the medial septum, but not the lateral septum, blocked CRH-enhanced startle. However, fiber-sparing chemical lesions of the medial septum failed to block CRH-enhanced startle, suggesting that the blockade seen with electrolytic lesions was probably caused by damage to fibers of passage, presumably the fornix. Supporting this conclusion, f unctional lesions of the fornix induced by knife cuts of the fimbria /fornix complete...

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“…(17,18,19) Although the PAG provides direct opioid modulation of spinal nociception, the amygdala also influences the activity of other brain stem nuclei including the raphe nuclei and LC that can alter the excitability of both supraspinal and spinal circuits. (17,18,20) The descending projections from the CeA to the brain stem that modulate sensory processing in the spinal cord produce neuronal hyperexcitability. Descending modulation of spinal nociceptive processing may be a mechanism for the GR and MR divergence seen in the present study since the effects of Corticosterone on spinal neuronal excitability were blocked by placing the MR antagonist spironolactone on the amygdala.…”

Section: Discussionmentioning

confidence: 99%

A study on the effect of Aldosterone antagonist on Nociception and anxiety in Swiss albino mice

Suresh¹

2012

iosrphr

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An aldosterone antagonist, used for the treatment of hypertension, edema, hyper-aldosteronism and also act as the antiinflammatory functions. Spironolactone is a steroid, easily available and marketed as a trade name aldactone. This drug is used for blocking aldosterone dependent sodium transport in the distal tubule of the kidney in order to reduce oedema and to treat essential hypertension and primary hyperaldosteronism. In this study aldosterone antagonist Spironolactone was administrated to find the effect of thermally induced pain, visceral pain and behavioral response in Swiss albino mice. The effects of spironolactone aldosterone antagonist, were examined on thermally-induced pain using the hot-plate and hot water tail immersion test (53-54°C). The visceral nociception was observed by intra-peritoneal acetic acid injection and the behavioral responses in the mice were examined by using open field behavioral model test. In hot plate test and hot water tail immersion test spironolactone significantly(0.01) reduces the pain threshold in dose dependent manner and increases the somatic pain, was as in visceral pain induced by acetic acid writhing spironolactone significantly(0.003) increases the pain threshold and decreases the visceral pain. In behavioral study spironolactone decrease the ambulation, rearing and grooming and significantly (0.01) increases immobilization time and urination. Spironolactone increased somatic pain in hot plate test and hot water tail immersion test and decreases visceral pain in writhing test. The spironolactone also altered the behavioral response in mice, such as increased immobilization and decreased ambulation.

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The organization of projections from the central nucleus of the amygdala to brainstem sites involved in central autonomic regulation: A combined retrograde transport-immunohistochemical study

Cited by 461 publications

References 76 publications

The central and basolateral nuclei of the amygdala exhibit opposite diurnal rhythms of expression of the clock protein Period2

The central and basolateral nuclei of the amygdala exhibit opposite diurnal rhythms of expression of the clock protein Period2

Role of the Hippocampus, the Bed Nucleus of the Stria Terminalis, and the Amygdala in the Excitatory Effect of Corticotropin-Releasing Hormone on the Acoustic Startle Reflex

A study on the effect of Aldosterone antagonist on Nociception and anxiety in Swiss albino mice

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