Regulation of the concentration of dynorphin A1–8 in the striatonigral pathway by the dopaminergic system

Li, S.; Sivam, Subbiah P.; Hong, Jau–Shyong

doi:10.1016/0006-8993(86)91502-7

Cited by 72 publications

(12 citation statements)

References 9 publications

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“…Cocaine induced a proportionally higher c-fos expression in striato-nigral compared to striatopallidal neurons, whereas apomorphine activated Fos almost exclusively in striato-nigral neurons. The present findings are consistent with the idea that striatal c-fos induction by dopaminergic agents is primarily mediated by an interaction with D1 -receptors, which are thought to be selectively localized on neurons projecting to SN.Repeated administration of direct or indirect dopaminergic agonists to rats is known to cause long-lasting behavioural alterations (Robinson, 1984;Morelli and Di Chiara, 1987) and has been reported to modulate the synthesis of several peptides in the striatum (Li et al, 1986;Hanson et al, 1988), a structure that is directly implicated in the effects of these drugs. The induction of immediateearly genes in striatal neurons obtained by dopaminergic agents in vivo appears as a possible intermediate step both in the molecular pathways leading to peptide-gene regulation and in the behavioural sensitization brought about by these drugs.…”

supporting

confidence: 92%

Striatal c‐fos Induction by Cocaine or Apomorphine Occurs Preferentially in Output Neurons Projecting to the Substantia Nigra in the Rat

Cenci

Campbell

Wictorin

et al. 1992

Eur J of Neuroscience

118

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Fluorogold or rhodamine-labelled latex beads were injected in the substantia nigra (SN) or the globus pallidus (GP) in order retrogradely to label striatal output neurons that project to the two target structures. Ten days later, striatal c-fos was induced by systemic administration of cocaine (five normal rats; 25 mg/kg cocaine i.p. 2 h before killing) or apomorphine (five unilaterally dopamine-denervated rats; 0.25 mg/kg apomorphine s. c. 2 h before killing), and detection of the Fos protein in the striatum was achieved by immunofluorescence. Sections through the caudate-putamen that displayed good labelling from both SN and GP were selected for a quantitative analysis: the number of retrogradely labelled cells that exhibited Fos immunoreactivity, as well as the total number of retrogradely labelled cells located within a grid (0.16 mm2 in size) were counted manually at 25 x magnification. Cocaine induced a proportionally higher c-fos expression in striato-nigral compared to striato-pallidal neurons, whereas apomorphine activated Fos almost exclusively in striato-nigral neurons. The present findings are consistent with the idea that striatal c-fos induction by dopaminergic agents is primarily mediated by an interaction with D1-receptors, which are thought to be selectively localized on neurons projecting to SN.

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supporting

confidence: 92%

Striatal c‐fos Induction by Cocaine or Apomorphine Occurs Preferentially in Output Neurons Projecting to the Substantia Nigra in the Rat

Cenci

Campbell

Wictorin

et al. 1992

Eur J of Neuroscience

118

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“…****Significant difference from controls, as tested with Mann-Whitney U per rostrocaudal level (P Ͻ 0.05). In contrast to the major effects of risperidone and haloperidol on ppEnk-A mRNA, only minor changes in ppEnk-B (increase) and ppT mRNA levels (decrease) were observed, which is consistent with earlier reports on haloperidol (Quirion et al, 1985, Bannon et al, 1987Li et al, 1987;Angulo et al, 1990a;Humpel et al, 1990;Shibata et al, 1990; however, see also Li et al, 1986;Morris et al, 1988a;Trujillo et al, 1990). The changes previously reported for ppT mRNA levels were more pronounced than those we observed.…”

Section: Comparison Of the Actions Of Risperidone And Haloperidol On supporting

confidence: 76%

Effects of risperidone and haloperidol on tachykinin and opioid precursor peptide mRNA levels in the caudate-putamen and nucleus accumbens of the rat

