Effects of multiple pretreatment with apomorphine and amphetamine on amphetamine-induced locomotor activity and its inhibition by apomorphine

Riffee, William H.; Wilcox, Richard E.

doi:10.1007/bf00427330

Cited by 28 publications

(11 citation statements)

References 14 publications

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“…Again, these e¤ects were consistent with the well known actions of d-amphetamine and apomorphine as established in numerous earlier studies (e.g. Ri¤ee and Wilcox 1985;Geyer et al 1987;Mazurski and Beninger 1988;Druhan et al 1993;Ott and Mandel 1995). The overall similarity between the basic dose-e¤ect relations obtained with PPI and activity measures in this study and results reported elsewhere underscores the reliability of the procedures and measures employed in this study.…”

Section: Discussionsupporting

confidence: 89%

Lack of sensitization to the effects of d -amphetamine and apomorphine on sensorimotor gating in rats

1998

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This study assessed whether repeated injections of d-amphetamine or apomorphine could induce sensitization to the disruptive effects of these psychomotor stimulants on sensorimotor gating in rats. In the first experiment, rats were given six pre-exposures to either 2.0 mg/kg d-amphetamine or saline before being tested for the effects of d-amphetamine (0.0, 0.5, 1.0, 2.0 or 4.0 mg/kg, i.p.) on prepulse inhibition of acoustic startle (PPI) and locomotor activity. The tests for PPI confirmed that sensorimotor gating could be disrupted by a high dose of d-amphetamine (4.0 mg/kg). However, comparison of the dose-response curves for the drug and saline pre-exposed groups did not reveal evidence for sensitization to this d-amphetamine effect in drug-pre-exposed rats, despite indications that sensitization had developed to the locomotor stimulant effects of d-amphetamine. A similar pattern of results was obtained in a second experiment that examined the effects of apomorphine (0.0, 0.1, 0.2, 0.4 and 0.8 mg/kg, s.c.) on PPI and locomotion in rats pre-exposed to 2.0 mg/kg of this drug or its vehicle. These findings demonstrate that treatments which induce sensitization to the behavioral activating effects of psychomotor stimulants do not necessarily produce sensitization to the disruptive effects of stimulants on sensorimotor gating. The implications of these results for hypotheses linking sensitization-like processes to the etiology of schizophrenia are discussed.

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Section: Discussionsupporting

confidence: 89%

Lack of sensitization to the effects of d -amphetamine and apomorphine on sensorimotor gating in rats

1998

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“…Also, repeated administration of APO or AMP produces an increased stereotypy and motor response to AMP (Segal and Mandell 1974;Wilcox et al 1980;Riffee and Wilcox 1985). Similar to the results in the present study, the regulation of presynaptic activity by DA agonists is not impaired following chronic APO, and there are no corresponding changes in the maximal number or affinity of 3H-spiroperidol binding sites (Riffee et al 1982;Riffee and Wilcox 1985).…”

Section: Discussionsupporting

confidence: 79%

“…Acute or repeated stress selectively activates mesocortical DA turnover (Fadda et al 1978;Herman et al 1982), increases the stereotypy response to AMP (Antelman and Chiodo 1983) and APO (Csernansky et al 1984), and the locomotor responses to AMP and APO (Herman et al 1984). Also, repeated administration of APO or AMP produces an increased stereotypy and motor response to AMP (Segal and Mandell 1974;Wilcox et al 1980;Riffee and Wilcox 1985). Similar to the results in the present study, the regulation of presynaptic activity by DA agonists is not impaired following chronic APO, and there are no corresponding changes in the maximal number or affinity of 3H-spiroperidol binding sites (Riffee et al 1982;Riffee and Wilcox 1985).…”

Section: Discussionmentioning

confidence: 99%

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Behavioral and biochemical studies of dopamine receptor sensitivity in differentially housed mice

VanderWende

1986

Psychopharmacology

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Group housed and individually housed mice were compared in (1) the motor activity responses to direct and indirect dopamine (DA) agonists, (2) in vivo presynaptic autoreceptor sensitivity and (3) in vitro binding of 3H-spiperone. Relative to group housed mice, individually housed mice showed an increased motor activity response to amphetamine, 1.25 and 0.625 mg/kg. Using two in vivo measures of presynaptic DA receptor sensitivity, the antagonism of spontaneous locomotor activity and the antagonism of dihydroxyphenylalanine (DOPA) accumulation by apomorphine (APO), individually housed mice showed greater activity counts and higher DOPA accumulations than group housed mice. Levels of tyrosine were significantly greater in individually housed mice. Significant effects of housing were also noted with the motor activity response to APO, 0.075-0.300 mg/kg, following pretreatment with reserpine, an in vivo measure of postsynaptic receptor sensitivity. However, there was no effect of housing on the number or affinity of 3H-spiperone binding sites in the striatum. These results are discussed in terms of the presynaptic activity of catecholaminergic neurons and the postsynaptic receptor sensitivity to APO in individually housed mice.

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“…Amphetamine becomes available in the brain within minutes following an i.p. injection (Riffee and Wilcox, 1985) and, therefore, we chose a time point of 2 h after amphetamine injection to test for changes in the AMPAR/NMDAR ratio. At 2 h following amphetamine injections, we prepared acute slices from those animals with a locomotor response greater than 120 ambulation counts/hour, (Figure 5a).…”

Section: Resultsmentioning

confidence: 99%

Rapid Synaptic Plasticity of Glutamatergic Synapses on Dopamine Neurons in the Ventral Tegmental Area in Response to Acute Amphetamine Injection

Faleiro

Jones

Kauer

2004

Neuropsychopharmacol

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Drugs of abuse activate the reward circuitry of the mesocorticolimbic system, and it has been hypothesized that drug exposure triggers synaptic plasticity of glutamatergic synapses onto dopamine (DA) neurons of the ventral tegmental area. Here, we show that just a 2 h in vivo exposure to amphetamine is sufficient to potentiate these synapses, measured as an increase in the synaptic AMPAR/NMDAR ratio. We tested the prediction that an increase in GluR1-containing AMPA receptors would result in an increase in GluR1 homomeric receptors at synapses, but were unable to observe any evidence of the predicted rectification in DA neurons from animals treated with amphetamine. We also examined the possibility of increased AMPA receptor insertion in the membrane, but did not detect a significant increase in biotinylated surface GluR1. We conclude that amphetamine induces rapid changes in synaptic AMPAR/NMDAR ratios, suggesting that potentiation of glutamatergic synapses is a relatively early event in the series of neuroadaptations in response to drugs of abuse.

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Effects of multiple pretreatment with apomorphine and amphetamine on amphetamine-induced locomotor activity and its inhibition by apomorphine

Cited by 28 publications

References 14 publications

Lack of sensitization to the effects of d -amphetamine and apomorphine on sensorimotor gating in rats

Lack of sensitization to the effects of d -amphetamine and apomorphine on sensorimotor gating in rats

Behavioral and biochemical studies of dopamine receptor sensitivity in differentially housed mice

Rapid Synaptic Plasticity of Glutamatergic Synapses on Dopamine Neurons in the Ventral Tegmental Area in Response to Acute Amphetamine Injection

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