Elsevier

Brain Research

Volume 1066, Issues 1–2, 20 December 2005, Pages 196-200
Brain Research

Short Communication
Immunodetection of heparin-binding growth associated molecule (pleiotrophin) in striatal interneurons

https://doi.org/10.1016/j.brainres.2005.10.055Get rights and content

Abstract

Pleiotrophin (PTN), a developmentally-regulated trophic factor, is over-expressed in the striatum of parkinsonian rats. Because striatal PTN can provide trophic support to dopamine neurons, we identified the cellular types containing PTN in the striatum of adult rats. By means of fluorescent double-immunolabeling, we found PTN to co-localize with a neuronal nuclei marker but not with glial fibrillary acidic protein. The number, distribution, and morphology of the PTN-immunolabeled cells suggested that they were interneurons. Further double-immunolabeling studies ruled out PTN localization to calretinin- and parvalbumin-containing interneurons. Instead, ∼40% of the PTN-immunolabeled neurons contained nitric oxide synthase or somatostatin and ∼60% expressed the vesicular acetylcholine transporter, supporting that they were GABAergic nitric oxide synthase/somatostatin-containing and cholinergic interneurons. Further work is necessary to determine if PTN from striatal interneurons can provide trophic support to dopamine neurons.

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Acknowledgments

This study was supported by CONICET PIP2196, ANPCYT PICT05-11063, and UBACYT M037 (Argentina), INSERM and ECOS A01S02 (France), and the National Parkinson Foundation (Florida, USA). J.E. Ferrario is funded by the FRM (Fondation pour la Recherche Médicale, grant no. ACE 20040700891). We wish to thank Pamela Rizk, Stephanie Laurens, and Daniele Caruelle for their help with some experiments, Dr. Merle Ruberg for helpful discussions, and Andrea Stefano for her continuous support.

References (25)

Cited by (18)

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    Despite the maladaptive behavioral outcomes, overactive ChIs may play a part in compensatory mechanisms that occur in PD, such as trophic support for DA-related targets. Following DA depletion, ChIs express increased levels of pleiotrophin (PTN), a growth-promoting factor for DA neurons (Salin et al., 2009; Taravini et al., 2005). This PTN increase corresponds with an upregulation in PTN receptor expression in striatal MSNs, suggesting an attempt to functionally reconstruct the striatal DA system (Ferrario et al., 2008; Marchionini et al., 2007).

  • Regulation of Pleiotrophin and Fyn in the striatum of rats undergoing L-DOPA-induced dyskinesia

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    Concerning the nigroestriatal system, PTN has been found to be neuroprotective for mesencephalic dopaminergic neurons in vitro [14] and in vivo [15]. In the adult striatum, PTN is expressed by two sub-population of interneurons: the GABAergic interneurons that co-express nitric oxide synthase (NOS)/somatostatin (SST)/Neuropeptide Y, and the cholinergic interneurons [9,10]. We have found that the PTN receptor RPTPζ/β is upregulated by L-DOPA and expressed by striatal MSNs [11].

  • The absence of pleiotrophin modulates gene expression in the hippocampus in vivo and in cerebellar granule cells in vitro

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    It was recently proposed that PTN may signal through a multi-receptor complex that activates different signaling pathways (Gonzalez-Castillo et al., 2014; Xu et al., 2014), which could explain the variety of activities in different tissues. Although PTN is widely distributed across the Central Nervous System (CNS) during early development (Li et al., 1990), it appears to be found constitutively in the adult brain and it is apparently limited to only a few cell types in the cortex, hippocampus and olfactory bulb (Lauri et al., 1996; Wanaka et al., 1993), as well as some striatal interneurons (Taravini et al., 2005) and cerebellar granule cells (Basille-Dugay et al., 2013). At these locations, PTN receptors could be differentially expressed, which might partially explain its diverse actions.

  • Changes to interneuron-driven striatal microcircuits in a rat model of Parkinson's disease

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    This anatomical reorganization may also contribute to the involvement of cholinergic transmission in the selective pruning of spines in striatopallidal neurons, a key structural change produced by dopamine depletion (Shen et al., 2007). Another interesting property of striatal cholinergic interneurons is that they express PTN, a factor promoting neurite outgrowth that has been suggested to play an important role in the compensatory mechanisms occurring in PD (Taravini et al., 2005). Our present data extend the previous finding that PTN levels increase in the striatum of dopamine-depleted rats, by showing that this increase occurs specifically in ChAT+ interneurons, irrespective of their connection to striatopallidal or striatonigral neurons.

  • The pro-angiogenic cytokine pleiotrophin potentiates cardiomyocyte apoptosis through inhibition of endogenous AKT/PKB activity

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    In these experiments, contaminating FBs only comprised 4.8 ± 2% of the total number of cells in the primary NNCM cultures. Interestingly, PTN immunostaining was observed in NNCMs both in the cytoplasmic and nuclear regions of the cells (Fig. 2C), similar to reports showing co-localization of PTN with nuclear markers in neurons (34). Transcripts to all five known PTN receptors (RPTP β/ζ, anaplastic lymphoma kinase, and syndecans -1, -3, and -4) were also present in hearts and in isolated CMs (Table 2), suggesting that PTN might be able to activate a signaling cascade in contractile cells.

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