Catecholaminergic regulation of proliferation and survival in rat forebrain paraventricular germinal cells

Pabbathi, Vijay K; Brennan, Hannah; Muxworthy, A; Gill, Lukhbir S; Holmes, Fiona E.; Vignes, Michel; Haynes, Laurence W.

doi:10.1016/s0006-8993(97)00272-2

Cited by 13 publications

(6 citation statements)

References 46 publications

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“…Noradrenaline is converted from dopamine by dopamine‐β‐hydroxylase but unlike dopamine, is widely distributed through the brain (Happe et al, 2004). Noradrenaline is important during cortical development, promoting survival and proliferation of germinal neuroepithelial cells (Pabbathi et al, 1997). In adult animals, noradrenaline levels in the hippocampus are thought to be involved in the modulation of neuroplasticity and thus may be integral to emotionally charged memory formation (Tully and Bolshakov, 2010) and long‐term memory consolidation (Smythies, 2005).…”

Section: Discussionmentioning

confidence: 99%

Developmental vitamin D deficiency alters multiple neurotransmitter systems in the neonatal rat brain

Kesby

Turner

Alexander

et al. 2017

Intl J of Devlp Neuroscience

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Our results confirm that DVD deficiency leads to changes in multiple neurotransmitter systems in the neonate brain. Importantly, this regionally-based assessment in DVD-deficient neonates identified both widespread neurotransmitter changes (glutamine/noradrenaline) and regionally selective neurotransmitter changes (dopamine/serotonin). Thus, vitamin D may have both general and local actions depending on the neurotransmitter system being investigated. Taken together, these data suggest that DVD deficiency alters neurotransmitter systems relevant to schizophrenia in the developing rat brain.

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Section: Discussionmentioning

confidence: 99%

Developmental vitamin D deficiency alters multiple neurotransmitter systems in the neonatal rat brain

Kesby

Turner

Alexander

et al. 2017

Intl J of Devlp Neuroscience

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“…In studies by others, the viability of progenitor cells in the developing motor cortex of rat brain are sustained through the PLC signal transduction pathway by activation of α 1 B‐adrenoreceptors (Pabbathi et al . 1997; Gill et al .…”

Section: Discussionmentioning

confidence: 99%

“…In studies by others, the viability of progenitor cells in the developing motor cortex of rat brain are sustained through the PLC signal transduction pathway by activation of a 1 Badrenoreceptors (Pabbathi et al 1997;Gill et al 1998). Ligand deprivation resulted in the translocation of tTG/Gah from the plasma membrane, the attenuation of inositol triphosphate (IP3) formation and apoptosis, accompanied in dying cells by the onset of cross-linking activity (isodipeptide bonds).…”

Section: Discussionmentioning

confidence: 99%

Injury‐induced ‘switch’ from GTP‐regulated to novel GTP‐independent isoform of tissue transglutaminase in the rat spinal cord

Festoff

SantaCruz

Arnold

et al. 2002

Journal of Neurochemistry

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We recently found that alternative transcripts of tissue transglutaminase (tTG or TG2) were present in hippocampal brain regions of Alzheimer's disease (AD), but not in control, nondemented, age-matched brains. Since antecedent non-severe trauma has been implicated in AD and other neurodegenerative diseases, such as Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS), we were interested in whether alternative transcripts might be detected in a model of neurotrauma, controlled-contusion spinal cord injury (SCI) in the rat. Implicated in diverse roles from growth and differentiation to apoptotic cell death, only bifunctional tTG, of the nine member TG family, has dual catalytic activities: guanine trinucleotide (GTP) hydrolyzing activity (GTPase), as well as protein cross-linking. These functions imply two physiological functions: programmed cell life and death. These may have profound roles in the nervous system since studies in cultured astrocytes found tTG short (S) mRNA transcripts induced by treatment with injury-related cytokines. In the developing rat spinal cord, tTG activity is concentrated in ventral horn alpha motoneurons, but neither studies of spinal cord tTG gene expression, nor evaluation of the GTP-regulated isoforms in tissues, have been reported. We now report increased tTG protein and gene expression occurring rapidly after SCI. In parallel, novel appearance of a second, short form transcript, in addition to the normal long (L) isoform, occurs by 8 h of injury. Up-regulation of tTG message and activity following neural injury. with appearance of a truncated GTP-unregulated S form, may represent new approaches to drug targets in neurotrauma.

