Thyroid Hormone-Dependent Regulation of Galanin Synthesis in Neurons and Glial Cells after Colchicine Administration

Calzà, L.; Giardino, Luciana; Hökfelt, Tomas

doi:10.1159/000054393

Cited by 22 publications

(10 citation statements)

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“…However, in a study using icv injections of colchicine, Calza et al [4] demonstrated that colchicine-induced NG2 cell-specific galanin up-regulation did not occur in thyroidectomised, hypothyroid adult rats, although neuronal galanin up-regulation was preserved in some neuronal populations. These data suggest that endogenous thyroid hormone could mediate injury-induced glial galanin production, potentially regulated by a thyroid hormone responsive element in the galanin promoter.…”

Section: Regulation Of Glial Galanin Expression and Secretionmentioning

confidence: 99%

“…Absence of co-labelling with another microglia/macrophage marker, ED1, confirmed that another glial cell type other than macrophages or microglia was likely to be responsible for trauma-induced galanin expression [4]. Ubink and colleagues [5] subsequently demonstrated that the glial cell type expressing galanin after icv colchicine injection was positive for the cell surface proteoglycan, NG2.…”

mentioning

confidence: 95%

“…Surprisingly, this was not only demonstrated in neurons but also in small, morphologically non-neuronal cells in the CNS grey matter and in many cells in the white matter [1]. In the same laboratory, these studies were extended using icv injection of either colchicine or the neurotoxic mitosis inhibitor, vinblastine, in adult rats [3,4]. Using autoradiographic techniques, this latter study confirmed marked, colchicine-and vinblastine-induced galanin mRNA up-regulation, evident at 24 h after injection.…”

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confidence: 99%

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Galanin in Glia: Expression and Potential Roles in the CNS

Butzkueven

Gundlach

2010

Experientia Supplementum

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The roles of galanin in central nervous system (CNS) development and the normal adult CNS have been extensively reviewed in this volume and elsewhere. There is also ample evidence that galanin expression is induced following neural injury in the CNS, and has neuroprotective properties separate from its role in normal physiology. Although strong injury-mediated up-regulation of galanin occurs in neurons, there is increasing evidence, accumulated over almost two decades, that glial cells can express galanin in the injured brain and during white matter development. In this chapter, we review the available evidence and canvas the potential functional significance of glial galanin expression.Keywords Cerebral ischemia Á Experimental autoimmune encephalomyelitis Á Galanin Á Multiple sclerosis Á NG2 cell surface proteoglycan Á Neural and glial plasticity Á Oligodendrocyte progenitor cell Experimental Central Nervous System InjuryA number of different experimental CNS insults result in increased glial galanin expression. The earliest experiments demonstrating this were reported by Hökfelt and co-workers in 1990, using intracerebroventricular (icv) injection of colchicine [1].

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Section: Regulation Of Glial Galanin Expression and Secretionmentioning

confidence: 99%

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confidence: 95%

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confidence: 99%

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Galanin in Glia: Expression and Potential Roles in the CNS

Butzkueven

Gundlach

2010

Experientia Supplementum

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“…2002; Barreda‐Gomez et al. 2005) whose expression has been shown to be TH‐regulated (Calza et al. 1998; Kolakowski et al.…”

Section: Discussionmentioning

confidence: 99%

Identification of genes mediating thyroid hormone action in the developing mouse cerebellum

Takahashi

Negishi

Tashiro

2007

Journal of Neurochemistry

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Despite the indispensable role thyroid hormone (TH) plays in brain development, only a small number of genes have been identified to be directly regulated by TH and its precise mechanism of action remains largely unknown, partly because most of the previous studies have been carried out at postnatal day 15 or later. In the present study, we screened for TH‐responsive genes in the developing mouse cerebellum at postnatal day 4 when morphological alterations because of TH status are not apparent. Among the new candidate genes selected by comparing gene expression profiles of experimentally hypothyroid, hypothyroid with postnatal thyroxine replacement, and control animals using oligoDNA microarrays, six genes were confirmed by real‐time PCR to be positively (orc1l, galr3, sort1, nlgn3, cdk5r2, and zfp367) regulated by TH. Among these, sort1, cdk5r2, and zfp367 were up‐regulated already at 1 h after a single injection of thyroxine to the hypothyroid or control animal, suggesting them to be possible primary targets of the hormone. Cell proliferation and apoptosis examined by BrdU incorporation and terminal deoxynucleotide transferase‐mediated dUTP nick‐end labeling assay revealed that hypothyroidism by itself did not enhance apoptosis at this stage, but rather increased cell survival, possibly through regulation of these newly identified genes.

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“…Impaired PTP in ganglia from hypothyroid rats reported here is in agreement with an earlier finding in hypothyroid cat ganglia (Pascalov‐Stoenescu and Sterescu, 1971). The mechanism responsible for impairment of PTP in hypothyroid ganglia is unknown, but could be due to decreased de novo synthesis of presynaptic voltage‐operated calcium channels, or other protein molecules involved in transmitter release, resulting from hypothyroidism‐decreased protein synthesis (Wibo et al, 1995; Calza et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Hypothyroidism impairs long‐term potentiation in sympathetic ganglia: Electrophysiologic and molecular studies

Alzoubi

Bedawi

Aleisa

et al. 2004

J of Neuroscience Research

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Electrophysiologic and molecular techniques were used to study the effect of adult-onset hypothyroidism on synaptic plasticity in the superior cervical sympathetic ganglion. Ganglia excised from adult thyroidectomized and sham-operated rats were subjected to a brief high-frequency stimulation of the preganglionic nerve to express long-term potentiation (gLTP). Western blotting was carried out to determine the protein levels of key signaling molecules that may be involved in the expression of gLTP. Input/output relationship in ganglia from hypothyroid rats indicated a normal basal synaptic transmission, whereas activity-dependent types of synaptic plasticity, posttetanic potentiation (PTP) and gLTP, were impaired. Immunoblot analysis showed that both calcium/calmodulin kinase II (CaMKII) and phosphorylated CaMKII (P-CaMKII) levels were reduced markedly in hypothyroid rat ganglia compared to those from euthyroid controls. Additionally, protein levels of nitric oxide synthase-1, heme oxygenase-2, calmodulin, protein kinase C (PKC), and calcineurin were also reduced in hypothyroid rat ganglia. The results indicate that abnormally low basal levels of signaling molecules may be responsible for hypothyroidism-induced impairment of gLTP in superior cervical ganglia. In addition, the results indicate that synaptic plasticity in sympathetic ganglia may involve a molecular sequence of events similar to that proposed for LTP in the hippocampus.

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Thyroid Hormone-Dependent Regulation of Galanin Synthesis in Neurons and Glial Cells after Colchicine Administration

Cited by 22 publications

References 49 publications

Galanin in Glia: Expression and Potential Roles in the CNS

Galanin in Glia: Expression and Potential Roles in the CNS

Identification of genes mediating thyroid hormone action in the developing mouse cerebellum

Hypothyroidism impairs long‐term potentiation in sympathetic ganglia: Electrophysiologic and molecular studies

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