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Birte Glenthøj - One of the best experts on this subject based on the ideXlab platform.

  • effects of blocking d2 d3 receptors on mismatch negativity and p3a amplitude of initially antipsychotic naive first episode schizophrenia patients
    The International Journal of Neuropsychopharmacology, 2016
    Co-Authors: Signe During, Bob Oranje, Birte Glenthøj
    Abstract:

    Background: Reduced mismatch negativity and P3a amplitude have been suggested to be among the core deficits in schizophrenia since the late 1970s. Blockade of dopamine D2 receptors play an important role in the treatment of schizophrenia. In addition, there is some evidence indicating that deficits in mismatch negativity and P3a amplitude are related to increased dopaminergic activity. This is the first study investigating the effect of Amisulpride, a potent D2-antagonist, on mismatch negativity and P3a amplitude in a large group of antipsychotic-naive, first-episode schizophrenia patients. Methods: Fifty-one antipsychotic-naive, first-episode schizophrenia patients were tested in a mismatch negativity paradigm at baseline and after 6 weeks of treatment with Amisulpride. We further examined 48 age- and gender-matched controls in this paradigm. Results: At baseline, the patients showed significantly reduced P3a amplitude compared with healthy controls, but no differences in mismatch negativity. Although the treatment with Amisulpride significantly improved the patients’ psychopathological (PANSS) and functional (GAF) scores, it did not influence their mismatch negativity amplitude, while also their reduced P3a amplitude persisted. Conclusion: Our findings show that antipsychotic naive, first-episode patients with schizophrenia have normal mismatch negativity yet reduced P3a amplitude compared with healthy controls. In spite of the fact that the 6-week Amisulpride treatment improved the patients both clinically and functionally, it had no effect on either mismatch negativity or P3a amplitude. This suggests that even though there is a dopaminergic involvement in global functioning and symptomatology in schizophrenia, there is no such involvement in these particular measures of early information processing.

  • frontal fasciculi and psychotic symptoms in antipsychotic naive patients with schizophrenia before and after 6 weeks of selective dopamine d2 3 receptor blockade
    Journal of Psychiatry & Neuroscience, 2016
    Co-Authors: Bjorn H Ebdrup, Jayachandra Mitta Raghava, Mette Odegaard Nielsen, Egill Rostrup, Birte Glenthøj
    Abstract:

    BACKGROUND Psychotic symptoms are core clinical features of schizophrenia. We tested recent hypotheses proposing that psychotic, or positive, symptoms stem from irregularities in long-range white matter tracts projecting into the frontal cortex, and we predicted that selective dopamine D2/3 receptor blockade would restore white matter. METHODS Between December 2008 and July 2011, antipsychotic-naive patients with first-episode schizophrenia and matched healthy controls underwent baseline examination with 3 T MRI diffusion tensor imaging and clinical assessments. We assessed group differences of fractional anisotropy (FA) using voxelwise tract-based spatial statistics (TBSS) and anatomic region of interest (ROI)-based analyses. Subsequently, patients underwent 6 weeks of antipsychotic monotherapy with Amisulpride. We repeated the examinations after 6 weeks. RESULTS We included 38 patients with first-episode schizophrenia and 38 controls in our analysis, and 28 individuals in each group completed the study. At baseline, whole brain TBSS analyses revealed lower FA in patients in the right anterior thalamic radiation (ATR), right cingulum, right inferior longitudinal fasciculus and right corticospinal tract (CT). Fractional anisotropy in the right ATR correlated with positive symptoms (z = 2.64, p= 0.008). The ROI analyses showed significant associations between positive symptoms and FA of the frontal fasciculi, specifically the right arcuate fasciculus (z = 2.83, p= 0.005) and right superior longitudinal fasciculus (z = -3.31, p= 0.001). At re-examination, all correlations between positive symptoms and frontal fasciculi had resolved. Fractional anisotropy in the ATR increased more in patients than in controls (z = -4.92, p< 0.001). The Amisulpride dose correlated positively with FA changes in the right CT (t= 2.52, p= 0.019). LIMITATIONS Smoking and a previous diagnosis of substance abuse were potential confounders. Long-term effects of Amisulpride on white matter were not evaluated. CONCLUSION Antipsychotic-naive patients with schizophrenia displayed subtle deficits in white matter, and psychotic symptoms appeared specifically associated with frontal fasciculi integrity. Six weeks of Amisulpride treatment normalized white matter. Potential remyelinating effects of dopamine D2/3 receptor antagonism warrant further clarification.

