One More Look at Propranolol for the Treatment of Refractory Schizophrenia

Berlant, Jeffrey

doi:10.1093/schbul/13.4.705

Cited by 18 publications

(7 citation statements)

References 52 publications

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“…There is some evidence for enhancement of antipsychotic function by compounds that reduce central NE transmission or block postsynaptic NE receptors, suggesting the possibility of NE-based therapeutics as adjunct treatments for schizophrenia, but there are also examples of no clinical improvement with these compounds in schizophrenia (Berlant, 1987; Freedman, et al 1982; Friedman, et al 2001; Maas, et al 1995; Wahlbeck, et al 2000). …”

Section: Discussionmentioning

confidence: 99%

Ventral Striatal Noradrenergic Mechanisms Contribute to Sensorimotor Gating Deficits Induced by Amphetamine

Alsene

Fallace

Bakshi

2010

Neuropsychopharmacol

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The psychotomimetic drug d-amphetamine (AMPH), disrupts prepulse inhibition of the startle response (PPI), an operational measure of sensorimotor gating that is deficient in schizophrenia patients. Historically, this effect has been attributed to dopaminergic substrates; however, AMPH also increases norepinephrine (NE) levels, and enhancement of central NE transmission has been shown recently to disrupt PPI. The present study examined the extent to which NE might participate in AMPH-induced disruptions of PPI and increases in locomotor activity, another classic behavioral effect of AMPH, by determining whether antagonism of postsynaptic NE receptors blocked these effects. Separate groups of male Sprague-Dawley rats received either the α1 receptor antagonist, prazosin (0, 0.3, 1 mg/kg), or the β receptor antagonist timolol (0, 3, 10 mg/kg) prior to administration of AMPH (0 or 1 mg/kg) before testing for PPI or locomotor activity. As an initial exploration of the anatomical substrates underlying possible α1 receptor-mediated effects on AMPH-induced PPI deficits, the α1 receptor antagonist terazosin (0, 40 μg/0.5 μl) was microinfused into the nucleus accumbens shell (NAccSh) in conjunction with systemic AMPH administration prior to startle testing in a separate experiment. Prazosin, but not timolol, blocked AMPH-induced hyperactivity; both drugs reversed AMPH-induced PPI deficits without altering baseline startle responses. Interestingly, AMPH-induced PPI deficits also were partially blocked by terazosin in NAccSh. Thus, behavioral sequelae of AMPH (PPI disruption and hyperactivity) may be mediated in part by NE receptors, with α1 receptors in NAccSh possibly playing an important role in the sensorimotor gating deficits induced by this psychotomimetic drug.

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Section: Discussionmentioning

confidence: 99%

Ventral Striatal Noradrenergic Mechanisms Contribute to Sensorimotor Gating Deficits Induced by Amphetamine

Alsene

Fallace

Bakshi

2010

Neuropsychopharmacol

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“…Several therapeutic interventions in psychotic or manic patients with centrally active anti-NA agents other than clozapine have led to less convincing results. These include putative additional benefits from adding reserpine (a non-specific monoaminedepleting agent) to neuroleptic treatment regimens, especially in affective psychoses (Berlant, 1986), as well as long-standing but still inconclusive reports that high doses of the centrally active {3-adrenergic antagonist propranolol may have benefit when added to standard neuroleptic treatments (Berlant, 1987;van Kammen & Gelernter, 1987;Lader, 1988). The centrally active direct al antagonist prazosin was found to be ineffectivein treating schizophrenia in one small study (Hommer et ai, 1984), but it has not been combined with neuroleptics to seek additional benefit or reduction of neurological side-effects.…”

mentioning

confidence: 99%

Do Central Antiadrenergic Actions Contribute to the Atypical Properties of Clozapine?

Baldessarini

Huston-Lyons²,

Campbell³

et al. 1992

Br J Psychiatry

121

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Full neuropharmacological understanding of the atypical antipsychotic agent clozapine remains elusive. Antidopaminergic actions of most neuroleptics probably contribute to their antipsychotic benefits, but also to neurological side-effects. Clinical evidence of abnormalities of dopamine (DA) and serotonin (5-HT) in psychotic disorders is inconsistent, but there is substantial metabolic and post-mortem evidence for hyperactivity of noradrenalin (NA). Clozapine is only weakly antidopaminergic but is a potent antagonist at brain α1-adrenergic, 5-HT2-serotonergic, and muscarinic receptors. Its apparent limbic-over-extrapyramidal neuro-physiological selectivity can be mimicked by combining a typical neuroleptic with a central α1 antagonist. Clozapine strongly upregulates α1, but not DA, receptor abundance, and may supersensitise α1 but not DA receptors in rat brain. Clozapine also selectively increases activity of NA neurons and metabolic turnover in NA more than DA areas of rat brain, and also increases NA, but not DA or 5-HT, metabolites in human CSF. Potential psychotropic effects of selective central antiadrenergic agents may deserve reconsideration.

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“…Propranolol may also be a useful adjunct to neuroleptic agents, separate from the issue of akathisia in terms of enhancing or augmenting antipsychotic action in patients otherwise considered to be refractory or hyporesponsive, although this issue remains controversial (Donaldson et ai, 1983;Ananth & Lin, 1986;Berlant, 1987;Lader, 1988;Lipinski et ai, 1988;Christison et ai, 1991). In this case, as in the case of treatment of akathisia, the strategy of propranolol dosing may be important in the avoidance of autonomic and toxic side-effects (Ananth & Lin, 1986).…”

Section: Adjunctive Propranololmentioning

confidence: 99%

Adjunctive Medication in the Maintenance Treatment of Schizophrenia and its Conceptual Implications

Siris

1993

Br J Psychiatry

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Beyond the continuing use of neuroleptic medication, psychopharmacological treatment approaches during the maintenance phase of schizophrenia often involve adjunctive medication. Appropriate use of such ‘polypharmacy’ can be crucial to patients in achieving their optimal levels of symptom management and functional capacity, although the risks of side-effects and medication interactions must be weighed. This paper reviews the use of adjunctive anti-Parkinsonian medication, benzodiazepines, propranolol, antidepressants, lithium, and carbamazepine in this context. It also explores a strategy of identifying secondary syndromes in the longitudinal course of schizophrenia which can be approached psychopharmacologically.

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One More Look at Propranolol for the Treatment of Refractory Schizophrenia

Cited by 18 publications

References 52 publications

Ventral Striatal Noradrenergic Mechanisms Contribute to Sensorimotor Gating Deficits Induced by Amphetamine

Ventral Striatal Noradrenergic Mechanisms Contribute to Sensorimotor Gating Deficits Induced by Amphetamine

Do Central Antiadrenergic Actions Contribute to the Atypical Properties of Clozapine?

Adjunctive Medication in the Maintenance Treatment of Schizophrenia and its Conceptual Implications

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