Mijnster

Schotte

Docter

et al. 1998

Synapse

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We investigated whether the two output pathways of the striatum are differently affected by the novel atypical drug risperidone and the conventional typical antipsychotic drug haloperidol. To this end, changes in mRNA levels of preproenkephalin-A, preproenkephalin-B, and preprotachykinin were determined in the rat striatum following chronic drug treatment for 14 days, using quantitative in situ hybridization. Furthermore, we studied the contribution of the dopamine D2 and serotonin 5-HT2A antagonist components of risperidone in establishing its effects on neuropeptide mRNA levels in the striatum. The results showed that both risperidone and haloperidol had major effects on the preproenkephalin-A mRNA and thus on the indirect striatal output route, whereas they had minor effects on preproenkephalin-B and preprotachykinin mRNA, contained by the direct output route. When both drugs were administered in the same dose, preproenkephalin-A mRNA was much more elevated by haloperidol than by risperidone. However, when doses of risperidone and haloperidol were modified to attain comparable dopamine D2 receptor occupancy, the drugs had comparable effects on preproenkephalin-A mRNA levels. It was further found that 5-HT2A/C receptor blockade with ritanserin had only modest effects on preproenkephalin-B and preprotachykinin mRNA levels and did not affect preproenkephalin-A mRNA levels. We conclude that risperidone and haloperidol, administered in the same dose, differently affect the striatal output routes. Furthermore, the results suggest that the effects of risperidone on neuropeptide mRNA levels are fully accounted for by its D2 antagonism and that no indication exists for a role of 5-HT2A receptor blockade in this action.

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“…Using in situ hybridization techniques, Young et al (1986) have shown that mesostriatal dopaminergic systems affect the expression of striatal peptide levels, demonstrating that 6-OHDA lesions of the entire system result in an up-regulation of enkephalin mRNA expression and a down-regulation of substance P mRNA expression. Chronic apomorphine treatment of rats causes a selective increase in dynorphin immunoreactivity in the striatonigral patch system (Li et al, 1986) despite the expression of dynorphin in both the patch and matrix striatonigral systems (Young et al, 1986; C. R. Gerfen and S. J. Young, unpublished observations).…”

Section: Functional Implicationsmentioning

confidence: 88%

“…For example, following pharmacologic treatments that deplete dopamine stores in mesostriatal terminals, there is a more rapid replenishment of dopamine in patch than in matrix areas (Olson et al, 1972;Fuxe et al, 1979;Fukui et al, 1986). Also, chronic apomorphine treatment results in an increase in dynorphin immunoreactivity in patch and not matrix striatonigral neurons (Li et al, 1986). The manner in which the patch-and matrix-directed mesostriatal dopaminergic neurons may be differentially regulated by the compartmental organization of striatonigral projections (Gerfen, 1984(Gerfen, , 1985 was discussed in the previous paper (Gerfen et al, 1987).…”

mentioning

confidence: 96%

The neostriatal mosaic: III. Biochemical and developmental dissociation of patch-matrix mesostriatal systems

1987

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In the previous paper (Gerfen et al., 1987) mesostriatal dopaminergic neurons were shown to be subdivided into dorsal and ventral tiers that project to the striatal matrix and patch compartments, respectively. The present study provides experimental evidence that these patch- matrix mesostriatal dopaminergic systems are biochemically and developmentally distinct. A 28 kDa calcium-binding protein (CaBP, or calbindin-D28 kDa) is expressed in dorsal tier mesostriatal dopaminergic neurons. The distribution of such neurons, located in the ventral tegmental area, dorsal tier of the substantia nigra pars compacta, and retrorubral area, matches that of dopaminergic neurons that project to the striatal matrix. Dopaminergic neurons that do not express CaBP--those in the ventral tier of the pars compacta and in the pars reticulata--are distributed in a pattern that matches the origin of the dopaminergic projection to the striatal patches. During development, dopaminergic afferents to the striatal patch compartment are in place prior to the development of those to the matrix. Injections of the neurotoxin 6-hydroxydopamine (6-OHDA) into the striatum of newborn rats result in a selective and long-lasting depletion of dopaminergic afferents in the striatal patches. The later- developing matrix projection is relatively spared by such lesions. The distribution of surviving dopaminergic neurons, labeled with tyrosine hydroxylase (TH) immunoreactivity, matches the pattern of dorsal tier neurons previously shown to provide inputs to the matrix. Surviving neurons also express CaBP immunoreactivity and have dendrites that spread mediolaterally, in the plane of the pars compacta. On the other hand, those neurons that project to the patches are selectively lesioned by the neonatal 6-OHDA striatal injections, do not express CaBP, and have dendrites that are directed ventrally into the pars reticulata.

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Regulation of the concentration of dynorphin A1–8 in the striatonigral pathway by the dopaminergic system

Cited by 72 publications

References 9 publications

Striatal c‐fos Induction by Cocaine or Apomorphine Occurs Preferentially in Output Neurons Projecting to the Substantia Nigra in the Rat

Striatal c‐fos Induction by Cocaine or Apomorphine Occurs Preferentially in Output Neurons Projecting to the Substantia Nigra in the Rat

Effects of risperidone and haloperidol on tachykinin and opioid precursor peptide mRNA levels in the caudate-putamen and nucleus accumbens of the rat

The neostriatal mosaic: III. Biochemical and developmental dissociation of patch-matrix mesostriatal systems

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