The effect of reserpine treatment in vivo upon L-dopa and amphetamine evoked dopamine and DOPAC efflux in vitro from the corpus striatum of male rats

Dluzen, Dean E.; Liu, B.

doi:10.1007/bf01271567

Cited by 11 publications

(8 citation statements)

References 40 publications

(29 reference statements)

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“…These results contrast with studies in reserpinized rats, where NSD-1015 decreased striatal decarboxylation of L-DOPA to dopamine, while extending the behavioural effect (Fisher et al 2000). However, their methodology is different from the present study, as reserpine affects only vesicular storage of dopamine (Dluzen & Liu, 1994). Several authors also report a discrepancy between the quantities of DA recovered by brain dialysis and the intensity of the motor response produced by L-DOPA (Spencer & Wooten, 1984;Zetterstrom et al, 1986;Nakazoto & Akiyama, 1989).…”

Section: Discussioncontrasting

confidence: 93%

“…2000). However, their methodology is different from the present study, as reserpine affects only vesicular storage of dopamine (Dluzen & Liu, 1994). Several authors also report a discrepancy between the quantities of DA recovered by brain dialysis and the intensity of the motor response produced by l ‐DOPA (Spencer & Wooten, 1984; Zetterstrom et al ., 1986; Nakazoto & Akiyama, 1989).…”

Section: Discussionmentioning

confidence: 99%

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The central aromatic amino acid DOPA decarboxylase inhibitor, NSD‐1015, does not inhibit l‐DOPA‐induced circling in unilateral 6‐OHDA‐lesioned‐rats

Treseder

Rose

Jenner

2001

Eur J of Neuroscience

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The centrally acting aromatic amino acid dopa decarboxylase (AADC) inhibitor, 3-hydroxybenzyl hydrazine (NSD-1015), is widely used to study the neurotransmitter-like actions of L-DOPA. However, the effects of NSD-1015 on L-DOPA-induced motor activity are unclear as both increases and decreases have been reported. We now investigate the effects of NSD-1015 on L-DOPA-induced contralateral circling behaviour in 6-OHDA-lesioned rats and on striatal levels of L-DOPA, 3-O-methyl-DOPA (3-OMD), dopamine, dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) using microdialysis techniques. NSD-1015 (50-200 mg/kg i.p.) inhibited AADC activity both in the liver and striatum of normal rats. Administration of NSD-1015 (50-200 mg/kg i.p.), delayed the onset of circling produced by administration of L-DOPA (25 mg/kg i.p.) and carbidopa (12.5 mg/kg i. p.), suggesting blockade of central AADC activity. However, the duration of the L-DOPA-induced circling was prolonged and overall no inhibition of circling behaviour occurred. L-DOPA (25 mg/kg i.p.) plus carbidopa (12.5 mg/kg i.p.) increased extracellular levels of L-DOPA, 3-OMD, dopamine, DOPAC and HVA in the 6-OHDA-lesioned striatum. Pretreatment of rats with the central AADC inhibitor, NSD-1015 (100 mg/kg i.p.), potentiated the increase in dialysate levels of L-DOPA and 3-OMD. However, it did not reduce striatal dopamine levels in the 6-OHDA-lesioned hemisphere, which were elevated following L-DOPA administration. The increases in DOPAC and HVA levels were abolished by NSD-1015 pretreatment. These results suggest that, while NSD-1015 blocks central AADC activity, it also acts as a monoamine oxidase inhibitor so maintaining striatal dopamine concentration by reducing dopamine metabolism. NSD-1015, therefore, may not be an appropriate tool for the study of brain AADC activity and for assessing the neuromodulatory role of L-DOPA.

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Section: Discussioncontrasting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

The central aromatic amino acid DOPA decarboxylase inhibitor, NSD‐1015, does not inhibit l‐DOPA‐induced circling in unilateral 6‐OHDA‐lesioned‐rats

Treseder

Rose

Jenner

2001

Eur J of Neuroscience

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“…Thus, a lack of effect of the mGlu2/3-receptor agonists on these levels indicates that dynamics of dopamine reuptake or vesicular storage, two processes that are disrupted by amphetamine (Sulzer et al 1995), are not targeted by these agonists. Amphetamine may also influence dopamine synthesis (Patrick et al 1981); however, we found that increasing extracellular levels of dopamine by L-dopa, which primarily is due to increasing pools of newly synthesized dopamine (Dluzen and Liu 1994), was not affected by mGlu2/3 receptor activation suggesting that these receptors do not influence packaging and release of newly synthesized dopamine.…”

Section: Discussionmentioning

confidence: 74%

“…Thus, low doses of amphetamine may release dopamine preferentially from the newly synthesized cytosolic dopamine pool; whereas, higher doses release dopamine from new and older pools of dopamine. Here we observed that mGlu2/3 receptor activation significantly reduces amphetamine-induced dopamine release, but has no effect on dopamine release evoked by the dopamine precursor L-dopa, which is insensitive to reserpine treatment and thus is derived from a newly synthesized pool (Dluzen and Liu 1994). This result is consistent with a recent paper showing that activation of mGlu 2/3 receptors has no effect on the rate of dopamine synthesis in reserpine-treated rats (Fell et al 2009).…”

Section: Discussionmentioning

confidence: 84%

Impact of metabotropic glutamate 2/3 receptor stimulation on activated dopamine release and locomotion

