Cocaine, amphetamine and cathinone, but not nomifensine and pargyline increase calcium inward current in internally perfused neurons

Вислобоков, А. И.; Mantsev, V.V.; Kuzmin, Alexander

doi:10.1016/0024-3205(93)90012-r

Cited by 16 publications

(9 citation statements)

References 9 publications

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“…Although calcium is not required for AMPH uptake through the carrier for DA release, AMPH could have an effect on increasing calcium in the synaptosome. AMPH at concentrations from 1 nM to 100 nM elicited an activation of an inward calcium current in internally perfused neurons of the snail (Vislobokov et al, 1993). Depletion of DA from a specific pool in the synaptosome, elicited by DA release, might have an activating effect on a signal transduction system.…”

Section: Discussionmentioning

confidence: 98%

Amphetamine increases the phosphorylation of neuromodulin and synapsin I in rat striatal synaptosomes

Iwata

Hewlett

Gnegy

1997

Synapse

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Amphetamine is taken up through the dopamine transporter in nerve terminals and enhances the release of dopamine. We previously found that incubation of rat striatal synaptosomes increases phosphorylation of the presynaptic neural-specific protein, neuromodulin (Gnegy et al., Mol. Brain Res. 20:289-293, 1993). Using a state-specific antibody, we now demonstrate that incubation of rat striatal synaptosomes with amphetamine increases levels of neuromodulin phosphorylated at ser41, the protein kinase C substrate site. Phosphorylation was maximal at 5 min at 37 degrees C at concentrations from 100 nM to 10 microM amphetamine. The effect of amphetamine on the phosphorylation of synapsin I at a site specifically phosphorylated by Ca2+/calmodulin-dependent protein kinase II (site 3), was examined using a state-specific antibody for site 3-phosphosynapsin I. Incubation with concentrations of amphetamine from 1 to 100 nM increased the level of site 3-phospho-synapsin I at times from 30 sec to 2 min. The effect of amphetamine on synapsin I phosphorylation was blocked by nomifensine. The presence of calcium in the incubating buffer was required for amphetamine to increase the level of site 3-phospho-synapsin I. The amphetamine-mediated increase in the content of phosphoser41-neuromodulin was less sensitive to extrasynaptosomal calcium. The amphetamine-mediated increase in the content of site 3-phospho-synapsin I persisted in the presence of 10 microM okadaic acid and was not significantly altered by D1 or D2 dopamine receptor antagonists. Preincubation of striatal synaptosomes with 10 microM of the protein kinase C inhibitor, Ro-31-8220, blocked the amphetamine-mediated increases in the levels of both phosphoser41-neuromodulin and site 3-phospho-synapsin I. Our results demonstrate that amphetamine can alter phosphorylation-related second messenger activities in the synaptosome.

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Section: Discussionmentioning

confidence: 98%

Amphetamine increases the phosphorylation of neuromodulin and synapsin I in rat striatal synaptosomes

Iwata

Hewlett

Gnegy

1997

Synapse

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“…Calcium ions play an important role in the control of Leydig cell steroidogenesis (Hall et al , 1981; Themmen et al , 1986; Foresta & Mioni, 1993; Foresta et al , 1995) and some studies have suggested that this ion contributes to the amphetamine signal transduction pathway (Dilullo & Martin‐Iverson, 1992; Giambalvo, 1992; Vislobokov et al , 1993). We evaluated the role of transmembrane Ca 2+ flux on amphetamine‐decreased steroidogenesis by use of the Ca 2+ channel blocker, nifedipine, and found that nifedipine reduced the basal release of testosterone but did not alter the effect induced by amphetamine.…”

Section: Discussionmentioning

confidence: 99%

“…Our previous results have suggested that amphetamine inhibits testosterone release via a mechanism associated with increased testicular adenosine 3′:5′‐cyclic monophosphate (cyclic AMP) (Tsai et al , 1996a). Amphetamine has a biphasic action on an inward calcium current in neurones of snail Lymnaea , causing activation at 10 −9 ‐10 −7 m , and inhibition at higher concentrations (Vislobokov et al , 1993). Combined nimodipine, a L‐type calcium channel antagonist, and haloperidol treatment have been shown to block the unconditioned and to attenuate the conditioned locomotor response to amphetamine in rats (DiLullo & Martin‐Iverson, 1992).…”

Section: Introductionmentioning

confidence: 99%

The role of cyclic AMP production, calcium channel activation and enzyme activities in the inhibition of testosterone secretion by amphetamine