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“…3 H]Prazosin binding sites are found in SVZ neuroepithelia in rat embryonic day-13 embryos (Pabbathi et al, 1997) and in adult mice engineered to overexpress ␣ 1A -ARs tagged with enhanced green fluorescent protein (EGFP) to localize the receptor (Papay et al, 2006). Using ␣ 1 -AR promoters expressing EGFP tags with or without the receptor (Papay et al, 2004(Papay et al, , 2006, we identified a cell type in the SVZ in vivo that coexpressed markers of NSCs and/or their progenitors that can be labeled by 5-bromo-2-deoxyuridine (BrdU).…”

mentioning

confidence: 99%

α₁-Adrenergic Receptors Regulate Neurogenesis and Gliogenesis

Gupta¹,

Papay²,

Jurgens³

et al. 2009

Mol Pharmacol

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The understanding of the function of ␣ 1 -adrenergic receptors in the brain has been limited due to a lack of specific ligands and antibodies. We circumvented this problem by using transgenic mice engineered to overexpress either wild-type receptor tagged with enhanced green fluorescent protein or constitutively active mutant ␣ 1 -adrenergic receptor subtypes in tissues in which they are normally expressed. We identified intriguing ␣ 1A -adrenergic receptor subtype-expressing cells with a migratory morphology in the adult subventricular zone that coexpressed markers of neural stem cell and/or progenitors. Incorporation of 5-bromo-2-deoxyuridine in vivo increased in neurogenic areas in adult ␣ 1A -adrenergic receptor transgenic mice or normal mice given the ␣ 1A -adrenergic receptor-selective agonist, cirazoline. Neonatal neurospheres isolated from normal mice expressed a mixture of ␣ 1 -adrenergic receptor subtypes, and stimulation of these receptors resulted in increased expression of the ␣ 1B -adrenergic receptor subtype, proneural basic helix-loop-helix transcription factors, and the differentiation and migration of neuronal progenitors for catecholaminergic neurons and interneurons. ␣ 1 -Adrenergic receptor stimulation increased the apoptosis of astrocytes and regulated survival of neonatal neurons through phosphatidylinositol 3-kinase signaling. However, in adult normal neurospheres, ␣ 1 -adrenergic receptor stimulation increased the expression of glial markers at the expense of neuronal differentiation. In vivo, S100-positive glial and ␤III tubulin neuronal progenitors colocalized with either ␣ 1 -adrenergic receptor subtype in the olfactory bulb. Our results indicate that ␣ 1 -adrenergic receptors can regulate both neurogenesis and gliogenesis that may be developmentally dependent. Our findings may lead to new therapies to treat neurodegenerative diseases.

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Catecholaminergic regulation of proliferation and survival in rat forebrain paraventricular germinal cells

Cited by 13 publications

References 46 publications

Developmental vitamin D deficiency alters multiple neurotransmitter systems in the neonatal rat brain

Developmental vitamin D deficiency alters multiple neurotransmitter systems in the neonatal rat brain

Injury‐induced ‘switch’ from GTP‐regulated to novel GTP‐independent isoform of tissue transglutaminase in the rat spinal cord

α₁-Adrenergic Receptors Regulate Neurogenesis and Gliogenesis

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Catecholaminergic regulation of proliferation and survival in rat forebrain paraventricular germinal cells

Cited by 13 publications

References 46 publications

Developmental vitamin D deficiency alters multiple neurotransmitter systems in the neonatal rat brain

Developmental vitamin D deficiency alters multiple neurotransmitter systems in the neonatal rat brain

Injury‐induced ‘switch’ from GTP‐regulated to novel GTP‐independent isoform of tissue transglutaminase in the rat spinal cord

α1-Adrenergic Receptors Regulate Neurogenesis and Gliogenesis

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Product

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α₁-Adrenergic Receptors Regulate Neurogenesis and Gliogenesis