Abstract
BackgroundThis study aimed to assess hypothalamic-pituitary dopaminergic (DA), noradrenergic (NA), thyroid (HPT), and adrenal (HPA) activity in schizophrenia, in schizoaffective disorder, and in bipolar disorder.MethodWe investigated a combined approach of hormone responses to (1) apomorphine (APO), a short-acting DA receptor agonist which decreases prolactin secretion (PRL), and stimulates secretion of growth hormone (GH), adrenocorticotropin (ACTH), and cortisol; (2) clonidine (CLO), an alpha 2-adrenoceptor agonist which stimulates GH secretion; (3) 8 AM and 11 PM protirelin (TRH) which stimulates thyrotropin (TSH) secretion; and (4) dexamethasone which suppresses cortisol secretion, in 13 hospitalized healthy male controls and 39 untreated male inpatients: 13 with DSM-IV paranoid schizophrenia, 13 with DSM-IV schizoaffective disorder (bipolar subtype, depressed at the time of the study), and 13 with DSM-IV bipolar disorder (depressed).ResultsCompared to controls, paranoid schizophrenic patients showed (1) lower APO-induced ACTH and cortisol stimulation, and (2) higher post-dexamethasone cortisol values. Compared to controls, schizoaffective and bipolar patients showed (1) lower ΔΔTSH values (i.e., difference between 11 PM and 8 AM TRH-TSH responses), (2) lower APO-induced PRL suppression, (3) lower CLO-induced GH stimulation, and (4) higher post-dexamethasone cortisol values.ConclusionsAlthough results must be interpreted with caution because of the small sample, this preliminary study suggests that depressed bipolar and schizoaffective patients share common biological dysregulations, distinct from that of paranoid schizophrenic patients. From a pathophysiological viewpoint, paranoid schizophrenic patients can be characterized by hyposensitivity of the hypothalamic DA receptors (possibly resulting from an increase in presynaptic DA release) associated with increased HPA axis activity, while depressed bipolar and schizoaffective patients can be characterized by hyposensitivity of the pituitary TRH and DA-D2 receptors (possibly linked to the activation of the hypothalamic TRH and tuberoinfundibular DA neurons, respectively), together with subsensitive postsynaptic α2-adrenoreceptors at the hypothalamic level (possibly secondary to an erratic release of NA) and increased HPA axis activity.
Highlights
It is well established that the secretion of the hypothalamic hypophysiotropic hormones is controlled by neurotransmitters posited to play a preeminent role in the pathophysiology of major psychiatric disorders such as schizophrenia (SCH), schizoaffective disorder (SAD), and bipolar disorder (BD) [1, 2]
Compared with hospitalized control (HC), PRLS values were lower in SADs and BDs, while in
Results obtained from the morning thyrotropin-releasing hormone (TRH)-thyroid-stimulating hormone (TSH) challenge agree with those of previous published reports [for review, see [21]]
Summary
It is well established that the secretion of the hypothalamic hypophysiotropic hormones is controlled by neurotransmitters posited to play a preeminent role in the pathophysiology of major psychiatric disorders such as schizophrenia (SCH), schizoaffective disorder (SAD), and bipolar disorder (BD) [1, 2]. Some studies found lower APO induced-PRL suppression in depressed BDs compared to healthy controls and unipolar depressed patients [9, 12] It has been reported in patients with major unipolar depressive disorder with HPA axis overactivity and melancholic and psychotic features altered ACTH/cortisol and GH responses to APO [13]. These latter findings are in line with the hypothesis that hypercortisolemia by increasing DA release may induce a hyposensitivity of hypothalamic DA receptors [14]. This study aimed to assess hypothalamic-pituitary dopaminergic (DA), noradrenergic (NA), thyroid (HPT), and adrenal (HPA) activity in schizophrenia, in schizoaffective disorder, and in bipolar disorder
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