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Vascular depression, stress link examined by Heather Woolwine Public Relations This article is second in a series of four on the 2004 Update in Psychiatry. The psychiatric disorder known as depression is common throughout the United States, even given its many different manifestations and classifications.  K. Ranga Krishnan, M.D., chairman of the Department of Psychiatry and Behavioral Sciences at Duke University, outlined his discovery of a believed stress-induced type of depression that directly affects the cardiovascular health of the brain. “It is a little like the chicken or the egg,” Krishnan said during his presentation June 4 at the MUSC 2004 Update in Psychiatry—Vulnerability and Stress conference. “Epidemiological studies demonstrate that depression is a risk factor for the development of coronary artery disease and cerebrovascular disease and that depression following myocardial infarction or stroke also increases the risk of death and functional impairment. The data support that depression is a significant risk factor for morbidity and mortality following cardiovascular disease. The interesting new focus is that when depression originates later in life, it is related to silent cerebrovascular disease.” Krishnan first identified and described the then-little-known condition dubbed vascular depression in the late '90s. The condition is believed to result from small strokes in the mood centers of the brain, which may have a direct link to the way a person handles stress. The studies related to vascular depression exhibit through MRI’s the existence of the condition, which is more common in the basal ganglia and frontal lobes. Krishnan and his colleagues identified factors associated with vascular depression, including older age, hypertension, greater impairment in carrying out daily activities, and loss of energy. Some of the consequences of this type of depression in patients with vascular lesions are less response to treatment, longer recovery times, decreases in cognitive functioning and increased stroke risk. A point that Krishnan reiterated numerous times was that because of the connection between depression and cardiovascular health, psychiatrists were just as responsible for looking out for their patients’ cardiovascular health as they are for their mental health. “We’ve told primary care doctors, cardiologists, etc. to look for depression when treating patients,” he said. “We should also treat the whole patient and look for hypertension. We must certainly keep this in mind, especially since we know that for most patients with psychiatric disorders, we are the only physicians they see.” The Neurobiology of Social Attachment Thomas Insel, M.D., director of the National Institute of Mental Health, concluded the June 4 session with a discussion of his work on the neurobiology of attachment through animal models. A particular focus of his work examined the role of neuropeptides oxytocin and vasopressin in social attachment, like maternal behavior and pair bond formation. “We’re trying to take on the seemingly impossible task of understanding brain mechanisms for complex behavior, specifically social attachment,” Insel said. “This task becomes tractable because of two insights. First, there are many mammals besides humans that form long-term social attachments …  and the second is that a family of neuropeptides, including oxytocin and vasopressin seem to have an important role in social behavior across evolution.” Attachment requires several cognitive processes that link sensory and motor outputs, including attention, memory, social recognition, and motivation. In animals, proximity seeking, a social preference or a separation response demonstrates motivation. In humans, the ultimate form of motivation is experienced as “love.” “To study the neural basis of attachment, model systems with three features must be used,” Insel said. “First, we need to observe a clear onset of behavior to identify factors that initiate/inhibit the formation of attachment bonds; second, the attachment behavior must be selective and enduring; and third, we need to measure and manipulate these behaviors.” The two neuropeptides mentioned by Insel—demonstrated through his work with prairie voles, a monogamous rodent—seem to be critical for the development of a long-term social bond. Naturally, this occurs after voles mate, but Insel and his colleagues found that if either neuropeptide is given in the absence of mating, the voles will still bond. Con-versley, if the voles mate but the neuropeptides are blocked, then they fail to bond.  An interesting application of Insel’s data may be in the study of autism, a neurodevelopmental disorder characterized by a reduction in social behavior and abnormal social attachment. So far, there have been reports of reduced oxytocin in children with autism. “We do not know yet whether the autistic brain has an altered distribution of vasopressin or oxytocin receptors,” Insel said. “Nevertheless, a principle elucidated from the vole studies, that the confluence of oxytocin or vasopressin circuits with the brain’s reward pathways is critical for social attachment, deserves careful study in autism.” Insel concluded his presentation with the point that social neuroscience is a translational science with implications for clinical syndromes of abnormal social behavior. Friday, June 25, 2004 Catalyst Online is published weekly, updated as needed and improved from time to time by the MUSC Office of Public Relations for the faculty, employees and students of the Medical University of South Carolina. Catalyst Online editor, Kim Draughn, can be reached at 792-4107 or by email, catalyst@musc.edu. Editorial copy can be submitted to Catalyst Online and to The Catalyst in print by fax, 792-6723, or by email to petersnd@musc.edu or catalyst@musc.edu. To place an ad in The Catalyst hardcopy, call Community Press at 849-1778.