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Cotard’s syndrome (le délire de négation)
Published in David Enoch, Basant K. Puri, Hadrian Ball, Uncommon Psychiatric Syndromes, 2020
David Enoch, Basant K. Puri, Hadrian Ball
When the syndrome is linked to a chronic schizophrenic illness, as in Case 5, who suffered with nihilistic delusions for over 30 years, the prognosis is clearly much worse. However, in other schizophrenic patients where the onset is more acute, although the symptoms are bizarre and severe, there may well be a rapid improvement with the administration of neuroleptic drugs, as was the situation in our Case 6. Sulpiride has been successfully used to treat Cotard’s syndrome in schizophrenia (Shiraishi et al., 2004), while amongst third-generation antipsychotics, aripiprazole monotherapy has been reported to be successful (De Berardis et al., 2010). In some cases, therapeutic success may follow the combined use of an antidepressant and an antipsychotic drug; reported cases include the successful use of imipramine with risperidone (Machado et al., 2016) and escitalopram with aripiprazole (De Berardis et al., 2015).
Intestinal Pharmacomanometry: Evidence for Two Antagonistic Dopaminergic Mechanisms in the Human
Published in Fuad Lechin, Bertha van der Dijs, Neurochemistry and Clinical Disorders: Circuitry of Some Psychiatric and Psychosomatic Syndromes, 2020
Fuad Lechin, Bertha van der Dijs, Francisco Gomez, Marcel Lechin, Luis Arocha, Emilio Acosta
The effects of haloperidol and sulpiride were investigated in 2729 subjects. The effects of DA-releasing and DA-suppressing agents (D-amphetamine and clonazepam, respectively) were also investigated. Results have been reported in several published papers.6,32-35,103-105 Motility records were obtained during 3 to 4 h at both sigmoidal and rectal levels, according to previously established procedure.6,34,38,104-106 Both DA-blocking agents induced deep, long-lasting, and antagonist changes of distal colon motility in 78.7% of the subjects. It is noteworthy that biperiden (a central-acting anti-ACh drug) counteracted the sulpiride- but not the haloperidol- induced changes.
Prejunctional Dopamine Receptor Stimulants
Published in M.D. Francesco Amenta, Peripheral Dopamine Pathophysiology, 2019
The effects of quinpirole on heart rate differ from those of other DA2 receptor stimulants, and as with blood pressure, differ also from one model to another. Modest reductions occur in the dog and monkey, whereas in the conscious rat, heart rate increases. In the anesthetized rat, however, the compound produces profound bradycardia which is not influenced by vagotomy.186,190,191 This is difficult to reconcile with the proven lack of effect of quinpirole on prejunctional α2-adrenoceptors, and the belief that the rat lacks prejunctional dopamine receptors on sympathetic neurones supplying the cardiac pacemaker.6 Involvement of a central action is suggested by a study demonstrating that metoclopramide (a DA2 receptor antagonist which penetrates the brain) prevents the bradycardia, whereas the peripherally active antagonist, domperidone, does not.192 The situation is further complicated by the fact that sulpiride, which also does not readily enter the brain, causes substantial inhibition of the response.190,191 Quinpirole has been shown to inhibit ganglionic transmission, and to produce a significant reduction in cAMP levels in isolated stellate ganglia of the dog; both effects are attenuated selectively by S-sulpiride.198,200 the concentrations required to produce these effects, however, are high (i.e., from 5 × 10−6M), and it cannot be said with any certainty whether such an effect contributes significantly to the bradycardia observed in the rat following doses in the μg/kg range.
