Differential Spatiotemporal Alterations in Adrenoceptor mRNAs and Binding Sites in Cerebral Cortex Following Spreading Depression: Selective and Prolonged Up-Regulation of α1B-Adrenoceptors

Shen, Peiyan; Gundlach, Andrew L.

doi:10.1006/exnr.1998.6915

Cited by 18 publications

(14 citation statements)

References 78 publications

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“…In addition, one‐way anova was used to compare mRNA levels between control and experimental groups. In all cases examined, no differences existed between mRNA levels in the unoperated hemisphere of CSD and sham‐operated animals, as previously observed (Shen and Gundlach 1998a,b, 1999). All data from the ipsilateral hemisphere were converted to percentages of control (left hemisphere) values for tabular presentation.…”

Section: Discussionsupporting

confidence: 82%

“…In situ hybridization histochemistry was carried out using described methods (Shen and Gundlach 1998b; Wisden and Morris 2002). For each transcript investigated, a total of four sections per rat were used, taken at intervals of 350 μm apart throughout the designated cortical areas.…”

Section: Oligonucleotide Probes and In Situ Hybridization Histochemistrymentioning

confidence: 99%

“…Slide‐mounted sections were hybridized overnight at 42°C with ∼ 0.02 pmol/slide (65 μL per slide, 200–500 000 c.p.m.) labelled probes in hybridization buffer containing 50% formamide; 4 × saline sodium citrate (SSC); 1 × SSC contains 0.15 m NaCl and 0.015 m sodium citrate, pH 7.0; 10% dextran sulfate and 200 m m dithiothreitol (Shen and Gundlach 1998b; Wisden and Morris 2002). Following hybridization, slides were washed in 1 × SSC at 55°C for 1 h, rinsed in 1 × SSC, 0.1 × SSC, ethanol dehydrated and air‐dried at room temperature (25°C).…”

Section: Oligonucleotide Probes and In Situ Hybridization Histochemistrymentioning

confidence: 99%

“…1993; Jacobs et al . 1994; Shen and Gundlach 1998a,b; Schaller and Graf 2002). Previous studies have suggested an important link between the regulation of neuronal nitric oxide synthase (nNOS) levels and activity and the neuroprotective effect of cortical spreading depression (CSD) against cerebral ischemia (Shen and Gundlach 1999; see also Caggiano and Kraig 1998).…”

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confidence: 99%

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Neuronal‐NOS adaptor protein expression after spreading depression: implications for NO production and ischemic tolerance

Wiggins

Shen

Gundlach

2003

Journal of Neurochemistry

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Cortical spreading depression (CSD) is characterized by slowly propagating waves of neuronal/astrocytic depolarization and metabolic changes, followed by a period of quiescent neuronal and electroencephalographic activity. CSD acts as a preconditioning stimulus in brain, reducing cell death when elicited up to several days prior to an ischemic insult. Precise mechanisms associated with this neuroprotection are not known, although CSD increases the expression of a number of potentially neuroprotective genes/proteins. The nitric oxide (NO) system may be of particular importance, as it is acutely activated and chronically up-regulated in cerebral cortex by CSD, and NO can ameliorate and exacerbate cell death under different conditions. Several molecules have recently been identified that modulate the production and/or cellular actions of NO, but it is not known whether their expression is altered by CSD. Therefore, the present study examined the effect of CSD on the spatiotemporal expression of PIN, CAPON, PSD-95, Mn-SOD and Cu/Zn-SOD mRNA in the rat brain. In situ hybridization using specific [35 S]-labelled oligonucleotides revealed that levels of PIN mRNA were significantly increased in the cortex and claustrum (30-180%; p £ 0.01) after 6 h and 1 and 2 days, but were again equivalent to contralateral (control) cortical values at 7, 14 and 28 days. CAPON mRNA levels were increased (30-180%; p £ 0.05) in the ipsilateral cortical hemisphere at 6 h and 2 days post treatment, but not at the other times examined. In contrast, levels of PSD-95, Mn-and Cu/Zn-SOD mRNA were not altered at any time after CSD. These results suggest that following CSD, nNOS activity and NO levels may be tightly regulated by both transcriptional and translational alterations in a range of nNOS adaptor proteins, which may contribute to CSD-induced neuroprotection against subsequent ischemia. Obrenovitch et al. 2002). CSD alone does not cause neuronal damage or loss, even when elicited for 4-5 h (Nedergaard and Hansen 1988), but when it occurs in haemodynamically or metabolically compromised tissue, the additional metabolic load induced potentiates the degree of cell damage, both in vivo and in vitro (Back et al. 1996;Busch et al. 1996;Obeidat and Andrew 1998). In contrast, an episode of CSD elicited 1-14 days prior to an ischemic insult significantly reduces Abbreviations used: CAPON, carboxy-terminal PDZ ligand of nNOS; CSD, cortical spreading depression; DHC, dynein heavy-chain; KLC, kinesin light-chain; Mn(Cu/Zn)-SOD, manganese (zinc/copper)-containing isoform of superoxide dismutase; NO, nitric oxide; nNOS, neuronal nitric oxide synthase; PDZ, postsynaptic-density zone; PIN, protein inhibitor of neuronal nitric oxide synthase; PSD-95, postsynaptic density-95; SSC, saline sodium citrate.