Tsai¹,

Chen

Chiao

et al. 1997

British J Pharmacology

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1 The aim of this study was to investigate the mechanism by which amphetamine exerts its inhibitory e ect on testicular interstitial cells of male rats. 2 Administration of amphetamine (10 712 ± 10 76 M) in vitro resulted in a dose-dependent inhibition of both basal and human chorionic gonadotropin (hCG, 0.05 iu ml 71 )-stimulated release of testosterone. 3 Amphetamine (10 79 M) enhanced the basal and hCG-increased levels of adenosine 3':5'-cyclic monophosphate (cyclic AMP) accumulation in vitro (P50.05) in rat testicular interstitial cells. 4 Administration of SQ22536, an adenylyl cyclase inhibitor, decreased the basal release (P50.05) of testosterone in vitro and abolished the inhibitory e ect of amphetamine. 5 Nifedipine (10 76 M) alone decreased the secretion of testosterone (P50.01) but it failed to modify the inhibitory action of amphetamine (10 710 ± 10 76 M). 6 Amphetamine (10 710 ± 10 76 M) signi®cantly (P50.05 or P50.01) decreased the activities of 3b-hydroxysteroid dehydrogenase (3b-HSD), P450c17, and 17-ketosteroid reductase (17-KSR) as indicated by thin-layer chromatography (t.l.c.). 7 These results suggest that increased cyclic AMP production, decreased Ca 2+ channel activity and decreased activities of 3b-HSD, P450c17, and 17-KSR are involved in the inhibition of testosterone production induced by the administration of amphetamine.

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“…The mechanism for this reduced inhibition at intermediate cocaine concentrations is unclear, but the effect may be related to a combined effect of cocaine on all three monoamine transporters. Cocaine in the range of 1·nmol·l -1 to 1·mol·l -1 could alter the dynamics of dopamine and other neurotransmitters because it significantly increases calcium influx in Lymnaea neurons (Vislobokov et al, 1993). However, at all doses tested, cocaine only partially inhibited dopamine uptake (about 70%), even in the presence of 10·mol·l -1 cocaine.…”

Section: Dopamine Uptake In Lymnaeamentioning

confidence: 96%

Repeated cocaine effects on learning, memory and extinction in the pond snail Lymnaea stagnalis

Carter

Lukowiak

Schenk

et al. 2006

Journal of Experimental Biology

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SUMMARY The persistence of drug addiction suggests that drugs of abuse enhance learning and/or impair extinction of the drug memory. We studied the effects of repeated cocaine on learning, memory and reinstatement in the pond snail, Lymnaea stagnalis. Respiratory behavior can be operantly conditioned and extinguished in Lymnaea, and this behavior is dependent on a critical dopamine neuron. We tested the hypothesis that repeated cocaine exposure promotes learning and memory or attenuates the ability to extinguish the memory of respiratory behavior that relies on this dopaminergic neuron. Rotating disk electrode voltammetry revealed a Km and Vmax of dopamine uptake in snail brain of 0.9 μmol l-1 and 558 pmol s-1 g-1 respectively, and the IC50 of cocaine for dopamine was approximately 0.03 μmol l-1. For operant conditioning, snails were given 5 days of 1 h day-1 immersion in water (control) or 0.1 μmol l-1cocaine, which was the lowest dose that maximally inhibited dopamine uptake,and snails were trained 3 days later. No changes were found between the two groups for learning or memory of the operant behavior. However, snails treated with 0.1 μmol l-1 cocaine demonstrated impairment of extinction memory during reinstatement of the behavior compared with controls. Our findings suggest that repeated exposure to cocaine modifies the interaction between the original memory trace and active inhibition of this trace through extinction training. An understanding of these basic processes in a simple model system may have important implications for treatment strategies in cocaine addiction.

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Cocaine, amphetamine and cathinone, but not nomifensine and pargyline increase calcium inward current in internally perfused neurons

Cited by 16 publications

References 9 publications

Amphetamine increases the phosphorylation of neuromodulin and synapsin I in rat striatal synaptosomes

Amphetamine increases the phosphorylation of neuromodulin and synapsin I in rat striatal synaptosomes

The role of cyclic AMP production, calcium channel activation and enzyme activities in the inhibition of testosterone secretion by amphetamine

Repeated cocaine effects on learning, memory and extinction in the pond snail Lymnaea stagnalis

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