Antidepressant drugs potentiate the α1-adrenoceptor effect in hippocampal slices

Bijak, M

doi:10.1016/0014-2999(89)90058-7

Cited by 18 publications

(2 citation statements)

References 42 publications

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“…As was demonstrated previously, similar changes (increased responsiveness to agonists) are observed after both OXAs -like after others AD -in the %-adrenergic system (Mogilnicka et al, 1987;Bijak, 1989;Maj etal., 1990c). The data on a decreased sensitivity of %-adrenergic receptors after repeated OXAs are controversal: a diminished sensitivity (Delini-Stula et al, 1983), but also the lack of changes (Maj et al, 1990 c) have been reported.…”

Section: Discussionsupporting

confidence: 79%

The effect of (+)- and (−)-oxaprotiline administered repeatedly on the dopamine system

Klimek

Rogóż

et al. 1991

J. Neural Transmission

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The behavioural and biochemical effects of repeated (14 and 28 days) treatment with (+)-oxaprotiline (a noradrenaline uptake inhibitor) and (-)-oxaprotiline (levoprotiline, without influence on noradrenaline uptake; the clinically active antidepressant) were studied in rats. Both those enantiomers given repeatedly increased the locomotor and exploratory activity and reduced the immobility time in Porsolt's test. The D-amphetamine-induced locomotor hyperactivity, as well as the stereotypies induced by D-amphetamine and apomorphine, were increased by the oxaprotilines. Single-dose treatment with both the oxaprotilines was not effective in the tests mentioned above. Repeated (+)-oxaprotiline administration reduced the binding (Bmax but not KD) to dopamine D-1 receptors in the striatum and limbic system; levoprotiline was inactive. The binding to dopamine D-2 receptors was not changed by either drug. Both the enantiomers showed only low affinity for brain dopamine D-1 and D-2 receptors in vitro. The obtained results indicate that chronic treatment with (+)- and (-)-oxaprotiline increases behavioural responsiveness of the dopamine mesolimbic and striatal systems.

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Section: Discussionsupporting

confidence: 79%

The effect of (+)- and (−)-oxaprotiline administered repeatedly on the dopamine system

Klimek

Rogóż

et al. 1991

J. Neural Transmission

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“…In the dog with narcolepsy there is evidence that the anticataplectic action of the tricyelics, like that of the stimulants described earlier, is mediated by the alpha-1- adrenoceptor because this therapeutic effect can be overcome with prazosin (Mignot et al, 1988a, 1988b). Under certain circumstances the tricyclic antidepressants, as well as the monoamine oxidase inhibitors to be discussed shortly, can also increase the number of alpha-1-adrenergic receptors or increase their sensitivity to agonists (Bijak, 1989; Johnson et al, 1987; Klimic, Nowak, Zak, & Maj, 1990; Menkes, Aghajanian, & Gallagher, 1983; Rehavi, Ramot, Yavetz, & Soholovsky, 1980). The implications of these recent observations for the treatment of narcolepsy require further study.…”

Section: Treatmentmentioning

confidence: 99%

A model for narcolepsy.

Mamelak

1991

Canadian Journal of Psychology / Revue canadienne de psychologi

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A model for narcolepsy is developed on the basis of data obtained from brains collected at post mortem from three patients with narcolepsy. The concentration of dopamine, noradrenaline, and serotonin and their metabolites was measured in many brain regions. The number and affiniiy of the 3-H-spiperone and 3-Hprazocin binding sites was also measured in many of these regions to characterize the O-2 dopamine and alpha-l-noradrenergic receptors, respectively.Evidence for significantly increased serotonin levels and serotonin turnover was found in many brain regions. Noradrenaline turnover was increased in the frontal cortex. DOPAC/DA was significantly reduced in the striatum. The number of D-2 dopamine receptors, however, was markedly increased in this region. The number of alpha-1-noradrenergic receptors was significantly decreased in the frontal cortex and amygdala.Our ncurochemical data demonstrating increased NA and 5-HT turnover suggest that locus cocrulcus noradrenergic neurones and raphe serotonergic neurones are ovcractivc in narcolepsy. Current evidence posits that increased activity in these neurones depresses the activity of cholinergic pcdunculopontinc (PP) RF.M sleep effector neurones. PP neurones project to and stimulate the dopamincrgic substantia nigra compacta neurones. Decreased PP activity in narcolepsy, thus, could lead to pontine cholinergic supersensitivity and could also reduce the firing rales of dopaminergic neurones, as the low slriatal ratio of DOPAC/DA suggests. An increase in the number of D-2 dopamine receptors in the striatum may result. The reason for the increased activity of the noradrenergic and serotonergic neurones remains to be determined, but immune inactivation of alpha-l-noradrenergic receptors may be the initiating event.Low alpha-1 -noradrencrgic receptor numbers may account for the chronic drowsiness of narcolepsy. The repealed entry into sleep, and into RHM sleep in particular, may represent a homeostalic response to increase these receptor numbers and, thus, to increase alertness. Some therapeutic implications of this model arc presented in the discussion. KKSUMK Un modclc dc la narcolepsic cst developpc a partir de donnees obtenucs sur des cerveaux post-mortem appanenant a trois patients souffrant de narcolepsie. Ix;s concentrations en dopamine, noradrenaline, serotonine et leurs metabolites ont ete mesurees dans plusieurs regions cerebralcs. On a mesure aussi lc nombre el raffiniie des sites d'attache de la 3H Spiperone et de la 3H frazocin dans plusieurs de ces regions en vue de caractcriscr les rcccptcurs dopamine D2 et noradrenergiques alpha-1.Dans dc nombrcuscs regions cerebralcs les nivcaux de serotonine et le changemenl scrotoninergique ctaient augmentcs significalivemenl. l.

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Neuromodulation of Hippocampal Cells and Circuits

Cobb

Lawrence

2010

Hippocampal Microcircuits

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Antidepressant drugs potentiate the α1-adrenoceptor effect in hippocampal slices

Cited by 18 publications

References 42 publications

The effect of (+)- and (−)-oxaprotiline administered repeatedly on the dopamine system

The effect of (+)- and (−)-oxaprotiline administered repeatedly on the dopamine system

A model for narcolepsy.

Neuromodulation of Hippocampal Cells and Circuits

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