Striatal axons to the globus pallidus, entopeduncular nucleus and substantia nigra come mainly from separate cell populations in cat

Beckstead, Robert M.; Cruz, Calvin J.

doi:10.1016/0306-4522(86)90012-6

Cited by 147 publications

(67 citation statements)

References 58 publications

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“…Clozapine 2 :: I 50 msec the accumbens shell region (Beckstead et al, 1979;Phillipson and Griffiths, 1985;Voom et al, 1986;Zahm, 1991). Since these measures were made following a 36 hr drug washout, we also performed a limited number of recordings on a subset of rats treated for 1 month with haloperidol, and confirmed that the DA cells were still in a nonfiring state under these conditions (unpublished observations).…”

Section: Differential Modulation Of Dye Coupling By Typical Versus Atsupporting

confidence: 53%

Repeated treatment with haloperidol and clozapine exerts differential effects on dye coupling between neurons in subregions of striatum and nucleus accumbens

Onn

Grace

1995

J. Neurosci.

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The delayed onset of action of antipsychotic drugs (APDs) during the treatment of schizophrenia has been hypothesized to temporally correlate with the induction of depolarization block in rat mesencephalic dopamine (DA) cell groups. Nevertheless, it is unknown whether these drugs also exert a delayed action on the dopaminoceptive postsynaptic target cells in the striatal complex. Using in vivo intracellular recording and dye labeling techniques, the effects of APDs on dye coupling were examined in subregions of the striatal complex defined by double staining for calbindin immunoreactivity. Rats treated repeatedly with APDs were found to exhibit a 66–71% higher incidence of coupling that occurred in a drug- and a region-specific manner, that is, both drug treatments increased dye coupling in the limbic-associated accumbens shell region whereas only haloperidol increased dye coupling in the motor-related striatal matrix and accumbens core regions. In addition, cells located in regions in which dye coupling was altered also showed significantly higher input resistance. These changes were not observed in response to DA receptor blockade by acute drug administration or when haloperidol was administered for a period sufficient to induce DA receptor supersensitivity but not DA cell depolarization block (i.e., 2 weeks). Therefore, alteration in dye coupling appears to be correlated temporally with the induction of DA cell depolarization block. The finding that both APDs exert a common action on neurons in the accumbens shell region is consistent with its identification as the site of therapeutic drug actions, whereas the capacity of haloperidol to also affect cells in the motor-related matrix and core regions correlates with its high propensity to induce extrapyramidal side effects.

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Section: Differential Modulation Of Dye Coupling By Typical Versus Atsupporting

confidence: 53%

Repeated treatment with haloperidol and clozapine exerts differential effects on dye coupling between neurons in subregions of striatum and nucleus accumbens

Onn

Grace

1995

J. Neurosci.

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“…In both birds and mammals, the striatum as a whole projects to the substantia nigra and the pallidum, with the projections arising from different populations of mediumsized neurons with heavily spiny dendrites (Gerfen, 1988, Graybiel, 1990Reiner and Anderson, 1990;Reiner et al, 1998a). In mammals, such striatonigral and striatopallidal neurons are intermingled throughout the caudate and putamen (Beckstead and Cruz, 1986;Reiner and Anderson, 1990;Selemon and Goldman-Rakic, 1990;Reiner et al, 1998a). By contrast, the LPO of birds contains spiny neurons projecting to the substantia nigra but few (if any) that target the pallidal part of the dorsal basal ganglia, whereas the lateral striatum (paleostriatum augmentatum) projects primarily to the dorsal pallidum (Karten and Dubbeldam, 1973;Brauth et al, 1978;Bottjer et al, 1989).…”

