5-hydroxydopamine-labeled dopaminergic axns: Three-dimensional reconstructions of axons, synapses and postsynaptic targets in rat neostriatum

Groves, Philip M.; Linder, Jean C.; Young, Stephen J.

doi:10.1016/0306-4522(94)90084-1

Cited by 128 publications

(93 citation statements)

References 52 publications

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“…These are strategic locations for D1Rs, since dopaminergic terminals preferentially contact dendritic spine necks (Sesack and Pickel, 1990;Groves et al, 1994). Accordingly, many D1R immunogold particles on spine necks were apposed by small unlabeled axonal profiles, characteristic of dopaminergic terminals (Groves et al, 1994;Pickel et al, 1996). The APO +AS group also had a significantly higher number of D1R-labeled spines compared to the VEH +AS group, without a significant change in the total (labeled and unlabeled) number of spines.…”

Section: Apomorphine-and As-induced Changes In D1r Distribution In Thmentioning

confidence: 95%

“…The main finding in the core, however, was that the VEH+AS group had smaller D1R-labeled dendrites compared with APO, VEH or APO+AS. One interpretation of this data is a movement of D1Rs from medium to smaller, more distal dendrites, where dopaminergic inputs are known to terminate (Groves et al, 1994). Unlike the Acb shell, the dopaminergic inputs to the Acb core principally originate from the substantia nigra pars compacta, which is associated with motor response (Brog et al, 1993;David et al, 2004).…”

Section: As-induced Changes In Dendritic D1r Distribution In the Acb mentioning

confidence: 96%

“…D1R immunogold particles in the APO+AS group were often located on extrasynaptic plasma membranes of spine necks. These are strategic locations for D1Rs, since dopaminergic terminals preferentially contact dendritic spine necks (Sesack and Pickel, 1990;Groves et al, 1994). Accordingly, many D1R immunogold particles on spine necks were apposed by small unlabeled axonal profiles, characteristic of dopaminergic terminals (Groves et al, 1994;Pickel et al, 1996).…”

Section: Apomorphine-and As-induced Changes In D1r Distribution In Thmentioning

confidence: 99%

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Dendritic distributions of dopamine D1 receptors in the rat nucleus accumbens are synergistically affected by startle-evoking auditory stimulation and apomorphine

Hara

Pickel

2007

Neuroscience

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Prepulse inhibition of the startle response to auditory stimulation (AS) is a measure of sensorimotor gating that is disrupted by the dopamine D1/D2 receptor agonist, apomorphine. The apomorphine effect on prepulse inhibition is ascribed in part to altered synaptic transmission in the limbicassociated shell and motor-associated core subregions of the nucleus accumbens (Acb). We used electron microscopic immunolabeling of dopamine D1 receptors (D1Rs) in the Acb shell and core to test the hypothesis that region-specific redistribution of D1Rs is a short-term consequence of AS and/or apomorphine administration. Thus, comparisons were made in the Acb of rats sacrificed one hour after receiving a single subcutaneous injection of vehicle (VEH) or apomorphine (APO) alone or in combination with startle-evoking AS (VEH+AS, APO+AS). In both regions of all animals, the D1R immunoreactivity was present in somata and large, as well as small, presumably more distal dendrites and dendritic spines. In the Acb shell, compared with the VEH+AS group, the APO+AS group had more spines containing D1R immunogold particles, and these particles were more prevalent on the plasma membranes. This suggests movement of D1Rs from distal dendrites to the plasma membrane of dendritic spines. Small-and medium-sized dendrites also showed a higher plasmalemmal density of D1R in the Acb shell of the APO+AS group compared with the APO group. In the Acb core, the APO+AS group had a higher plasmalemmal density of D1R in medium-sized dendrites compared with the APO or VEH+AS group. Also in the Acb core, D1R-labeled dendrites were significantly smaller in the VEH+AS group compared to all other groups. These results suggest that alerting stimuli and apomorphine synergistically affect distributions of D1R in Acb shell and core. Thus adaptations in D1R distribution may contribute to sensorimotor gating deficits that can be induced acutely by apomorphine or develop over time in schizophrenia.

