Identification of a cortical site for stress-induced cardiovascular dysfunction |
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Authors: | David F Cechetto PhD |
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Institution: | 1. Robarts Research Institute, 100 Perth Dr., P.O. Box 5015, N6A 5K8, London, Ontario, Canada
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Abstract: | The evidence indicating that the insular cortex is a likely candidate to mediate stress-induced cardiovascular responses is
reviewed. Both neuroanatomical and electrophysiological investigations demonstrate that the insular cortex receives an organized
representation of visceral information. In addition, the insular cortex also receives highly processed association cortex
information. The insular cortex is also highly interconnected with many subcortical limbic and autonomic regions. This combination
of sensory input and limbic/autonomic connectivity would be necessary to permit the insular cortex to be a critical site for
the integration of emotional and autonomic responses. Stimulation of the insular cortex elicits specific cardiovascular and
autonomic responses from discrete sites. Phasic stimulation entrained to the cardiac cycle is even capable of causing severe
arrhythmias. The efferent pathways and some of the neurotransmitter mechanisms have determined. It appears that the lateral
hypothalamic area is the primary site of synapse for autonomic responses originating in the insular cortex and this information
is relayed by NMDA glutamatergic receptors and modulated by neuropeptides including neuropeptide Y, neurotensin, leu-enkephalin
and dynorphin. Finally, a rat stroke model, which includes the insular cortex in the infarct region indicates that disruption
of the insula can produce substantial cardiac and autonomic abnormalities, which might be similar to those produced by stress.
Some of the chronic neurochemical changes, including increases in opioids, neuropeptide Y and neurotensin in the central nucleus
of the amygdala, which might be mediating these cardiovascular disturbances, have been determined. |
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