Pehrson

Moghaddam

2010

Psychopharmacology

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Rationale-Activation of metabotropic glutamate (mGlu) 2/3 receptors may provide a novel strategy for treating schizophrenia. This effect is thought to be mediated through dopamineindependent mechanisms because mGlu2/3-receptor agonists have no considerable affinity for dopamine receptors. These agonists, however, reduce amphetamine-induced hyperlocomotion suggesting that they influence dopamine neurotransmission.Objective-We evaluated whether the inhibitory effect of mGlu2/3-receptor activation on amphetamine-induced hyper-locomotion correlates with attenuated dopamine release. We also assessed whether mGlu 2/3 receptor activation has inhibitory effects on activity-dependent vesicular release of dopamine in behaving animals.Methods-Microdialysis was used to measure extracellular levels of dopamine in the dorsal striatum (DStr) and nucleus accumbens (NAc) of freely moving rats. The effect of the mGlu2/3-receptor agonist LY354740 on dopamine release and locomotion elicited by amphetamine, electrical stimulation of the ventral tegmental area, or L-dopa was assessed.Results-We find that the inhibitory effect of mGlu2/3 activation on amphetamine-induced hyperlocomotion correlates with an attenuated increase in dopamine release in the NAc and DStr. However, when dopamine levels were increased by electrical stimulation of dopamine neurons or by administration of the dopamine precursor L-dopa, activation of mGlu2/3 receptors had no effect on dopamine release or on behavior.Conclusions-Activation of mGlu2/3 receptors attenuates amphetamine-induced dopamine release through a mechanism that does not affect activity dependent vesicular release, reuptake or synthesis of dopamine.

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“…Finally, at high doses, amphetamine redistributes DA from the vesicular to the cytoplasmic pool (Sulzer et aI., 1993; Sulzer et aI., 1995). Thus, reserpine pretreat ment affects amphetamine-induced DA release, at least after high doses of amphetamine (Dluzen and Liu, 1994; Cadoni et aI., 1995; Florin et aI., 1995; Pift et aI., 1995). (1988) showed that pretreatment with the DAT blocker GBR 12909 blocked the effect of amphetamine on [ I I C Jraclo pride BP, as measured during radiotracer constant infu sion paradigm.…”

mentioning

confidence: 99%

Imaging Synaptic Neurotransmission within VivoBinding Competition Techniques: A Critical Review

Laruelle

2000

J Cereb Blood Flow Metab

910

756

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Summary: Several groups have provided evidence that posi tron emission tomography (PET) and single-photon emission computed tomography (SPECT) neuroreceptor imaging tech niques might be applied to measure acute t1uctuations in do pamine (OA) synaptic concentration in the living human brain. Competition between OA and radioligands for binding to O2 receptor is the principle underlying this approach. This new application of neuroreceptor imaging provides a dynamic mea surement of neurotransmission that is likely to be informative to our understanding of neuropsychiatric conditions. This ar ticle reviews and discusses the body of data supporting the feasibility and potential of this imaging paradigm. Endogenous competition studies performed in rodents, nonhuman primates, and humans are first summarized. After this overview, the va lidity of the model underlying the interpretation of these im aging data is critically assessed. The current reference model is defined as the occupancy model, since changes in radiotracer binding potential (BP) are assumed to be directly caused by changes in occupancy of O2 receptors by OA. Experimental data supporting this model are presented. The evidence that manipulation of OA synaptic levels induces change in the BP of several O2 radiotracers (catecholamines and benzamides) is unequivocal. The fact that these changes in BP are mediated by changes in OA synaptic concentration is well documented. The relationship between the magnitude of BP changes measured with PET or SPECT and the magnitude of changes in OA concentration measured by microdialysis supports the use of these noninvasive techniques to measure changes in neuro transmission. On the other hand, several observations remain unexplained. First, the amphetamine-induced changes in the BP of O2 receptor antagonists [1 2 3IJIBZM and [I I Clraclopride last longer than amphetamine-induced changes in OA extracellular concentration. Second, nonbenzamide O2 receptor antagonists, such as spiperone and pimozide, are not affected by changes in OA release, or are affected in a direction opposite to that pre dicted by the occupancy model. Similar observations are re ported with 0 I radiotracers. These results suggest that the changes in BP following changes in OA concentration might not be fully accounted by a simple occupancy model. Specifi cally, the data are reviewed supporting that agonist-mediated receptor internalization might play an important role in char acterizing receptor-ligand interactions. Finally, it is proposed that a better understanding of the mechanism underlying the effects observed with benzamides is essential to develop this imaging technique to other receptor systems. Key Words: Pos itron emission tomography-Single-photon emission computed tomography-Oopamine-Raclopride-IBZM-Spiperone Internalization.Received August 2S, 1999; final revision received December 3, 1999; accepted December 3, 1999. Supported by the National Institute of Mental Health (K02 MHO I 603-0 1). Address correspondence and reprint requests to Ma...

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The effect of reserpine treatment in vivo upon L-dopa and amphetamine evoked dopamine and DOPAC efflux in vitro from the corpus striatum of male rats

Cited by 11 publications

References 40 publications

The central aromatic amino acid DOPA decarboxylase inhibitor, NSD‐1015, does not inhibit l‐DOPA‐induced circling in unilateral 6‐OHDA‐lesioned‐rats

The central aromatic amino acid DOPA decarboxylase inhibitor, NSD‐1015, does not inhibit l‐DOPA‐induced circling in unilateral 6‐OHDA‐lesioned‐rats

Impact of metabotropic glutamate 2/3 receptor stimulation on activated dopamine release and locomotion

Imaging Synaptic Neurotransmission within VivoBinding Competition Techniques: A Critical Review

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