Section: Rationale For Individual Changesmentioning

confidence: 99%

“…As for the avian medial striatum compared with the mammalian caudate nucleus, there is no compelling evidence that the lateral striatum of birds is homologous in a one-to-one fashion with the lateral part of the mammalian striatum, namely, the putamen. For example, the LSt in birds contains spiny neurons that mainly project to the pallidal part of basal ganglia but not to the substantia nigra (Karten and Dubbeldam, 1973;Anderson and Reiner, 1991a;Veenman et al, 1995a;Mezey and Csillag, 2002), whereas striatonigral and striatopallidal neurons are intermingled throughout the putamen (Beckstead and Cruz, 1986;Reiner and Anderson, 1990;Selemon and Goldman-Rakic, 1990;Reiner et al, 1998a).…”

Section: Rationale For Individual Changesmentioning

confidence: 99%

Revised nomenclature for avian telencephalon and some related brainstem nuclei

Reiner

Perkel

Bruce

et al. 2004

J of Comparative Neurology

1,064

1,170

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The standard nomenclature that has been used for many telencephalic and related brainstem structures in birds is based on flawed assumptions of homology to mammals. In particular, the outdated terminology implies that most of the avian telencephalon is a hypertrophied basal ganglia, when it is now clear that most of the avian telencephalon is neurochemically, hodologically, and functionally comparable to the mammalian neocortex, claustrum, and pallial amygdala (all of which derive from the pallial sector of the developing telencephalon). Recognizing that this promotes misunderstanding of the functional organization of avian brains and their evolutionary relationship to mammalian brains, avian brain specialists began discussions to rectify this problem, culminating in the Avian Brain Nomenclature Forum held at Duke University in July 2002, which approved a new terminology for avian telencephalon and some allied brainstem cell groups. Details of this new terminology are presented here, as is a rationale for each name change and evidence for any homologies implied by the new names.Revisions for the brainstem focused on vocal control, catecholaminergic, cholinergic, and basal ganglia-related nuclei. For example, the Forum recognized that the hypoglossal nucleus had been incorrectly identified as the nucleus intermedius in the Karten and Hodos (1967) pigeon brain atlas, and what was identified as the hypoglossal nucleus in that atlas should instead be called the supraspinal nucleus. The locus ceruleus of this and other avian atlases was noted to consist of a caudal noradrenergic part homologous to the mammalian locus coeruleus and a rostral region corresponding to the mammalian A8 dopaminergic cell group. The midbrain dopaminergic cell group in birds known as the nucleus tegmenti pedunculopontinus pars compacta was recognized as homologous to the mammalian substantia nigra pars compacta and was renamed accordingly; a group of ␥-aminobutyric acid (GABA)ergic neurons at the lateral edge of this region was identified as homologous to the mammalian substantia nigra pars reticulata and was also renamed accordingly. A field of cholinergic neurons in the rostral avian hindbrain was named the nucleus pedunculopontinus tegmenti, whereas the anterior nucleus of the ansa lenticularis in the avian diencephalon was renamed the subthalamic nucleus, both for their evident mammalian homologues.For the basal (i.e., subpallial) telencephalon, the actual parts of the basal ganglia were given names reflecting their now evident homologues. For example, the lobus parolfactorius and paleostriatum augmentatum were acknowledged to make up the dorsal subdivision of the striatal part of the basal ganglia and were renamed as the medial and lateral striatum. The paleostriatum primitivum was recognized as homologous to the mammalian globus pallidus and renamed as such. Additionally, the rostroventral part of what was called the lobus parolfactorius was acknowledged as comparable to the mammalian nucleus accumbens, which, together with the...

