The crossed mesostriatal projection: neurochemistry and developmental response to lesion

Altar, Anthony; Neve, Kim A.; Loughlin, Sandra E.; Marshall, John F.; Fallon, James H.

doi:10.1016/0006-8993(83)90157-9

Cited by 50 publications

(16 citation statements)

References 26 publications

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“…Tile reductions in striatal dopamine levels following either nigral or intrastriatal 6-OHDA are in agreement with the results of others Marshall et al, 1983;Altar et al, 1983;Neve et al, 1982;. Since local depletion ofstriatal dopamine lowered spontaneous MUA and antagonized the dexamphetamineinduced increase in MUA, it is apparent that depletion ofdopamine within the striatum is by itself sufficient to abolish excitatory responses to dexamphetamine.…”

Section: Discussionsupporting

confidence: 90%

Activation of striatal neurons by dexamphetamine is antagonized by degeneration of striatal dopaminergic terminals

Warenycia

McKenzie

1987

J. Neural Transmission

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Unilateral degeneration of nigrostriatal dopaminergic terminals by the intranigral infusion of 6-OHDA produced a decrease in spontaneous multiple unit activity (MUA) in both the ipsilateral and contralateral striata of freely moving rats. Nigral lesions also attenuated the dexamphetamine-induced increase in MUA in the ipsilateral but not in the contralateral striatum. The magnitude of the attenuation in the ipsilateral striatum was directly proportional to the percent depletion of dopamine. Similarly degeneration of dopaminergic terminals produced by a unilateral application of 6-OHDA into the striatum lowered spontaneous MUA and completely antagonized the dexamphetamine-induced increase in MUA in the dopamine-depleted striatum. Although the spontaneous MUA in striata contralateral to a local 6-OHDA treatment was significantly reduced, the response to dexamphetamine was normal. Both striatal and nigral application of 6-OHDA produced dopamine depletion in the ipsilateral striatum and an increase in striatal dopamine levels on the contralateral side. Striatal application of 6-OHDA did not alter dopamine levels in either the olfactory tubercles, piriform cortex or cingulate cortex. It is concluded that the increase in MUA observed in the striatum following dexamphetamine treatment is critically dependent upon the release of dopamine in the striatum. These results support the concept that dopamine may have an excitatory action on some striatal neurons.

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Section: Discussionsupporting

confidence: 90%

Activation of striatal neurons by dexamphetamine is antagonized by degeneration of striatal dopaminergic terminals

Warenycia

McKenzie

1987

J. Neural Transmission

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“…Although some NMDA receptors may be located on nigrostriatal dopamine terminals (Krebs et al, 1991) the size of the crossed nigrostriatal pathway appears to be too small to account for the magnitude of the receptor changes (Altar et al, 1983). In contrast, unilateral electrical stimulation of SNr produces a bilateral 25-30% increase in striatal glucose utilization (Savaki et al, 1983) that is similar in magnitude to the 30% reduction in NMDA receptors we found.…”

Section: Discussionmentioning

confidence: 99%

Polysynaptic regulation of glutamate receptors and mitochondrial enzyme activities in the basal ganglia of rats with unilateral dopamine depletion

et al. 1994

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After nigrostriatal dopaminergic denervation, the output nuclei of the basal ganglia, the medial globus pallidus and substantia nigra pars reticulata (Snr), become overactive, in part, because of increased activity of excitatory afferents from the subthalamic nucleus (STN). Because STN uses glutamate as a transmitter, we examined whether there are regulatory changes in glutamate receptor binding in the basal ganglia. Rats received unilateral 6-hydroxydopamine lesions of the medial forebrain bundle and substantia nigra pars compacta that were confirmed by apomorphine-induced rotation and 3H-GBR-12935 binding. As an indirect index of relative synaptic activity, succinate dehydrogenase and cytochrome oxidase activities were assayed histochemically in sections adjacent to those used for receptor binding. There were increases in enzymatic activity in entopeduncular nucleus (EP; the rodent homolog of medial globus pallidus), SNr, and globus pallidus (GP, the rodent homolog of lateral globus pallidus) in the lesioned hemisphere, suggesting increased synaptic activity, perhaps due to increased firing of the STN. Ipsilateral to the lesion, and postsynaptic to the STN, there were profound decreases in the binding of 3H-AMPA (alpha-amino-3-hydroxy-5-methylisoxazole propionic acid) in EP and SNr (45% and 30%, respectively); there were no alterations in the striatum, globus pallidus, or STN, and binding throughout the unlesioned hemisphere was equivalent to that in unlesioned control animals. In contrast, 3H-MK-801 binding to the NMDA receptor ion channel was not reduced in SNr, and was too low to be measured reliably in EP and STN. 3H-MK-801 binding was reduced by 6% in striatum and 39% in globus pallidus.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Approximately 1–3% of the DA fibers reaching the striatum come from the contralateral SNc, the VTA and the posterior lateral hypothalamic area (Veening et al, 1980; Gerfen et al, 1982; Swanson, 1982; Altar et al, 1983; Fallon et al, 1983; Consolazione et al, 1985; Lieu and Subramanian, 2012). Less than 10% of the VTA efferents cross the midline to the contralateral side (Swanson, 1982) where they give rise to about 8% of the fibers reaching the NAc and about 1–3% of the fibers reaching the dStr (Carter and Fibiger, 1977; Altar et al, 1983; Douglas et al, 1987).…”

Section: Anatomy and Connectivitymentioning

confidence: 99%

Hemispheric differences in the mesostriatal dopaminergic system

Molochnikov

Cohen

2014

Front. Syst. Neurosci.

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The mesostriatal dopaminergic system, which comprises the mesolimbic and the nigrostriatal pathways, plays a major role in neural processing underlying motor and limbic functions. Multiple reports suggest that these processes are influenced by hemispheric differences in striatal dopamine (DA) levels, DA turnover and its receptor activity. Here, we review studies which measured the concentration of DA and its metabolites to examine the relationship between DA imbalance and animal behavior under different conditions. Specifically, we assess evidence in support of endogenous, inter-hemispheric DA imbalance; determine whether the known anatomy provides a suitable substrate for this imbalance; examine the relationship between DA imbalance and animal behavior; and characterize the symmetry of the observed inter-hemispheric laterality in the nigrostriatal and the mesolimbic DA systems. We conclude that many studies provide supporting evidence for the occurrence of experience-dependent endogenous DA imbalance which is controlled by a dedicated regulatory/compensatory mechanism. Additionally, it seems that the link between DA imbalance and animal behavior is better characterized in the nigrostriatal than in the mesolimbic system. Nonetheless, a variety of brain and behavioral manipulations demonstrate that the nigrostriatal system displays symmetrical laterality whereas the mesolimbic system displays asymmetrical laterality which supports hemispheric specialization in rodents. The reciprocity of the relationship between DA imbalance and animal behavior (i.e., the capacity of animal training to alter DA imbalance for prolonged time periods) remains controversial, however, if confirmed, it may provide a valuable non-invasive therapeutic means for treating abnormal DA imbalance.

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The crossed mesostriatal projection: neurochemistry and developmental response to lesion

Cited by 50 publications

References 26 publications

Activation of striatal neurons by dexamphetamine is antagonized by degeneration of striatal dopaminergic terminals

Activation of striatal neurons by dexamphetamine is antagonized by degeneration of striatal dopaminergic terminals

Polysynaptic regulation of glutamate receptors and mitochondrial enzyme activities in the basal ganglia of rats with unilateral dopamine depletion

Hemispheric differences in the mesostriatal dopaminergic system

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