Behavioural and ECoG spectrum power effects after intraventricular injection of drugs altering dopaminergic transmission in rats

Bagetta, Giacinto; Corasaniti, Maria Tiziana; Strongoli, M.C.; Sakurada, Shinobu; Nisticò, Giuseppe

doi:10.1016/0028-3908(87)90247-4

Cited by 16 publications

(7 citation statements)

References 19 publications

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“…Arguing against a presynaptic site of action in the wake-promoting actions of quinpirole is the finding that i.c.v. administration of the D2 autoreceptor-preferring agonist (Ϫ)- 3-propylpiperidine HCl, elicits increased time spent asleep (Bagetta et al, 1987). Similar effects were observed after infusion of the D2 agonist (ϩ)-3-propylpiperidine HCl into the ventral tegmental area, a region containing DA-synthesizing neurons.…”

Section: Discussionsupporting

confidence: 55%

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Wake-Promoting Actions of Dopamine D1 and D2 Receptor Stimulation

Isaac

Berridge²

2003

J Pharmacol Exp Ther

107

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Multiple ascending neurotransmitter systems participate in the regulation of behavioral state. For example, noradrenergic, cholinergic, and serotonergic systems increase EEG and, in some cases, behavioral indices of arousal. The extent to which dopaminergic systems exert a similar activating influence on behavioral state remains unclear. The current studies examined the wake-promoting actions of centrally administered D1 and D2 receptor agonists. In these studies, intracerebroventricular infusions of a D1 (SKF-82958; 2.5 and 25 nmol) or D2 (quinpirole; 40 and 140 nmol)-agonist were made into sleeping animals. The effects of these infusions on electroencephalogram/ electromyographic indices of sleep-wake state and behavior were examined. D1 agonist administration dose dependently increased time spent awake and suppressed rapid eye movement and slow-wave sleep in the 2 h immediately after infusion. D1 agonist administration also elicited modest increases in measures of locomotion and time spent grooming and eating. D2 agonist administration had similar wake-promoting actions, accompanied by modest effects on drinking and locomotion. Interestingly, D2 agonist administration also significantly increased time spent chewing on inedible material, an arousal/ stress-related behavior. Overall, these results demonstrate that dopamine contributes to the alert waking state via actions of D1 and D2 receptors. Additionally or alternatively, these results further suggest a potential involvement of dopamine receptors in the induction of high-arousal states, including stress.

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Section: Discussionsupporting

confidence: 55%

“…Limited observations indicate sedative effects of D1 antagonist administration into the cerebral ventricles (i.c.v. ; Bagetta et al, 1987). Similar effects were observed after suppression of dopaminergic neurotransmission induced by ventral tegmental area D2 autoreceptor stimulation (Bagetta et al, 1988).…”

supporting

confidence: 62%

Wake-Promoting Actions of Dopamine D1 and D2 Receptor Stimulation

Isaac

Berridge²

2003

J Pharmacol Exp Ther

107

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“…Electrophysiological evidence indicates that dopamine and dopamine D2-receptor agonists (i.e. N-propyl norapomorphine, apomorphine, lisuride, pergolide, LY141865, bromocriptine) inhibit the firing rate of VTA dopamine cell bodies (Trulson & Precussler, 1984;Wang et al, 1987 Longo, 1978, Bagetta et al, 1987bWauquier et al, 1985). On the contrary, drugs acting by potentiating dopaminergic transmission either acting as dopamine D1-and D2-postsynaptic agonists, as precursors (L-DOPA) or by releasing catecholamines or inhibiting catecholamine reuptake, i.e.…”

Section: Discussionmentioning

confidence: 99%

“…In favour of a presynaptic site for the mediation of soporific effects of (-}3PPP and of small doses of apomorphine is the antagonism of these effects by selective antagonists at D2-receptors, i.e. (-)-sulpiride and small doses of haloperidol Bagetta et al, 1987b). The present study was designed to ascertain the site through which the behavioural and ECoG sleep induced by apomorphine and (+)-3PPP were mediated.…”

Section: Introductionmentioning

confidence: 99%

“…In fact, we have recently reported that the i.c.v. injection of R-(-)3(3-hydroxy-phenyl-npropyl-piperidine hydrochloride ((-)-3PPP), a specific agonist at dopamine autoreceptors (Hjorth et al, 1981) produced in freely moving rats dosedependent behavioural and ECoG sleep (Bagetta et al, 1987b). In favour of a presynaptic site for the mediation of soporific effects of (-}3PPP and of small doses of apomorphine is the antagonism of these effects by selective antagonists at D2-receptors, i.e.…”

