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Review
. 2017 Apr 1:172:49-59.
doi: 10.1016/j.physbeh.2016.10.015. Epub 2016 Oct 25.

Corticolimbic regulation of cardiovascular responses to stress

Brent Myers  1
Affiliations
Review

Corticolimbic regulation of cardiovascular responses to stress

Brent Myers. Physiol Behav. .

Abstract

Cardiovascular disease, a leading cause of death worldwide, is frequently initiated or exacerbated by stress. In fact, chronic stress exposure and heightened reactions to acute psychological stress are both associated with increased cardiovascular morbidity. This brief review focuses on the mechanisms by which corticolimbic nuclei, critical for stress appraisal and emotional reactivity, regulate heart rate and blood pressure responses to psychological stress. Both human and rodent data are examined with a major emphasis on basic studies investigating prefrontal cortex, amygdala, and hippocampus. A detailed literature review reveals substantial limitations in our understanding of this circuitry, as well as significant opportunities for future investigation that may ultimately reduce the burden of cardiovascular illness.

Keywords: Amygdala; Blood pressure; Heart rate; Hippocampus; Prefrontal cortex.

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Figures

Fig. 1
Fig. 1
Hypothesized anatomical pathways translating mPFC output into autonomic processes. Simplified direct connections are illustrated without indirect multisynaptic circuits. Glutamate outflow from the PL targets GABAergic neurons in the BST and both 5-HT and GABAergic cells in the raphe. These structures then provide direct input to preganglionic neurons of the parasympathetic and sympathetic nervous systems. The IL targets local GABAergic interneurons within the glutamatergic PH to gate stress responding. Additional glutamatergic IL efferents target the NTS, although the neurochemistry of these targets has yet to be determined. See text for references. PL: prelimbic cortex, BST: bed nucleus of the stria terminalis, DMV: dorsal motor nucleus of the vagus, NA: nucleus ambiguus, IML intermediolateral cell column, IL: infralimbic cortex, NTS: nucleus of the solitary tract, PH: posterior hypothalamus, Glu: glutamate, 5-HT: serotonin, ACh: acetylcholine.
Fig. 2
Fig. 2
Hypothesized anatomical pathways mediating BLA and MeA effects on autonomic outflow. Simplified direct connections are illustrated without indirect multisynaptic circuits. The BLA has limited interaction with cell groups providing direct input to preganglionic neurons; however, the region sends excitatory projections to GABAergic cells in the BST and CeA. The MeA sends predominantly GABAergic projections to the BST, mPOA, and PH, although the neurochemistry of post-synaptic targets has not been directly investigated. See text for references. BLA: basolateral amygdala, BST: bed nucleus of the stria terminalis, CeA: central amygdala, DMV: dorsal motor nucleus of the vagus, NA: nucleus ambiguus, IML intermediolateral cell column, MeA: medial amygdala, mPOA: medial preoptic area, PH: posterior hypothalamus, Glu: glutamate, ACh: acetylcholine.
Fig. 3
Fig. 3
Hypothesized anatomical pathways translating CeA output into cardiovascular stress responses. Simplified direct connections are illustrated without indirect multisynaptic circuits. The CeA provides abundant innervation of stress-regulatory centers, particularly in the brainstem, representing a major source of descending limbic outflow. These projections are predominantly GABAergic but also co-release peptides to target a diverse array of postsynaptic cell groups. Generally, the CeA targets the GABAergic BST and mPOA, the neurochemically diverse LHA, and key brainstem centers (PB, NTS, VLM, LC, Raphe). The precise functional outcomes of CeA inputs to these distinct regions remains to be determined. See text for references. CeA: central amygdala, BST: bed nucleus of the stria terminalis, mPOA: medial preoptic area, PB: parabrachial nuclei, NTS: nucleus of the solitary tract, LHA: lateral hypothalamic area, VLM: ventrolateral medulla, LC: locus coeruleus, DMV: dorsal motor nucleus of the vagus, NA: nucleus ambiguus, IML intermediolateral cell column, Glu: glutamate, 5-HT: serotonin, NE: norepinephrine, ACh: acetylcholine.
Fig. 4
Fig. 4
Hypothesized anatomical circuitry by which the ventral hippocampus (subiculum and CA1) mediates autonomic responses. Simplified direct connections are illustrated without indirect multisynaptic circuits. The glutamatergic outflow of the ventral hippocampus targets GABAergic cells in the BST and mPOA and diffusely innervates the neurochemically mixed LHA. To date, the functional effects of hippocampal outputs on cardiovascular stress responses have not been investigated. See text for references. Hipp: hippocampus, BST: bed nucleus of the stria terminalis, mPOA: medial preoptic area, LHA: lateral hypothalamic area, DMV: dorsal motor nucleus of the vagus, NA: nucleus ambiguus, IML intermediolateral cell column, Glu: glutamate, ACh: acetylcholine.
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