Units in the amygdala responding to activation of carotid baro- and chemoreceptors

Cechetto, David F.; Calaresu, F. R.

doi:10.1152/ajpregu.1984.246.5.r832

Cited by 19 publications

(10 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Walker et al . (1953) and Weiskrant (1956) have shown that the amygdaloid complex plays an essential role in the genesis of emotions: (i) amygdalectomy results in several behavioural effects, including tameness, hypoemotionality, psychic blindness and changes in feeding and sexual behaviour referred as the Klüver–Bucy syndrome; (ii) amygaloid neurons are more sensitive to sensory events with biological and/or emotional significance (aversive or rewarding stimuli, faces); (iii) stimulation of the amygdala produces general arousal with a number of autonomic and behavioural defensive or aggressive responses [see review in Ledoux (1992)]. The amygdala appears to be involved in processing of aversive emotion.…”

Section: Discussionmentioning

confidence: 99%

Projections from the nociceptive area of the central nucleus of the amygdala to the forebrain: a PHA‐L study in the rat

Bourgeais

Gauriau

Bernard

2001

Eur J of Neuroscience

135

View full text Add to dashboard Cite

The lateral capsular division (CeLC) of the central nucleus (Ce) of the amygdala, in the rat, has been shown to be the main terminal area of a spino(trigemino)-parabrachio-amygdaloid nociceptive pathway [Bernard & Besson (1990) J. Neurophysiol. 63, 473-490; Bernard et al. (1992) J. Neurophysiol. 68, 551-569; Bernard et al. (1993) J. Comp. Neurol. 329, 201-229]. The projections to the forebrain from the CeLC and adjacent regions were studied in the rat by using microinjections of Phaseolus vulgaris leucoagglutinin (PHA-L) restricted in subdivisions of the Ce and the basolateral amygdaloid nucleus anterior (BLA). Our data showed that the entire CeLC projects primarily and extensively to the substantia innominata dorsalis (SId). The terminal labelling is especially dense in the caudal aspect of the SId. The other projections of the CeLC in the forebrain were dramatically less dense. They terminate in the bed nucleus of the stria terminalis (BST) and the posterior hypothalamus (pLH). No (or only scarce) other projections were found in the remaining forebrain areas. The Ce lateral division (CeL) and the Ce medial division (CeM), adjacent to the CeLC, also project to the SId with slightly lower density labelling. However, contrary to the case of the CeLC, both the CeL and the CeM extensively project to the ventrolateral subnucleus of the BST (BSTvl) with a few additional terminals found in other regions of the lateral BST. Only the CeM projects densely to both the interstitial nucleus of the posterior limb of the anterior commissure and the caudal most portion of the pLH. The projections of the BLA are totally different from those of the Ce as they terminate in the dorsal striatum, the accumbens nucleus, the olfactory tubercle, the nucleus of olfactory tract and the rostral pole of the cingulate/frontal cortex. This study demonstrates that the major output of the nociceptive spino(trigemino)-parabrachio-CeLC pathway is to the SId. It is suggested that the CeLC-SId pathway could have an important role in anxiety, aversion and genesis of fear in response to noxious stimuli.

show abstract

Section: Discussionmentioning

confidence: 99%

Projections from the nociceptive area of the central nucleus of the amygdala to the forebrain: a PHA‐L study in the rat

Bourgeais

Gauriau

Bernard

2001

Eur J of Neuroscience

135

View full text Add to dashboard Cite

show abstract

“…Bilateral lesions of the amygdala inhibit the response of corticosterone to several stimuli [6, 7, 8]with recent studies implicating the medial [9]and central [9, 10, 11]amygdaloid nuclei specifically. The central nucleus has also been shown to contain neurons that respond to cardiovascular inputs [12, 13, 14]and to project to several brain areas [15, 16, 17, 18]that influence the release of ACTH [19, 20, 21, 22]. …”

Section: Introductionmentioning

confidence: 99%

Potentiated Response of Corticotropin (ACTH) to Repeated Moderate Hemorrhage Requires Amygdalar Neuronal Processing<footref rid="foot01"><sup>1</sup></footref>