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Section: Discussionsupporting

confidence: 82%

Section: Oligonucleotide Probes and In Situ Hybridization Histochemistrymentioning

confidence: 99%

Section: Oligonucleotide Probes and In Situ Hybridization Histochemistrymentioning

confidence: 99%

mentioning

confidence: 99%

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Neuronal‐NOS adaptor protein expression after spreading depression: implications for NO production and ischemic tolerance

Wiggins

Shen

Gundlach

2003

Journal of Neurochemistry

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“…First, one of the genes whose upregulation by synaptic activity was specific to hiPSCd neurons was ADRA1B (Table S7; Figure S7), which is associated with attention deficit/hyperactivity disorder (Mick et al., 2010). If ADRA1B is activity regulated in vivo, it could be involved in the regulation of mood, cognition, and behavior as an activity-induced component of the monoaminergic system in humans that is not synaptic activity dependent in mice (but see Kobori et al., 2011 and Shen and Gundlach, 1998). Second, we detected CAMTA1 , which is associated with human episodic memory performance (Huentelman et al., 2007) and intellectual disability (Thevenon et al., 2012), to be upregulated by activity in hiPSCd neurons but not in mouse neurons (Table S7).…”

Section: Discussionmentioning

confidence: 98%

Networks of Cultured iPSC-Derived Neurons Reveal the Human Synaptic Activity-Regulated Adaptive Gene Program

2017

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SummaryLong-term adaptive responses in the brain, such as learning and memory, require synaptic activity-regulated gene expression, which has been thoroughly investigated in rodents. Using human iPSC-derived neuronal networks, we show that the human and the mouse synaptic activity-induced transcriptional programs share many genes and both require Ca2+-regulated synapse-to-nucleus signaling. Species-specific differences include the noncoding RNA genes BRE-AS1 and LINC00473 and the protein-coding gene ZNF331, which are absent in the mouse genome, as well as several human genes whose orthologs are either not induced by activity or are induced with different kinetics in mice. These results indicate that lineage-specific gain of genes and DNA regulatory elements affects the synaptic activity-regulated gene program, providing a mechanism driving the evolution of human cognitive abilities.

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Prolonged Induction of Neuronal NOS Expression and Activity Following Cortical Spreading Depression (SD): Implications for SD- and NO-Mediated Neuroprotection

Shen

Gundlach

1999

Experimental Neurology

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Differential Spatiotemporal Alterations in Adrenoceptor mRNAs and Binding Sites in Cerebral Cortex Following Spreading Depression: Selective and Prolonged Up-Regulation of α1B-Adrenoceptors

Cited by 18 publications

References 78 publications

Neuronal‐NOS adaptor protein expression after spreading depression: implications for NO production and ischemic tolerance

Neuronal‐NOS adaptor protein expression after spreading depression: implications for NO production and ischemic tolerance

Networks of Cultured iPSC-Derived Neurons Reveal the Human Synaptic Activity-Regulated Adaptive Gene Program

Prolonged Induction of Neuronal NOS Expression and Activity Following Cortical Spreading Depression (SD): Implications for SD- and NO-Mediated Neuroprotection

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