Long-term effects of postnatal amphetamine treatment on striatal protein kinase A activity, dopamine D1-like and D2-like binding sites, and dopamine content

Crawford, Cynthia A.; Zavala, Arturo R.; Karper, Patrick E.; McDougall, Sanders A.

doi:10.1016/s0892-0362(00)00109-4

Cited by 10 publications

(9 citation statements)

References 30 publications

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“…We previously hypothesized that psychostimulant-induced decreases in dorsal striatal PKA activity were due to either a down-regulation of DA D 1 receptors (which are coupled to G s G proteins) or an up-regulation of DA D 2 receptors (which are coupled to G i G proteins). This explanation is probably incorrect because PKA activity shows robust drug-induced declines despite inconsistent changes in dopamine receptor density (Crawford et al, 2000b(Crawford et al, , 2003. Instead, we hypothesize that psychostimulant-induced decreases in PKA activity are due to altered receptor sensitivity caused by changes in receptor/G protein coupling.…”

Section: Discussionmentioning

confidence: 83%

Neonatal 3,4-methylenedioxymethamphetamine (MDMA) exposure alters neuronal protein kinase A activity, serotonin and dopamine content, and [35S]GTPγS binding in adult rats

et al. 2006

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Recreational use of methylenedioxymethamphetamine (MDMA) has dramatically increased among juveniles and young adults of child-bearing age, and the potential for fetal exposure has increased. For this reason, it is surprising that comparatively few studies have assessed the long-term impact of early MDMA exposure on serotonin (5-HT) and dopamine (DA) neurotransmitter systems. The purpose of this study was to determine whether repeated exposure to MDMA during the preweanling period would cause long-term changes in 5-HT and DA functioning. Rats were treated with saline or 20 mg/kg MDMA (two injections per day) from postnatal day (PD) 11-20. At PD 90, rats were killed, and their dorsal striatum, prefrontal cortex, and hippocampus were removed. 5-HT and DA content, as well as their metabolites, were measured using HPLC. In addition, cAMP-dependent protein kinase A (PKA) activity and agonist-stimulated [ 35 S]GTPγS binding was assayed using tissue homogenates from each brain region. Results indicated that early MDMA exposure caused a decrease in PKA activity and 5-HT content in the prefrontal cortex and hippocampus while increasing the efficacy of 5-HT 1A receptors as measured by agonist-stimulated [ 35 S]GTPγS binding. Additionally, DA content was reduced in the dorsal striatum and prefrontal cortex. These data indicate that early MDMA exposure has long-term effects on the 5-HT and DA neurotransmitter systems that may be mediated, at least partially, by changes in 5-HT 1A receptor sensitivity.

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Section: Discussionmentioning

confidence: 83%

Neonatal 3,4-methylenedioxymethamphetamine (MDMA) exposure alters neuronal protein kinase A activity, serotonin and dopamine content, and [35S]GTPγS binding in adult rats

et al. 2006

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“…Although preweanling METH or AMPH exposure causes long-term reductions in PKA activity, the exact mechanism responsible for this effect has yet to be determined. Previously, we hypothesized that a psychostimulant-induced increase in D 2 -like receptors may have caused the persistent decline in PKA activity (Crawford et al, 2000b). This idea was based on studies showing that the cAMP-dependent PKA pathway is negatively coupled to D 2 -like receptors (Kebabian and Calne, 1979;Sibley and Monsma, 1992).…”

Section: Discussionmentioning

confidence: 99%

“…The purpose of this study, therefore, was to determine whether repeated exposure to METH (10 mg/kg ϫ 4 injections per day) during the preweanling period causes reductions in PKA activity that are still detectable in adulthood. DA content and D 2 -like binding sites were also assessed, because preweanling AMPH treatment has been shown to decrease striatal DA levels while increasing the number of D 2 -like receptors (Crawford et al, 2000b). If preweanling METH exposure does cause long-term reductions in PKA activity, then it is possible that behavioral deficits exhibited by METH-exposed rats are due to altered functioning of PKA-dependent transduction mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Methamphetamine exposure during the preweanling period causes prolonged changes in dorsal striatal protein kinase A activity, dopamine D₂‐like binding sites, and dopamine content

