An Open Field Study of Antidepressant Drugs

Dahl, Carl Bredo; Götestam, K. Gunnar

doi:10.1111/j.1600-0773.1989.tb00652.x

Cited by 4 publications

(3 citation statements)

References 33 publications

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“…However, other mechanisms could potentially explain the changes in motor behavior we observed after MGE cell transplantation. Our results are similar to those showing that L-dopa administration increases open field activity levels in control rats (Dahl and Götestam, 1989; Ljungberg and Ungerstedt, 1976). Thus, it is also possible that the transplantation of MGE cells induced secondary changes in the striatum that produced or contributed to the behavioral changes (Goto et al, 1997).…”

Section: Discussionsupporting

confidence: 92%

Embryonic MGE Precursor Cells Grafted into Adult Rat Striatum Integrate and Ameliorate Motor Symptoms in 6-OHDA-Lesioned Rats

et al. 2010

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SUMMARY We investigated a strategy to ameliorate the motor symptoms of rats that received 6-hydroxydopamine (6-OHDA) lesions, a rodent model of Parkinson’s disease, through transplantation of embryonic medial ganglionic eminence (MGE) cells into the striatum. During brain development, embryonic MGE cells migrate into the striatum and neocortex where they mature into GABAergic interneurons and play a key role in establishing the balance between excitation and inhibition. Unlike most other embryonic neurons, MGE cells retain the capacity for migration and integration when transplanted into the postnatal and adult brain. We performed MGE cell transplantation into the basal ganglia of control and 6-OHDA-lesioned rats. Transplanted MGE cells survived, differentiated into GABA+ neurons, integrated into host circuitry, and modifed motor behavior in both lesioned and control rats. Our data suggest that MGE cell transplantation into the striatum is a promising approach to investigate the potential benefits of remodeling basal ganglia circuitry in neurodegenerative diseases.

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Section: Discussionsupporting

confidence: 92%

Embryonic MGE Precursor Cells Grafted into Adult Rat Striatum Integrate and Ameliorate Motor Symptoms in 6-OHDA-Lesioned Rats

et al. 2010

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“…It has been demonstrated that NPY modulates the release of dopamine via an NPY Y 2 receptor controlled mechanism (Ault and Werling 1997). In addition, dopamimetics have been shown to display antidepressant-like activity in the forced swimming test (Willner 1997), as well as increased activity in the open field (Dahl and Gotestam 1989). As there is little or no behavioral data published to date using BIIE0246, a full and more detailed psychopharmacological profile of this molecule is warranted before any firm conclusions can be made.…”

Section: Discussionmentioning

confidence: 99%

The Neuropeptide Y (NPY) Y1 Receptor Subtype Mediates NPY-induced Antidepressant-like Activity in the Mouse Forced Swimming Test