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Section: Apomorphine-and As-induced Changes In D1r Distribution In Thmentioning

confidence: 95%

Section: As-induced Changes In Dendritic D1r Distribution In the Acb mentioning

confidence: 96%

Section: Apomorphine-and As-induced Changes In D1r Distribution In Thmentioning

confidence: 99%

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Dendritic distributions of dopamine D1 receptors in the rat nucleus accumbens are synergistically affected by startle-evoking auditory stimulation and apomorphine

Hara

Pickel

2007

Neuroscience

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“…With strong influences on corticostriatal synaptic efficacy and striatal function, dopamine is one such putative factor. Nigrostriatal dopaminergic fibers densely innervate the striatum (Bjorklund and Hokfelt, 1984), and both dopaminergic and corticostriatal glutamatergic afferent axons synapse onto target medium spiny neurons (Bouyer et al, 1984,Groves et al, 1994,Smith et al, 1994,Centonze et al, 2003b. Within the striatum, dopamine is instrumental in determining the efficacy of glutamatergic signaling at corticostriatal synapses (Centonze et al, 1999,Centonze et al, 2001,Cepeda et al, 2001,West et al, 2003, and striatal dopamine-glutamate interactions may play a role in the re-formation of behaviorally relevant functional connections after cortical injury.…”

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confidence: 99%

Intrastriatal dopamine D1 antagonism dampens neural plasticity in response to motor cortex lesion

2007

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Motor cortex lesions in rats partially denervate the striatum, producing behavioral deficits and inducing reactive neuroplasticity. Plastic responses include changes in growth-associated protein marker expression and anatomical restructuring. Corticostriatal plasticity is dependent on dopamine at the striatal target, where D1 receptor signaling reinforces behaviorally relevant neural activity. To determine whether striatal dopamine D1 receptor signaling is important for the growth-associated protein responses and behavioral recovery that follow unilateral motor cortex aspiration, the dopamine D1 receptor antagonist SCH23390 was intrastriatally infused in cortically lesioned animals. After a cortical aspiration lesion in Long Evans rats, the growth-associated proteins SCG10 and GAP-43 were upregulated in the cortex contralateral to the lesion at 30 days post-lesion. However, continuous unilateral intrastriatal infusion of SCH23390 prevented this aspiration-induced upregulation. Furthermore, lesioned rats demonstrated spontaneous sensorimotor improvement, in terms of limb-use symmetry, about one month post-lesion. This improvement was prevented with chronic intrastriatal SCH23390 infusion. The D1 receptor influence may be important to normalize corticostriatal activity (and observable behavior), either in a long-term manner or temporarily until other more permanent means of synaptic regulation, such as sprouting or synaptogenesis, may be implemented. Keywords cortical ablation; striatum; SCH23390The ability to reorganize neural connections according to changing environmental cues is essential to the formation of the wide network of limbic, striatal, and cortical circuits that regulate the complex array of human behaviors. Generally referred to as neural plasticity, these adaptive processes are most obvious in the developing brain, but are also utilized throughout adulthood as new skills and memories are acquired. Likewise, when the brain is damaged by trauma or disease, adaptive mechanisms of plasticity are brought into play and are critical for determining the limits of functional recovery (Ivanco and Greenough, 2000,Johansson, 2000,Nudo et al., 2001,Gonzalez and Kolb, 2003. These adaptive processes are governed by local extra-and intracellular signals and can be manipulated by various experimental interventions including: exercise (Cotman and Berchtold, 2002,Gomez-Pinilla et al., 2002) Tel: 323-442-2126; Fax: 323-442-2127. E-mail address: elizabjd@usc.edu Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. (van Praag et al., 2000), motor skills training (Plautz et a...

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“…11,34 A large fraction of the mesencephalic dopaminergic neurons are located in the substantia nigra pars compacta, which projects via the medial forebrain bundle (MFB) to the neostriatum, where dopaminergic terminals synapse on medium spiny neurons as well as on interneurons. 18,28,39,40,45 Although most dopaminergic neurons appear to be spontaneously active, it has been widely reported that a significant fraction are silent in vivo under normal conditions. 6,9,10,30,33,43,55 This concept was originally introduced in an in vivo extracellular recording study of the effects of the neuroleptic drug, haloperidol, on substantia nigra dopaminergic neurons.…”

mentioning

confidence: 99%

Do silent dopaminergic neurons exist in rat substantia nigra in vivo?

Dai

Tepper

1998

Neuroscience

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5-hydroxydopamine-labeled dopaminergic axns: Three-dimensional reconstructions of axons, synapses and postsynaptic targets in rat neostriatum

Cited by 128 publications

References 52 publications

Dendritic distributions of dopamine D1 receptors in the rat nucleus accumbens are synergistically affected by startle-evoking auditory stimulation and apomorphine

Dendritic distributions of dopamine D1 receptors in the rat nucleus accumbens are synergistically affected by startle-evoking auditory stimulation and apomorphine

Intrastriatal dopamine D1 antagonism dampens neural plasticity in response to motor cortex lesion

Do silent dopaminergic neurons exist in rat substantia nigra in vivo?

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