Effect of sulpiride on menopausal hot flashes: a randomized, double-blind, placebo-controlled clinical trial
Published in Gynecological Endocrinology, 2020
Clarissa Moreira Borba, Charles Francisco Ferreira, Fernanda Vargas Ferreira, Faustino R. Pérez-López, Maria Celeste Osório Wender
During the menopause transition, estrogen deficiency causes the loss of the gonadotropin-releasing hormone feedback and a hypertrophied kisspeptin-neurokinin B (NKB)-dynorphin (KNDy) signaling system in the hypothalamus [30,31]. This is where sulpiride may exert its effects on dopaminergic signaling. This effect would restore intracellular dopamine concentrations of dopamine. One should bear in mind that an imbalance in serum dopamine levels and increased dopamine availability in the CNS is also related to the onset of hot flashes [4]. Furthermore, sulpiride interacts with serotonin hypothalamic serotonin receptors in a similar manner as SSRIs and SNRIs do [15].
A novel nasal co-loaded loratadine and sulpiride nanoemulsion with improved downregulation of TNF-α, TGF-β and IL-1 in rabbit models of ovalbumin-induced allergic rhinitis
Published in Drug Delivery, 2021
Soad A. Mohamad, Mohamed A. Safwat, Mahmoud Elrehany, Sherif A. Maher, Ahmed M. Badawi, Heba F. Mansour
Sulpiride, an antipsychotic drug, is a selective dopamine receptor antagonist. It has high affinity to D2 and D4 receptors. It has been reported that sulpiride has an anti-inflammatory effect through increasing the intracellular cAMP level regardless the presence of dopamine signaling at D2 receptors (Brustolim et al., 2006). Based on this finding, it can be speculated that the drug can have a beneficial effect in the management of allergic rhinitis inflammatory manifestations. Sulpiride experiences a limited oral bioavailability not more than 27% due to its poor water solubility (Zidan et al., 2015).
Involvement of D2 receptor in the NAc in chronic unpredictable stress-induced depression-like behaviors
Published in Stress, 2020
Hui Qiao, Sha Yang, Chang Xu, Xin-Ming Ma, Shu-Cheng An
Dopamine D2 receptors (D2Rs) in the NAc are expressed not only in presynaptic neurons (D2autoreceptors), which exert negative feedback regulation on the synthesis and release of DA, but also in postsynaptic neurons and alter several intracellular downstream signaling pathways, including cAMP and Akt (Bonci & Hopf, 2005), to induce behavioral changes (Trifilieff et al., 2013). Previous clinical and preclinical studies have demonstrated that sensitization of D2Rs in the mesolimbic dopamine system may represent a ‘final common pathway’ in the antidepressant process (Willner, Hale, & Argyropoulos, 2005). Acute administration of D2R antagonists (sulpiride and raclopride) blocks the effect of several antidepressants (desipramine, imipramine, or amitriptyline) on depression-like behaviors (Gershon, Vishne, & Grunhaus, 2007). D2R agonists, such as pramipexole and aripiprazole, are effective in patients with depression who have failed to respond to previous medications (Choi et al., 2017; Hori & Kunugi, 2012). Another clinical study found that low-dose sulpiride (D2R antagonist) acts as an antidepressant (Ruther et al., 1999), but in antidepressant-treated patients, sulpiride caused a substantial reinstatement of depressed mood (Willner et al., 2005). Therefore, the effects of agonists and antagonists of D2Rs on depression are complicated. The paradox of these effects may be due to the complicated distribution and pre- and postsynaptic function of D2Rs, the diversity of the research techniques (Enman, Arthur, Ward, Perrine, & Unterwald, 2015; Maj, Papp, Skuza, Bigajska, & Zazula, 1989; Sim et al., 2013), the various agonists and antagonists (Choi et al., 2017; Hori & Kunugi, 2012), or the different stress protocols (D'Aquila, Peana, Carboni, & Serra, 2000). The role of D2Rs in CUS-induced depression-like behaviors is not completely clear. The aim of our study was to determine the effect of D2Rs on CUS-induced depression-like behaviors. Considering the structural plasticity found in the NAc after stress, our aim was to investigate the involvement of kalirin-7 in this process. Kalirin-7 is a key player in spine formation. In our previous studies, we found that CUS significantly reduce the expression of kalirin-7 in the hippocampus, and is closely related to stress-mediated alteration in the spine density (Qiao et al., 2014; Qiao, An, Xu, & Ma, 2017).