2000

View full text Add to dashboard Cite

We examined the role of the amygdala in the potentiation of the corticotropin (ACTH) response to a 10 mg/kg hemorrhage by a 1-hour episode of equivalent hypovolemia done 24 h earlier. Unanesthetized rats were studied on the fourth (D1) and fifth (D2) day after chronic implantation of arterial and venous catheters. Immunocytochemistry for Fos protein indicated that neurons in the central and medial nuclei of the caudal amygdala were activated by hemorrhage. We then tested the effect of excitotoxic destruction of the neurons in these areas by bilateral injections of ibotenic acid 10 days prior to catheter placement. In rats that were hemorrhaged on both D1 and D2, the responses of ACTH and corticosterone increased significantly from the first (H1) to the second hemorrhage (H2) in a control group injected with saline (p < 0.05) and in lesioned groups without bilateral damage of the Fos-responsive areas (p < 0.01). In the group with bilateral damage to these sites, the responses to H1 and H2 did not differ. Additional rats had H1 on D2 to control for the long-term effects of the chronic cannulation. The responses of ACTH to H1 on either D1 or D2 did not differ between the saline-injected controls and any of the lesioned groups. In contrast, the response of ACTH to H2 on D2 in rats with bilateral damage of the caudal amygdala was not significant and was less than the response of ACTH to H2 in both rats with unilateral damage of this area (p < 0.05) and those injected with saline (p < 0.05). We conclude that bilateral neuronal processing within the caudal amygdala is required for the potentiation of the response of ACTH to H2 by H1.

show abstract

“…A major system involving cardiovascular regulation is the neuronal network that encompasses the baroreflex including peripheral receptors in the cardiac chambers, aorta and carotid sinus, medullary relay nuclei, and the efferent signals to the heart and vasculature. In addition, specific cortical regions associated with baroreceptor‐mediated cardiovascular function include the insular cortex (Butcher & Cechetto, 1995; Zhang et al 1999), anterior cingulate cortex (ACC) (Terreberry & Neafsey, 1987; Verberne & Owens, 1998), amygdala (Cechetto & Calaresu, 1983, 1984, 1985; Gelsema et al 1989) and the cerebellum (Bradley et al 1987 b ; Nisimaru et al 1998). There have been a limited number of cortical stimulation experiments performed in humans.…”

mentioning

confidence: 99%

Cortical regions associated with autonomic cardiovascular regulation during lower body negative pressure in humans

Kimmerly¹,

O’Leary²,

Menon³

et al. 2005

The Journal of Physiology

200

160

View full text Add to dashboard Cite

The purpose of the present study was to determine the cortical structures involved with integrated baroreceptor-mediated modulation of autonomic cardiovascular function in conscious humans independent of changes in arterial blood pressure. We assessed the brain regions associated with lower body negative pressure (LBNP)-induced baroreflex control using functional magnetic resonance imaging with blood oxygen level-dependent (BOLD) contrast in eight healthy male volunteer subjects. The levels of LBNP administered were 5, 15 and 35 mmHg. Heart rate (HR; representing the cardiovascular response) and LBNP (representing the baroreceptor activation level) were simultaneously monitored during the scanning period. In addition, estimated central venous pressure (CVP), arterial blood pressure (ABP) and muscle sympathetic nerve activity were recorded on a separate session. Random effects analyses (SPM2) were used to evaluate significant (P < 0.05) BOLD signal changes that correlated separately with both LBNP and HR (15-and 35-mmHg versus 5-mmHg LBNP). Compared to baseline, steady-state LBNP at 15 and 35 mmHg decreased CVP (from 7 ± 1 to 5 ± 1 and 4 ± 1 mmHg, respectively) and increased MSNA (from 12 ± 1 to 23 ± 3 and 36 ± 4 bursts min −1 , respectively, both P < 0.05 versus baseline). Furthermore, steady-state LBNP elevated HR from 54 ± 2 beats min −1 at baseline to 64 ± 2 beats min −1 at 35-mmHg suction. Both mean arterial and pulse pressure were not different between rest and any level of LBNP. Cortical regions demonstrating increased activity that correlated with higher HR and greater LBNP included the right superior posterior insula, frontoparietal cortex and the left cerebellum. Conversely, using the identical statistical paradigm, bilateral anterior insular cortices, the right anterior cingulate, orbitofrontal cortex, amygdala, midbrain and mediodorsal nucleus of the thalamus showed decreased neural activation. These data corroborate previous investigations highlighting the involved roles of the insula, anterior cingulate cortex and amygdala in central autonomic cardiovascular control. In addition, we have provided the first evidence for the identification of the cortical network involved specifically with baroreflex-mediated autonomic cardiovascular function in conscious humans.

show abstract

Units in the amygdala responding to activation of carotid baro- and chemoreceptors

Cited by 19 publications

References 0 publications

Projections from the nociceptive area of the central nucleus of the amygdala to the forebrain: a PHA‐L study in the rat

Projections from the nociceptive area of the central nucleus of the amygdala to the forebrain: a PHA‐L study in the rat

Potentiated Response of Corticotropin (ACTH) to Repeated Moderate Hemorrhage Requires Amygdalar Neuronal Processing<footref rid="foot01"><sup>1</sup></footref>

Cortical regions associated with autonomic cardiovascular regulation during lower body negative pressure in humans

Contact Info

Product

Resources

About