  • striatal reward activity and antipsychotic associated weight change in patients with schizophrenia undergoing initial treatment
    JAMA Psychiatry, 2016
    Co-Authors: Mette Odegaard Nielsen, Birte Glenthøj, Egill Rostrup, Sanne Wulff, Bjorn H Ebdrup
    Abstract:

    Importance Weight gain is a common and serious adverse effect of antipsychotic treatment. A variable individual predisposition to development of metabolic disturbances calls for predictive biological markers. Objectives To investigate whether attenuated striatal activity during reward anticipation is associated with Amisulpride-induced weight change in antipsychotic-naive patients with schizophrenia undergoing initial treatment and to examine the association between weight change and changes in reward anticipation activity after treatment. Design, Setting, and Participants Sixty-nine antipsychotic-naive inpatients and outpatients with schizophrenia were included in a multimodal longitudinal cohort study from December 16, 2008, to December 11, 2013. Fifty-eight patients underwent functional magnetic resonance imaging (fMRI) while performing a monetary reward task. After 6 weeks of treatment with Amisulpride, a relatively selective dopamine D 2 antagonist, 39 patients underwent a second fMRI scan and measurement of change in body weight. Final follow-up was completed on January 14, 2014, and data were analyzed from October 25, 2014, to June 15, 2015 and August 31 to September 19, 2015. Exposures Six weeks of individually dosed Amisulpride treatment. Main Outcomes and Measures Reward-anticipation activity in the striatum before and after treatment and weight change. Results Of the 69 patients who consented to the study, 39 underwent the follow-up fMRI and weight measurement (age range, 18-45 years; 17 women and 22 men). The mean (SD) daily dose of Amisulpride was 272 (168; range, 50-800) mg, and patients gained a mean (SD) of 2.3 (2.8; range, −4 to 8) kg in body weight. Improvement from baseline to follow-up was found on the mean (SD) positive (19.9 [4.1] to 14.3 [3.8]), general (39.7 [7.7] to 30.5 [7.7]), and total (78.5 [15.3] to 63.2 [13.9]) scores on the Positive and Negative Syndrome Scale ( P F 35,3  = 5.64; P  = .003). After 6 weeks, weight gain was associated with an increase in mean (SD) reward activity in the same region during treatment (0.28 [0.74]; F 37,1  = 4.48; P  = .04). Conclusions and Relevance Activity in striatal regions of the reward system appears to be associated with the individual variability in the predisposition for antipsychotic-associated weight gain. Moreover, pharmacologic modulation of the reward system may play a role in antipsychotic-associated weight gain.

  • effects of dopamine d2 d3 blockade on human sensory and sensorimotor gating in initially antipsychotic naive first episode schizophrenia patients
    Neuropsychopharmacology, 2014
    Co-Authors: Signe During, Bob Oranje, Birte Glenthøj, Gitte Saltoft Andersen
    Abstract:

    It has been suggested that psychophysiological measures of sensory and sensorimotor gating, P50 gating and prepulse inhibition of the startle reflex (PPI), underlie core features of schizophrenia and are linked to dopaminergic pathways in the striatum and prefrontal cortex. In the present study, the effects of a potent D2/D3 receptor antagonist, Amisulpride, were investigated on PPI and P50 gating in a large sample of antipsychotic-naive, first-episode patients with schizophrenia. A total of 52 initially antipsychotic-naive, first-episode schizophrenia patients were assessed for their P50 gating, PPI, and habituation/sensitization abilities at baseline and after 2 and 6 weeks of treatment with flexible doses of Amisulpride. In addition, 47 matched healthy controls were assessed at baseline and after 6 weeks. At baseline, the patients showed significantly reduced PPI, yet normal levels of P50 gating, habituation, and sensitization. Treatment with Amisulpride showed no effects on these measures, either at 2 or 6 weeks of follow-up. This is the first study investigating the effects of monotherapy with a relatively selective dopamine D2/D3 receptor antagonist (Amisulpride) on sensory and sensorimotor gating deficits in a longitudinal study of a large group of initially antipsychotic-naive, first-episode patients with schizophrenia. Our finding that Amisulpride effectively reduced symptom severity in our patients without reducing their PPI deficits indicates that increased activity of dopamine D2 receptors may be involved in symptomatology of patients with schizophrenia, but not in their sensorimotor gating deficits.

