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  • 1
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Medicine 41 (1990), S. 437-446 
    ISSN: 0066-4219
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 92 (1987), S. 14-24 
    ISSN: 1432-2072
    Keywords: Serotonin ; MCPP ; Cortisol ; Prolactin ; Growth hormone ; Anxiety
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To assess the role of serotonin function in the development of panic anxiety, the behavioral and biochemical responses to the serotonin receptor agonist, m-chlorophenylpiperazine (MCPP) was examined in healthy subjects and agoraphobic and panic disorder patients. MCPP had anxiogenic effects in both the healthy subjects and patients. Panic attacks meeting DSM-III criteria occurred following MCPP in 12 of 23 patients and 6 of 19 healthy subjects (NS) and other ratings of anxiety also did not distinguish the two groups. MCPP resulted in significant but similar increases in cortisol, prolactin, and growth hormone in the healthy subjects and patients. The results of this investigation suggest that serotonin neuronal dysfunction may not be of etiologic significance in most panic disorder patients. However, the observed anxiogenic properties of MCPP suggest that additional studies of the role of serotonin systems in the pathophysiology of human anxiety disorders are indicated.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 92 (1987), S. 431-437 
    ISSN: 1432-2072
    Keywords: Reserpine ; Desipramine ; Antidepressants ; Refractory depression ; MHPG ; HVA ; 5-HIAA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Early studies showed dramatic improvement in some depressed patients when a brief course of parenteral reserpine was added to ineffective tricyclic antidepressant (TCA) treatment. We treated eight patients with DSM-III melancholic major depression with desipramine (DMI)≥2.5 mg/kg/day (plasma levels〉125 ng/ml) for at least 4 weeks. All patients failed to respond and received reserpine 5 mg IM b.i.d. over 2 days, in seven cases as a placebo-controlled, double-blind trial. One patient had dramatic resolution of depressive and psychotic symptoms within 48 h, but relapsed within 2 weeks; two other patients had transient hypomanic symptoms. Depression ratings did not significantly change for the sample as a whole, but plasma and cerebrospinal fluid (CSF) levels of 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) decreased and CSF levels of homovanillic acid (HVA) and 5-hydroxy-indoleacetic acid (5-HIAA) increased. Despite robust effects on central monoamine metabolism, reserpine augmentation appears insufficiently effective for routine use in managing refractory depression.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 110 (1993), S. 342-346 
    ISSN: 1432-2072
    Keywords: Yohimbine ; Noradrenergic ; Anxiety
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Preclinical studies have suggested the acoustic startle reflex (ASR) may be a useful animal model to investigate the neurochemical basis of anxiety and fear states. This work has revealed that the anxiogenic alpha-2 receptor antagonist, yohimbine, increases the amplitude of the ASR in laboratory animals. The present investigation evaluated the effects of yohimbine on the ASR in healthy subjects. Seven healthy subjects received IV yohimbine (0.4 mg/kg) or saline placebo on two separate days in a randomized double blind placebo control design. A trial of 2 tone frequencies with varied intensity (90, 96, 102, 108, 114 dB) white noise, instantaneous rise time, was delivered binaurally through headphones. Tones were delivered every 25–60 sec, for a 30 ms duration. Startle testing was done 80 minutes post infusion and lasted 15–20 minutes. Sign rank testing indicated yohimbine caused an overall increase in startle amplitude, as well as significant augmentation of startle amplitude at 96, 102, 108, 114 decibels but not at the 90 dB intensity. Sign rank tests indicated a significant reduction of startle latency by yohimbine at only the 96 dB intensity. Significant correlations were observed between startle and peak anxiety, startle and plasma MHPG, peak anxiety and plasma MHPG. This study demonstrates in healthy human subjects an excitatory effect of yohimbine on the mangnitude of the ASR and a decrease in its latency. In the context of the key role of this reflex in the alarm response, this finding adds to the array of documented behavioral, biochemical and cardiovascular effects of yohimbine in humans which support the relationship between increased noradrenergic function and anxiety states.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-2072
    Keywords: Yohimbine ; Noradrenergic ; Anxiety PTSD
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Preclinical and clinical studies have suggested that the acoustic startle reflex (ASR) is a useful model to investigate the neurochemical basis of anxiety and fear states. This work has revealed that the anxiogenic alpha-2 receptor antagonist, yohimbine, increases the amplitude of the ASR in laboratory animals and in healthy human controls. Because of the growing body of data that support the hypothesis that severe stress results in substantial alterations in noradrenergic neuronal reactivity, the present investigation evaluated the effects of yohimbine on the ASR of 18 patients with PTSD and 11 healthy combat controls. Subjects received IV yohimbine (0.4 mg/kg) or saline placebo on 2 separate days in a randomized double blind placebo control design. A trial of two tone frequencies with varied intensity (90, 96, 102, 108, 114 dB) white noise and instantaneous rise time, was delivered binaurally through headphones. Tones were delivered every 25–60 s, for a 40-ms duration. Startle testing was performed 80 min post-infusion and lasted 15–20 min. Yohimbine significantly increased the amplitude, magnitude and probability of the ASR in combat veterans with PTSD, but did not do so in combat controls. Overall startle was significantly larger in the PTSD subjects; however, this did not account for the differential effect of yohimbine, since yohimbine had no significant effect in the control group. This study demonstrates an excitatory effect of yohimbine on the amplitude, magnitude and probability of the ASR in PTSD patients that is not seen in combat controls. In the context of the key role of this reflex in the alarm response, this finding adds to the array of documented behavioral, biochemical and cardiovascular effects of yohimbine in humans which support the relationship between increased noradrenergic function and exaggerated startle symptomatology of PTSD.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 93 (1987), S. 308-313 
    ISSN: 1432-2072
    Keywords: Yohimbine ; Obsessive compulsive disorder ; MHPG ; Cortisol ; Norepinephrine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The α2-adrenergic receptor antagonist yohimbine was administered to 12 drug-free patients with obsessive compulsive disorder (OCD) and to 12 healthy subjects. Changes in behavior, cardiovascular symptoms, and in plasma levels of cortisol and the norepinephrine metabolite, 3-methoxy-4-hydroxyphenylglycol (MHPG), were assessed. Yohimbine had no significant effect on OCD symptoms. The OCD patients did not differ from healthy controls in their behavioral and MHPG response to yohimbine. In contrast to healthy subjects, OCD patients, like previous reports of depressed and panic disorders patients, had an increased cortisol response to yohimbine. These data suggest it is unlikely that abnormal noradrenergic function plays a primary role in the pathogenesis of OCD.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 94 (1988), S. 24-28 
    ISSN: 1432-2072
    Keywords: β-Adrenergic receptors ; Anxiety ; Panic disorder ; Lymphocytes ; Noradrenergic dysfunction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Lymphocyte beta adrenergic receptor binding using [125I]CNP was determined in patients with panic disorder (N=4) or agoraphobia with panic attacks (N=17) and age- and sex-matched healthy subjects (N=22). The patients showed a significantly lower number of β-adrenergic receptor binding sites and a significantly higher affinity of binding than healthy subjects. A past or present history of major depression in the patients did not alter these findings. These results are consistent with a growing body of knowledge implicating noradrenergic dysfunction in the pathophysiology of panic anxiety.
    Type of Medium: Electronic Resource
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