Section: Introductionmentioning

confidence: 99%

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Ventral tegmental area: site through which dopamine D₂‐receptor agonists evoke behavioural and electrocortical sleep in rats

Bagetta

Sarro

E³

et al. 1988

British J Pharmacology

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1 In freely moving rats the effects on behaviour and electrocortical (ECoG) spectrum power of some dopamine agonists, i.e. apomorphine and (+-3PPP, given directly into different areas of the rat brain were studied. In particular, dopamine agonists were microinfused in the ventral tegmental area (VTA) and substantia nigra (SN) or into the caudate nucleus, n. accumbens and prefrontal cortex. The ECoG spectrum power effects were continuously analysed by means of a computerized Berg-Fourier analyser as total spectrum power and power in preselected frequency bands.2 Apomorphine and (+)-3PPP (0.01, 0.1 and 1.0nmol) given bilaterally into the VTA produced behavioural and ECoG sleep in a dose-dependent fashion. A statistically significant (P < 0.01) increase in ECoG total spectrum power with a predominant increase in the lower frequency bands (0.25-3, 3-6 and 6-9 Hz) occurred. No behavioural and ECoG changes were evoked by the same doses of apomorphine bilaterally microinfused into the SN or into the caudate nucleus or by (+)-3PPP (1.0 nml) microinjected into the n. accumbens or applied onto the prefrontal cortex. 3 Behavioural and ECoG sleep was also induced in rats after systemic administration of apomorphine (263 nmol kg-1, i.p.). 4 The behavioural and ECoG spectrum power effects of apomorphine (1.0 nmol) bilaterally microinfused into the VTA were prevented by a previous microinjection into the same site of (-)-sulpiride (9.8 nmol). Similarly, behavioural and ECoG effects evoked by (+)-3PPP (0.1 nmol) given bilaterally into the VTA, were completely antagonized by a previous injection into the same site of haloperidol (16pmol given 10min before). In contrast, pretreatment with SCH 23390 (50 pgkg-1, s.c.), a selective antagonist at dopamine Dl-receptors, was unable to antagonize the behavioural and ECoG spectrum power effects of ( +)-3PPP. 5 Soporific effects induced by systemic administration of apomorphine were antagonized by (-)-sulpiride (9.8 nmol) given bilaterally into the VTA 10min before, whereas, yohimbine (1.3 nmol), (an antagonist at a2-adrenoceptors) bilaterally microinfused into the VTA, was ineffective in this respect.6 The present experiments provide evidence suggesting that stimulation of dopamine D2-receptors located at the cell body level and/or the dendrites of dopaminergic neurones in the VTA may represent the mechanism through which apomorphine or (+)-3PPP exert their soporific effects in rats.

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Dopaminergic regulation of cortical acetylcholine release

Day

Fibiger

1992

Synapse

109

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The extent to which the activity of basal forebrain cholinergic neurons is influenced by dopamine (DA) was investigated using in vivo microdialysis of cortical acetylcholine (ACh). Systemic administration of the DA receptor agonist apomorphine significantly increased dialysate concentrations of ACh. Systemic, but not local, administration of d-amphetamine produced similar effects. Both D1 (SCH 23390) and D2 (haloperidol, raclopride) DA receptor antagonists attenuated the amphetamine-induced increase in cortical ACh release; however, only the D1 antagonist significantly reduced basal output of cortical ACh. These findings suggest that the activity of cortically projecting cholinergic neurons in the nucleus basalis is regulated in an excitatory manner by central dopaminergic neurons and that both D1 and D2 receptors are involved.

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Behavioural and ECoG spectrum power effects after intraventricular injection of drugs altering dopaminergic transmission in rats

Cited by 16 publications

References 19 publications

Wake-Promoting Actions of Dopamine D1 and D2 Receptor Stimulation

Wake-Promoting Actions of Dopamine D1 and D2 Receptor Stimulation

Ventral tegmental area: site through which dopamine D₂‐receptor agonists evoke behavioural and electrocortical sleep in rats

Dopaminergic regulation of cortical acetylcholine release

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Behavioural and ECoG spectrum power effects after intraventricular injection of drugs altering dopaminergic transmission in rats

Cited by 16 publications

References 19 publications

Wake-Promoting Actions of Dopamine D1 and D2 Receptor Stimulation

Wake-Promoting Actions of Dopamine D1 and D2 Receptor Stimulation

Ventral tegmental area: site through which dopamine D2‐receptor agonists evoke behavioural and electrocortical sleep in rats

Dopaminergic regulation of cortical acetylcholine release

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Product

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Ventral tegmental area: site through which dopamine D₂‐receptor agonists evoke behavioural and electrocortical sleep in rats