Bob Oranje - One of the best experts on this subject based on the ideXlab platform.

  • effects of blocking d2 d3 receptors on mismatch negativity and p3a amplitude of initially antipsychotic naive first episode schizophrenia patients
    The International Journal of Neuropsychopharmacology, 2016
    Co-Authors: Signe During, Bob Oranje, Birte Glenthøj
    Abstract:

    Background: Reduced mismatch negativity and P3a amplitude have been suggested to be among the core deficits in schizophrenia since the late 1970s. Blockade of dopamine D2 receptors play an important role in the treatment of schizophrenia. In addition, there is some evidence indicating that deficits in mismatch negativity and P3a amplitude are related to increased dopaminergic activity. This is the first study investigating the effect of Amisulpride, a potent D2-antagonist, on mismatch negativity and P3a amplitude in a large group of antipsychotic-naive, first-episode schizophrenia patients. Methods: Fifty-one antipsychotic-naive, first-episode schizophrenia patients were tested in a mismatch negativity paradigm at baseline and after 6 weeks of treatment with Amisulpride. We further examined 48 age- and gender-matched controls in this paradigm. Results: At baseline, the patients showed significantly reduced P3a amplitude compared with healthy controls, but no differences in mismatch negativity. Although the treatment with Amisulpride significantly improved the patients’ psychopathological (PANSS) and functional (GAF) scores, it did not influence their mismatch negativity amplitude, while also their reduced P3a amplitude persisted. Conclusion: Our findings show that antipsychotic naive, first-episode patients with schizophrenia have normal mismatch negativity yet reduced P3a amplitude compared with healthy controls. In spite of the fact that the 6-week Amisulpride treatment improved the patients both clinically and functionally, it had no effect on either mismatch negativity or P3a amplitude. This suggests that even though there is a dopaminergic involvement in global functioning and symptomatology in schizophrenia, there is no such involvement in these particular measures of early information processing.

  • effects of dopamine d2 d3 blockade on human sensory and sensorimotor gating in initially antipsychotic naive first episode schizophrenia patients
    Neuropsychopharmacology, 2014
    Co-Authors: Signe During, Bob Oranje, Birte Glenthøj, Gitte Saltoft Andersen
    Abstract:

    It has been suggested that psychophysiological measures of sensory and sensorimotor gating, P50 gating and prepulse inhibition of the startle reflex (PPI), underlie core features of schizophrenia and are linked to dopaminergic pathways in the striatum and prefrontal cortex. In the present study, the effects of a potent D2/D3 receptor antagonist, Amisulpride, were investigated on PPI and P50 gating in a large sample of antipsychotic-naive, first-episode patients with schizophrenia. A total of 52 initially antipsychotic-naive, first-episode schizophrenia patients were assessed for their P50 gating, PPI, and habituation/sensitization abilities at baseline and after 2 and 6 weeks of treatment with flexible doses of Amisulpride. In addition, 47 matched healthy controls were assessed at baseline and after 6 weeks. At baseline, the patients showed significantly reduced PPI, yet normal levels of P50 gating, habituation, and sensitization. Treatment with Amisulpride showed no effects on these measures, either at 2 or 6 weeks of follow-up. This is the first study investigating the effects of monotherapy with a relatively selective dopamine D2/D3 receptor antagonist (Amisulpride) on sensory and sensorimotor gating deficits in a longitudinal study of a large group of initially antipsychotic-naive, first-episode patients with schizophrenia. Our finding that Amisulpride effectively reduced symptom severity in our patients without reducing their PPI deficits indicates that increased activity of dopamine D2 receptors may be involved in symptomatology of patients with schizophrenia, but not in their sensorimotor gating deficits.

B Scatton - One of the best experts on this subject based on the ideXlab platform.

