Noradrenergic and dopaminergic interrelation in schizophrenia

Brambilla, Frăncesca; Marini, Stefano; Saito, Anna; Fassone, Giovanni; Picardi, Angelo; Nerozzi, Dina; Pancheri, P.

doi:10.1016/0165-1781(94)90052-3

Cited by 9 publications

(6 citation statements)

References 39 publications

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“…Despite there is a trend towards blunting in SCHs, ΔGH APO values are not significantly different across patients and HCs. This latter result is in agreement with previous published reports ( 5 – 7 , 36 , 37 ) but not all ( 38 , 39 ). As previously discussed ( 8 ), the effect of APO on GH involves different pathways from those mediating ACTH/cortisol response, since this response requires the participation of GH-releasing-hormone (GHRH) neurons and acetylcholine, and other neurotransmitters/hormones such as NA, 5-HT, GABA, ghrelin, and cholecystokinin are probably involved in the GH response to APO.…”

Section: Discussionsupporting

confidence: 94%

“…Thus, the comparable ΔGH values found in depressed BDs and SADs suggest a possible biological link between these two diseases (i.e., NA dysregulation). In agreement with a previous study of our group ( 16 ), ΔGH CLO values in paranoid SCHs are not altered (suggesting normal sensitivity of hypothalamic α 2 -adrenoreceptors in these patients), although in disorganized SCHs it has been found greater CLO-induced GH responses ( 37 ) (suggesting hypersensitivity of α 2 -adrenoreceptors in these patients). However, this latter finding has not been replicated ( 16 ).…”

Section: Discussionsupporting

confidence: 92%

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Dopaminergic, Noradrenergic, Adrenal, and Thyroid Abnormalities in Psychotic and Affective Disorders

et al. 2020

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Background: 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. Method: We 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). Results: Compared to controls, paranoid schizophrenic patients showed (1) lower APOinduced ACTH and cortisol stimulation, and (2) higher post-dexamethasone cortisol values. Compared to controls, schizoaffective and bipolar patients showed (1) lower DDTSH 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. Conclusions: Although 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 DAD 2 receptors (possibly linked

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Section: Discussionsupporting

confidence: 94%

Section: Discussionsupporting

confidence: 92%

Dopaminergic, Noradrenergic, Adrenal, and Thyroid Abnormalities in Psychotic and Affective Disorders

et al. 2020

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“…Increased sensitivity of the HT2a-receptor and subsensitive alpha-2 receptors have been hypothesized to be contributory factors in schizophrenia (e.g. Brambilla et al, 1994). While these altered receptor states could underlie our results, our conclusions are limited by the absence of a suitable control for the binding of antipsychotic drugs to these receptors.…”

Section: Paranoid Vs Nonparanoid Diagnosesmentioning

confidence: 70%

Relations of clinical features, subgroups and medication to serum monoamines in schizophrenia

Oades¹,

Klimke

Henning

et al. 2002

Human Psychopharmacology

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“…Relatively lower anterior cingulate metabolism was noted in our better performing patients and the metabolic rates of these better-performing patients were identical to the normal control mean. Interestingly, a number of studies of schizophrenia and paranoid schizophrenia have found evidence of central noradrenergic abnormality (Brambilla et al 1994;Breier 1994;Farley et al 1978;Litman et al 1996;Van Kammen and Antelman 1984). Abnormalities in anterior cingulate metabolism may reflect relative inability to appropriately activate the noradrenergic system.…”

Section: Anterior Cingulate-incongruent Trial Error Linkagementioning

confidence: 99%

Anterior Cingulate Metabolism Correlates with Stroop Errors in Paranoid Schizophrenia Patients

Nordahl

Carter

Salo

et al. 2001

Neuropsychopharmacology

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Noradrenergic and dopaminergic interrelation in schizophrenia

Cited by 9 publications

References 39 publications

Dopaminergic, Noradrenergic, Adrenal, and Thyroid Abnormalities in Psychotic and Affective Disorders

Dopaminergic, Noradrenergic, Adrenal, and Thyroid Abnormalities in Psychotic and Affective Disorders

Relations of clinical features, subgroups and medication to serum monoamines in schizophrenia

Anterior Cingulate Metabolism Correlates with Stroop Errors in Paranoid Schizophrenia Patients

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