Redrobe

Dumont

Fournier

et al. 2002

Neuropsychopharmacology

187

123

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The present study was undertaken to investigate the possible antidepressant-like effects of neuropeptide Y (NPY)inNeuropeptide Y (NPY) is a 36-amino acid peptide that is widely distributed in the central nervous system (CNS). Intracerebroventricular (ICV) administration of NPY stimulates food intake (Clark et al. 1985;Levine and Morley 1984;Stanley and Leibowitz 1984), modulates cognition (Flood et al. 1987;Redrobe et al. 1999), inhibits neuronal excitability (Colmers and Bleakman 1994) and has anticonvulsant effects (Vezzani et al. 1999). NPY modulates the secretion of various hypothalamic neuropeptides, stimulates the corticotrophic axis (Krysiak et al. 1999;Small et al. 1997) and has potent inhibitory effects on gonadotrophic and somatotrophic axes (Catzeflis et al. 1993). In addition, NPY is thought to play a role in the pathophysiology of certain mood disorders and in the mechanism of action of antidepressant drugs (Heilig et al. 1988;Caberlotto et al. 1998 (Michel et al. 1998).Clinical studies have demonstrated decreased NPY levels in the cerebrospinal fluid (CSF) (Heilig and Widerlov 1990) and plasma (Nilsson et al. 1996) of depressed patients, when compared with healthy control subjects. In addition, NPY levels have been shown to be negatively correlated to scores of anxiety in clinically depressed patients (Heilig and Widerlov 1990), suggesting a possible link between low levels of NPY and predisposition to anxiety-related or stress-induced depression.Moreover, pre-clinical studies have shown that electroconvulsive shock stimulation increased NPY gene expression (Heilig et al. 1988), as well as the expression of NPY mRNA in distinct brain regions in rats (Caberlotto et al. 1998;Mikkelsen et al. 1994). In addition, chronic antidepressant treatment has been shown to alter NPY and NPY Y 1 -type receptor mRNA levels (Caberlotto et al. 1998), and to reduce NPY Y 2 -type receptor densities in certain brain regions (Widdowson and Halaris 1991). Interestingly, NPY-like immunoreactivity and NPY Y 1 -type receptor binding sites were shown to be decreased or increased, depending on the brain region studied, in the recently developed Flinders Sensitive Line (FSL) rats (Caberlotto et al. 1999), a purported genetic animal model of depression (Overstreet 1993;Overstreet et al. 1995).Additional evidence of a role for NPY in depressive disorders is found in studies using the olfactory bulbectomized (OB) rat model of depression. Sub-chronic ICV administration of NPY attenuated the increase in ambulation, rearing, grooming and defecation scores consistently found when OB animals are tested in the open field (Song et al. 1996). Treatment with NPY also increased noradrenaline (NA) and serotonin (5-HT) levels in the amygdala and hypothalamus (Song et al. 1996). In addition, NPY reversed the supression of lymphocyte proliferation seen following OB (Song et al. 1994). A decrease in lymphocyte proliferation has also been reported in depressed patients (Kronfol and House 1989). Another study demonstrated that OB caused long term...

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“…In open ®eld studies in rats, amineptine and nomifensine show a dose dependent activating effect (Dahl and Gotestam, 1989). Misuse of dothiepin and amitriptyline to produce sedation or euphoria has been reported in patients receiving methadone maintenance (Cohen et al, 1978;Cantor, 1979;Dorman et al, 1995).…”

Section: Pharmacological Issuesmentioning

confidence: 99%

Do antidepressants have any potential to cause addiction?

Haddad

1999

J Psychopharmacol

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Addiction/dependence is a syndrome in which the hallmark is a compulsive pattern of drug use. Most authorities do not regard antidepressants as causing addiction but this has been challenged. This debate is explored drawing on case reports and related clinical and pharmacological data. An extensive literature review identified 21 English language case reports of antidepressant addiction (DSM-IV 'substance dependence' criteria) published since 1963. Sixteen involved tranylcypromine or amineptine and may reflect their dopaminergic and stimulant properties. Subject characteristics included male sex (14/21), personality problems (10/21) and prior substance misuse (14/21). Withdrawal or discontinuation symptoms have long been recognized with antidepressants but other features of addiction such as tolerance and compulsive use are exceptionally rare. Common clinical problems are patients taking subtherapeutic dosages and prematurely stopping antidepressants. The pharmacodynamic profiles of most antidepressants and the absence of acute 'desirable' effects make addiction theoretically unlikely. It is concluded that, with the exception of tranylcypromine and amineptine, antidepressants do not have a clinically significant liability to cause addiction. Tranylcypromine and amineptine should be avoided in those with a history of substance misuse. Patients prescribed other antidepressants should be told that they are not addictive.

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An Open Field Study of Antidepressant Drugs

Cited by 4 publications

References 33 publications

Embryonic MGE Precursor Cells Grafted into Adult Rat Striatum Integrate and Ameliorate Motor Symptoms in 6-OHDA-Lesioned Rats

Embryonic MGE Precursor Cells Grafted into Adult Rat Striatum Integrate and Ameliorate Motor Symptoms in 6-OHDA-Lesioned Rats

The Neuropeptide Y (NPY) Y1 Receptor Subtype Mediates NPY-induced Antidepressant-like Activity in the Mouse Forced Swimming Test

Do antidepressants have any potential to cause addiction?

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