Crawford¹,

Williams²,

Newman³

et al. 2003

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Exposure to methamphetamine (METH) during the preweanling period produces few, if any, neurotoxic effects (using criteria established in adult rats), yet it has substantial long-term effects on a variety of behavioral measures (e.g., locomotor activity, acoustic startle response, and spatial learning). The purpose of the present study was to examine the long-term changes in dopaminergic functioning brought about by early METH exposure. Rats were injected with METH (10 mg/kg) or saline four times daily on postnatal days (PD) 11-20 and housed undisturbed until PD 90, at which time they were killed and their dorsal striata (i.e., caudate-putamen) were removed and frozen for assay. The ability of early METH exposure to alter protein kinase A (PKA) activity and dopamine (DA) D(2)-like binding sites, as well as DA and DOPAC content, were assessed. Results showed that METH exposure on PD 11-20 caused long-term reductions in all of the dopaminergic markers assayed. METH-induced reductions in DA content and D(2)-like receptors were observed. Some sex differences were apparent, as the METH-induced decreases in PKA activity and DOPAC content were more evident in male rats. In conclusion, preweanling METH exposure caused changes in DA markers that were still detectable at PD 90; however the magnitude of many of these effects (e.g., the reductions in DA and DOPAC levels) was substantially less than typically reported for rats treated with METH in adulthood. The ability of METH to cause long-term reductions in PKA activity may partially account for some of behavioral deficits exhibited by rats exposed to METH prior to weaning.

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“…The pieces of foil (containing brain slices) were coded to ensure the dopamine analysis was performed blind. Following the procedure of Crawford et al (2000), frozen slices were sonicated in 10 volumes of 0.1 N HClO 4 and then centrifuged at 20,000 ′ g for 20 min at 4°C. The supernatant was then filtered through a 0.22 mm centrifugation unit for 5 min at 2,000 ′ g at 4°C.…”

Section: Methodsmentioning

confidence: 99%

Decreased Striatal Dopamine Release Underlies Increased Expression of Long-Term Synaptic Potentiation at Corticostriatal Synapses 24 h after 3-Nitropropionic-Acid-Induced Chemical Hypoxia

Akopian¹,

Crawford²,

Beal³

et al. 2008

J. Neurosci.

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The striatum is particularly sensitive to the irreversible inhibitor of succinate dehydrogenase 3-nitropropionic acid (3-NP). In the present study, we examined early changes in behavior and dopamine and glutamate synaptic physiology created by a single systemic injection of 3-NP in Fischer 344 rats. Hindlimb dystonia was seen 2 h after 3-NP injections, and rats performed poorly on balance beam and rotarod motor tests 24 h later.

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Long-term effects of postnatal amphetamine treatment on striatal protein kinase A activity, dopamine D1-like and D2-like binding sites, and dopamine content

Cited by 10 publications

References 30 publications

Neonatal 3,4-methylenedioxymethamphetamine (MDMA) exposure alters neuronal protein kinase A activity, serotonin and dopamine content, and [35S]GTPγS binding in adult rats

Neonatal 3,4-methylenedioxymethamphetamine (MDMA) exposure alters neuronal protein kinase A activity, serotonin and dopamine content, and [35S]GTPγS binding in adult rats

Methamphetamine exposure during the preweanling period causes prolonged changes in dorsal striatal protein kinase A activity, dopamine D₂‐like binding sites, and dopamine content

Decreased Striatal Dopamine Release Underlies Increased Expression of Long-Term Synaptic Potentiation at Corticostriatal Synapses 24 h after 3-Nitropropionic-Acid-Induced Chemical Hypoxia

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Long-term effects of postnatal amphetamine treatment on striatal protein kinase A activity, dopamine D1-like and D2-like binding sites, and dopamine content

Cited by 10 publications

References 30 publications

Neonatal 3,4-methylenedioxymethamphetamine (MDMA) exposure alters neuronal protein kinase A activity, serotonin and dopamine content, and [35S]GTPγS binding in adult rats

Neonatal 3,4-methylenedioxymethamphetamine (MDMA) exposure alters neuronal protein kinase A activity, serotonin and dopamine content, and [35S]GTPγS binding in adult rats

Methamphetamine exposure during the preweanling period causes prolonged changes in dorsal striatal protein kinase A activity, dopamine D2‐like binding sites, and dopamine content

Decreased Striatal Dopamine Release Underlies Increased Expression of Long-Term Synaptic Potentiation at Corticostriatal Synapses 24 h after 3-Nitropropionic-Acid-Induced Chemical Hypoxia

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Methamphetamine exposure during the preweanling period causes prolonged changes in dorsal striatal protein kinase A activity, dopamine D₂‐like binding sites, and dopamine content