  • psychopharmacological profile of Amisulpride an antipsychotic drug with presynaptic d2 d3 dopamine receptor antagonist activity and limbic selectivity
    Journal of Pharmacology and Experimental Therapeutics, 1997
    Co-Authors: Gh Perrault, R Depoortere, E Morel, D J Sanger, B Scatton
    Abstract:

    Amisulpride, a benzamide derivative, is an antipsychotic drug with a pharmacological profile distinct from that of classical neuroleptics such as haloperidol and from that of another benzamide, remoxipride. In mice, Amisulpride antagonized hypothermia induced by apomorphine, quinpirole or (+/-) 7-hydroxy-2-(di-n-propylamino)-tetralin, an effect involving D2/D3 receptors, at similar doses (ED50 approximately 2 mg/kg i.p.), which were much lower than doses that blocked apomorphine-induced climbing, an effect involving postsynaptic D2 and D1 receptor activation (ED50 = 21 mg/kg i.p.). Much higher doses (ED50 = 54 mg/kg i.p.) of Amisulpride were needed to block grooming behavior observed after a short period in water, a D1 receptor-mediated behavior. In rats, Amisulpride preferentially inhibited effects produced by low doses of apomorphine (hypomotility and yawning), related to stimulation of presynaptic D2/D3 dopamine autoreceptors (ED50 = 0.3 and 0.19 mg/kg i.p.). By contrast, Amisulpride antagonized apomorphine-induced hypermotility, a postsynaptic dopamine receptor-mediated effect, at a much higher dose (ED50 = 30 mg/kg i.p.). Amisulpride (100 mg/kg i.p.) only partially inhibited apomorphine-induced stereotypies (gnawing) and had no effect on stereotypies induced by d-amphetamine. However, d-amphetamine-induced hyperactivity was antagonized by doses of Amisulpride as low as 3 mg/kg i.p., which may indicate selectivity of this drug for limbic dopaminergic mechanisms. In addition, in contrast to haloperidol or remoxipride, which produced catalepsy at doses 2 or 3 times higher than those that antagonized stereotypies induced by apomorphine, Amisulpride did not induce catalepsy up to a dose of 100 mg/kg i.p., which occupies 80% of striatal D2 receptors. This pharmacological profile of Amisulpride, characterized by a preferential blockade of effects involving presynaptic mechanisms and limbic structures, may explain the clinical efficacy of this drug against both negative and positive symptoms of schizophrenia and its low propensity to produce extrapyramidal side effects.

  • psychopharmacological profile of Amisulpride an antipsychotic drug with presynaptic d2 d3 dopamine receptor antagonist activity and limbic selectivity
    Journal of Pharmacology and Experimental Therapeutics, 1997
    Co-Authors: Gh Perrault, R Depoortere, E Morel, D J Sanger, B Scatton
    Abstract:

    Amisulpride, a benzamide derivative, is an antipsychotic drug with a pharmacological profile distinct from that of classical neuroleptics such as haloperidol and from that of another benzamide, remoxipride. In mice, Amisulpride antagonized hypothermia induced by apomorphine, quinpirole or (±) 7-hydroxy-2-(di- n -propylamino)-tetralin, an effect involving D 2 /D 3 receptors, at similar doses (ED 50 ∼ 2 mg/kg i.p.), which were much lower than doses that blocked apomorphine-induced climbing, an effect involving postsynaptic D 2 and D 1 receptor activation (ED 50 = 21 mg/kg i.p.). Much higher doses (ED 50 = 54 mg/kg i.p.) of Amisulpride were needed to block grooming behavior observed after a short period in water, a D 1 receptor-mediated behavior. In rats, Amisulpride preferentially inhibited effects produced by low doses of apomorphine (hypomotility and yawning), related to stimulation of presynaptic D 2 /D 3 dopamine autoreceptors (ED 50 = 0.3 and 0.19 mg/kg i.p.). By contrast, Amisulpride antagonized apomorphine-induced hypermotility, a postsynaptic dopamine receptor-mediated effect, at a much higher dose (ED 50 = 30 mg/kg i.p.). Amisulpride (100 mg/kg i.p.) only partially inhibited apomorphine-induced stereotypies (gnawing) and had no effect on stereotypies induced by d-amphetamine. However, d-amphetamine-induced hyperactivity was antagonized by doses of Amisulpride as low as 3 mg/kg i.p., which may indicate selectivity of this drug for limbic dopaminergic mechanisms. In addition, in contrast to haloperidol or remoxipride, which produced catalepsy at doses 2 or 3 times higher than those that antagonized stereotypies induced by apomorphine, Amisulpride did not induce catalepsy up to a dose of 100 mg/kg i.p., which occupies 80% of striatal D 2 receptors. This pharmacological profile of Amisulpride, characterized by a preferential blockade of effects involving presynaptic mechanisms and limbic structures, may explain the clinical efficacy of this drug against both negative and positive symptoms of schizophrenia and its low propensity to produce extrapyramidal side effects.