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“…[11][12][13] One subpopulation contains substance P and dynorphin and projects directly to substantia nigra pars reticulata and the entopeduncular nucleus (the direct striatonigral pathway). The other subpopulation contains enkephalin and projects indirectly to these structures via relays in the globus pallidus and subthalamic nucleus (the indirect striatopallidal pathway).…”

Section: Darpp-32 a Multifunctional Regulator Of Protein Kinases Andmentioning

confidence: 99%

DARPP-32 mediates the actions of multiple drugs of abuse

Svenningsson

Nairn

Greengard

2005

AAPS J

151

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A BSTRACTDrugs of abuse share the ability to enhance dopaminergic neurotransmission in the dorsal and ventral striatum. The action of dopamine is modulated by additional neurotransmitters, including glutamate, serotonin and adenosine. All these neurotransmitters regulate the phosphorylation state of Dopaminal serine/threonine protein phosphatase, PP-1. Phosphorylatine-and cAMP-regulated phosphoprotein, Mr 32 kDa . Phosphorylation at Thr 34 by protein kinase A converts DARPP-32 into a potent inhibitor of the multifunctioon at Thr 75 by Cdk5 converts DARPP-32 into an inhibitor of protein kinase A. The state of phosphorylation of DARPP-32 at Thr 34 also depends on the phosphorylation state of Ser 97 and Ser 130 , which are phosphorylated by CK2 and CK1, respectively. By virtue of regulation of these 4 phosphorylation sites, and through its ability to modulate the activity of PP-1 and protein kinase A, DARPP-32 plays a key role in integrating a variety of biochemical, electrophysiological, and behavioral responses controlled by dopamine and other neurotransmitters. Importantly, there is now a large body of evidence that supports a key role for DARPP-32-dependent signaling in mediating the actions of multiple drugs of abuse including cocaine, amphetamine, nicotine, caffeine, LSD, PCP, ethanol and morphine.K EYWORDS : protein phosphorylation, psychostimulants, dopamine, striatum DARPP-32, A MULTIFUNCTIONAL REGULATOR OF PROTEIN KINASES AND PROTEIN PHOSPHATASESDopamine-and cAMP-regulated phosphoprotein, Mr 32 kDa (DARPP-32), was initially discovered as a major target for dopamine-activated adenylyl cyclase and protein kinase A (PKA) in striatum. 1 Phosphorylation by PKA at Thr 34 converts DARPP-32 into a potent high-affi nity inhibitor of the multifunctional serine/threonine protein phosphatase, PP-1. The IC 50 for inhibition of PP-1 is ~10 − 9 M. 2 Since DARPP-32 is expressed in very high concentration (~50 m M) in all medium spiny neurons, 3 including those in both the striatonigral and striato pallidal projection pathways (see below), and the concentration of all PP-1 isoforms is likely less than 20 m M, 4 a substantial proportion of PP-1 activity will be inhibited in response to even moderate increases in DARPP-32 phosphorylation.Detailed structure-function studies have established that the fi rst 40 amino acids at the NH 2 -terminus of DARPP-32 are suffi cient (when Thr 34 is phosphorylated) for DARPP-32 to bind to and inhibit PP-1. Moreover, several different types of biochemical approaches have revealed that the remaining COOH-terminal portion of DARPP-32 serves an important role in the modulation of DARPP-32 function. In intact neurons, DARPP-32 is highly phosphorylated at Ser 97 and Ser 130 under basal conditions. Ser 97 is phosphorylated by CK2 and Ser 130 is phosphorylated by CK1. In vitro, phosphorylation of Ser 97 of DARPP-32 increases the effi ciency of phosphorylation of Thr 34 by PKA. 5 In vitro, phosphorylation of Ser 130 decreases the rate of dephosphorylation of Thr 34 by PP-2B, 6 and in striatal slic...

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Striatal axons to the globus pallidus, entopeduncular nucleus and substantia nigra come mainly from separate cell populations in cat

Cited by 147 publications

References 58 publications

Repeated treatment with haloperidol and clozapine exerts differential effects on dye coupling between neurons in subregions of striatum and nucleus accumbens

Repeated treatment with haloperidol and clozapine exerts differential effects on dye coupling between neurons in subregions of striatum and nucleus accumbens

Revised nomenclature for avian telencephalon and some related brainstem nuclei

DARPP-32 mediates the actions of multiple drugs of abuse

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