Physiological effects of electroconvulsive therapy and transcranial magnetic stimulation in major depression

Abstract

Major depressive episodes are associated with dysregulation of various physiologic systems. Antidepressant medications alter regulation of the hormonal and sleep systems. A thorough understanding of these changes may elucidate the pathophysiologic basis of the disorder [Amsterdam et al., 1989: Psychoneuroendocrinology 14:43–62], and interventions targeted directly at these systems are being increasingly recognized as possible treatments for depression [Wong et al., 2000: Proc Natl Acad Sci USA 97:325–330; Szuba et al., 1996: Proc Am Coll Neuropsychopharmacol Ann Meet]. These physiologic systems are regulated by the major neurotransmitters implicated in the etiology of mood disorders—norepinephrine, serotonin, and dopamine. Many of the hormones of import for this article also act as neurotransmitters and thus alter cerebral activity themselves [Owens and Nemeroff, 1993: Ciba Found Symp 172:296–308; Weitzner, 1998: Psychother Psychosom 67:125–132]. Parenteral infusion of hydrocortisone [DeBattista, 2000: Am J Psychiatry 157:1334–1337] and thyrotropin‐releasing hormone (TRH) [Prange et al., 1972: Lancet 2:999–1002; Marangell et al., 1997: Arch Gen Psychiatry 54:214–222; Szuba, 1996: Proc Am Coll Neuropsychopharmacol Ann Meet.] produce acute antidepressant effects. Antagonists to corticotropin‐releasing hormone and repeated parenteral infusion of TRH may have antidepressant activity when given during several weeks [Wong, 2000: Proc Natl Acad Sci USA 97:325–330; Arborelius et al., 1999: J Endocrinol 160:1–12; Callahan et al., 1997: Biol Psychiatry 41:264–272]. Manipulations of the sleep system through sleep deprivation can ameliorate depression [Szuba et al., 1994: Psychiatry Res 51:283–295; see Wirz‐Justice et al., 1999: Biol Psychiatry 46:445–453 for review]. Sleep deprivation has been shown in more than three dozen studies published in the last three decades to produce marked, acute antidepressant effects in the majority of depressed individuals [Wirz‐Justice, et al., 1999: Biol Psychiatry 46:445–453]. Thus, examination of the effects the two nonpharmacologic treatments, electroconvulsive therapy (ECT) and transcranial magnetic stimulation (TMS), produce in these physiologic systems may help elucidate their mechanisms of action, while enhancing understanding of the neurobiology of depressive illness. We will review these physiologic changes associated with depression, the effects that manipulations of these systems can have on depressive disorders, and then describe the effects the two techniques that can stimulate the human brain in vivo, ECT and TMS, exert on these systems. Depression and Anxiety 12:170–177, 2000. © 2000 Wiley‐Liss, Inc.

A role for galanin in antidepressant actions with a focus on the dorsal raphe nucleus

“…The length of each treatment was chosen to correlate with the onset of clinical benefit of each treatment and previous experience in the animal studies (26)(27)(28)(29). To further examine the contribution of altered galaninergic signaling to the FLX-mediated antidepressant-like effect, we tested whether a galanin receptor antagonist, M40, can block the antidepressant-like effect of chronic FLX treatment (10 mg͞kg i.p., 14 days) and whether a galanin receptor agonist, galnon, can exert an antidepressant-like effect in the rat forced swim test.…”

Pregnancy and depression: Exploring a new potential treatment option

“…In healthy individuals, neuroendocrine measurements have included cortisol, prolactin, follicular-stimulating hormone, and thyroid-stimulating hormone. Suprathreshold stimulation showed no deleterious or clinically signifi cant changes in levels of these hormones [45]. In depressed women, normalization of the dexamethasone suppression test with treatment has been demonstrated [46].…”

Translational Research in Late-Life Mood Disorders: Implications for Future Intervention and Prevention Research

“…The mechanism of action of interventions that are effective in treatment-resistant patients such as ECT should be further investigated. The neurobiological effects of such treatments remain poorly understood (Mann, 1998;Szuba et al, 2000). Mechanisms such as greater enhancements of monoaminergic function and increased trophic responses have been suggested to underlie the greater efficacy of ECT compared to antidepressant medications.…”