Boris B Quednow - One of the best experts on this subject based on the ideXlab platform.

  • dopamine d2 3 and μ opioid receptor antagonists reduce cue induced responding and reward impulsivity in humans
    Translational Psychiatry, 2016
    Co-Authors: Susanna C Weber, Boris B Quednow, B Beckschimmer, Me Kajdi, Daniel Muller, Philippe N Tobler
    Abstract:

    Increased responding to drug-associated stimuli (cue reactivity) and an inability to tolerate delayed gratification (reward impulsivity) have been implicated in the development and maintenance of drug addiction. Whereas data from animal studies suggest that both the dopamine and opioid system are involved in these two reward-related processes, their role in humans is less clear. Moreover, dopaminergic and opioidergic drugs have not been directly compared with regard to these functions, even though a deeper understanding of the underlying mechanisms might inform the development of specific treatments for elevated cue reactivity and reward impulsivity. In a randomized, double-blind, between-subject design we administered the selective dopamine D2/D3 receptor antagonist Amisulpride (400 mg, n=41), the unspecific opioid receptor antagonist naltrexone (50 mg, n=40) or placebo (n=40) to healthy humans and measured cue-induced responding with a Pavlovian-instrumental transfer task and reward impulsivity with a delay discounting task. Mood was assessed using a visual analogue scale. Compared with placebo, Amisulpride significantly suppressed cue-induced responding and reward impulsivity. The effects of naltrexone were similar, although less pronounced. Both Amisulpride and naltrexone decreased average mood ratings compared with placebo. Our results demonstrate that a selective blockade of dopamine D2/D3 receptors reduces cue-induced responding and reward impulsivity in healthy humans. Antagonizing μ-opioid receptors has similar effects for cue-induced responding and to a lesser extent for reward impulsivity.

  • sensorimotor gating and habituation of the startle response in schizophrenic patients randomly treated with Amisulpride or olanzapine
    Biological Psychiatry, 2006
    Co-Authors: Boris B Quednow, Michael Wagner, Jens Westheide, Wolfgang Maier, Katrin Beckmann, Niclaas Bliesener, Kai-uwe Kühn
    Abstract:

    Background Schizophrenic patients exhibit impairments in prepulse inhibition (PPI) and habituation of the acoustic startle response (ASR). Recent studies suggested that PPI deficits and habituation deficits are normalized after antipsychotic treatment. Despite clear evidence of gating and habituation mechanisms in animal models, it is still unknown which neurotransmitter systems are involved in schizophrenic patients. Thus, we compared the effects of a combined 5-HT 2A /D 2 and a pure D 2 /D 3 antagonist on PPI and habituation of ASR in patients with schizophrenia. Methods The ASR was measured in 37 acute schizophrenic patients who were randomized and double-blinded as to treatment with Amisulpride or olanzapine. Patients were assessed during the first week and after four and eight weeks of treatment. Twenty healthy matched control subjects were examined likewise. Results Schizophrenic patients showed a significant PPI deficit and significantly decreased startle amplitude at baseline. The gating deficit disappeared after antipsychotic treatment in both treatment groups. Amisulpride sensitized the startle amplitude, whereas startle amplitude was not changed by olanzapine. After correcting for startle amplitude, patients did not show a habituation deficit; however, Amisulpride accelerated habituation, whereas olanzapine had no effect. Conclusions Our findings suggest that the PPI-restoring effect of antipsychotics is probably attributed to a dopamine D 2 receptor blockade.

  • cognitive improvement in schizophrenic patients does not require a serotonergic mechanism randomized controlled trial of olanzapine vs Amisulpride
    Neuropsychopharmacology, 2005
    Co-Authors: Michael Wagner, Boris B Quednow, Jens Westheide, Thomas E Schlaepfer, Wolfgang Maier, K U Kuhn
    Abstract:

    Combined serotonin-2A (5-HT2A) and dopamine-2 (D2) receptor blockade has been proposed as a candidate mechanism by which second-generation antipsychotics (SGAs) improve both cognition and negative symptoms in schizophrenic patients, in contrast to antipsychotics of the first generation. The SGA Amisulpride, however, only binds to D2/D3 receptors, which makes it an interesting tool to test this assumption. In a randomized controlled trial, 52 schizophrenic patients were allocated to treatment with either olanzapine (10–20 mg/day) or Amisulpride (400–800 mg/day). A comprehensive neuropsychological test battery and clinical ratings were used to assess participants at inclusion and after 4 and 8 weeks. Cognitive improvements of moderate size were observed, with effect sizes similar to those obtained in previous studies on the cognitive effects of SGAs. Importantly, Amisulpride was not inferior to olanzapine for any cognitive domain. Combined 5-HT2A/D2 receptor blockade is probably not necessary for cognitive improvement by SGAs.

Signe During - One of the best experts on this subject based on the ideXlab platform.

  • effects of blocking d2 d3 receptors on mismatch negativity and p3a amplitude of initially antipsychotic naive first episode schizophrenia patients
    The International Journal of Neuropsychopharmacology, 2016
    Co-Authors: Signe During, Bob Oranje, Birte Glenthøj
    Abstract:

    Background: Reduced mismatch negativity and P3a amplitude have been suggested to be among the core deficits in schizophrenia since the late 1970s. Blockade of dopamine D2 receptors play an important role in the treatment of schizophrenia. In addition, there is some evidence indicating that deficits in mismatch negativity and P3a amplitude are related to increased dopaminergic activity. This is the first study investigating the effect of Amisulpride, a potent D2-antagonist, on mismatch negativity and P3a amplitude in a large group of antipsychotic-naive, first-episode schizophrenia patients. Methods: Fifty-one antipsychotic-naive, first-episode schizophrenia patients were tested in a mismatch negativity paradigm at baseline and after 6 weeks of treatment with Amisulpride. We further examined 48 age- and gender-matched controls in this paradigm. Results: At baseline, the patients showed significantly reduced P3a amplitude compared with healthy controls, but no differences in mismatch negativity. Although the treatment with Amisulpride significantly improved the patients’ psychopathological (PANSS) and functional (GAF) scores, it did not influence their mismatch negativity amplitude, while also their reduced P3a amplitude persisted. Conclusion: Our findings show that antipsychotic naive, first-episode patients with schizophrenia have normal mismatch negativity yet reduced P3a amplitude compared with healthy controls. In spite of the fact that the 6-week Amisulpride treatment improved the patients both clinically and functionally, it had no effect on either mismatch negativity or P3a amplitude. This suggests that even though there is a dopaminergic involvement in global functioning and symptomatology in schizophrenia, there is no such involvement in these particular measures of early information processing.

  • effects of dopamine d2 d3 blockade on human sensory and sensorimotor gating in initially antipsychotic naive first episode schizophrenia patients
    Neuropsychopharmacology, 2014
    Co-Authors: Signe During, Bob Oranje, Birte Glenthøj, Gitte Saltoft Andersen
    Abstract:

    It has been suggested that psychophysiological measures of sensory and sensorimotor gating, P50 gating and prepulse inhibition of the startle reflex (PPI), underlie core features of schizophrenia and are linked to dopaminergic pathways in the striatum and prefrontal cortex. In the present study, the effects of a potent D2/D3 receptor antagonist, Amisulpride, were investigated on PPI and P50 gating in a large sample of antipsychotic-naive, first-episode patients with schizophrenia. A total of 52 initially antipsychotic-naive, first-episode schizophrenia patients were assessed for their P50 gating, PPI, and habituation/sensitization abilities at baseline and after 2 and 6 weeks of treatment with flexible doses of Amisulpride. In addition, 47 matched healthy controls were assessed at baseline and after 6 weeks. At baseline, the patients showed significantly reduced PPI, yet normal levels of P50 gating, habituation, and sensitization. Treatment with Amisulpride showed no effects on these measures, either at 2 or 6 weeks of follow-up. This is the first study investigating the effects of monotherapy with a relatively selective dopamine D2/D3 receptor antagonist (Amisulpride) on sensory and sensorimotor gating deficits in a longitudinal study of a large group of initially antipsychotic-naive, first-episode patients with schizophrenia. Our finding that Amisulpride effectively reduced symptom severity in our patients without reducing their PPI deficits indicates that increased activity of dopamine D2 receptors may be involved in symptomatology of patients with schizophrenia, but not in their sensorimotor gating deficits.