Phosphorylation of proteins of the postsynaptic density: Effect of development on protein tyrosine kinase and phosphorylation of the postsynaptic density glycoprotein, PSD‐GP180

Jw, Gurd; Bissoon, Nankie

doi:10.1002/jnr.490250310

Cited by 19 publications

(11 citation statements)

References 57 publications

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“…The increase in tyrosine phosphorylation of NR2B between P7 and P21 supports our earlier finding of a developmental increase in the phosphorylation of NR2B on tyrosine 1472 (Nakazawa et al . 2001) and is in general accord with previous studies describing developmentally related changes in the tyrosine phosphorylation of synaptic proteins (Gurd and Bissoon 1990; Cudmore and Gurd 1991; Girault et al . 1992; Soulliere et al .…”

Section: Discussionsupporting

confidence: 90%

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Differential effects of hypoxia–ischemia on subunit expression and tyrosine phosphorylation of the NMDA receptor in 7‐ and 21‐day‐old rats

Gurd

Bissoon

Beesley

et al. 2002

Journal of Neurochemistry

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The effect of cerebral hypoxia-ischemia (HI) on levels and tyrosine phosphorylation of the NMDA receptor was examined in 7-(P7) and 21 (P21)-day-old rats. Unilateral HI was administered by ligation of the right common carotid artery and exposure to an atmosphere of 8% O 2 /92% N 2 for 2 (P7) or 1.5 (P21) h. This duration of HI produces significant infarction in nearly all of the survivors with damage being largely restricted to the cortex, striatum, and hippocampus of the hemisphere ipsilateral to the carotid artery ligation. NR2A levels in the right hemisphere of P7 pups were markedly reduced after 24 h of recovery, while NR1 and NR2B remained unchanged. In contrast, NR2B, but not NR2A, was reduced after HI at P21. At both ages, HI resulted in a transient increase in tyrosine phosphorylation of a number of forebrain proteins that peaked between 1 and 6 h of recovery. At both P7 and P21, tyrosine phosphorylation of NR2B was enhanced 1 h after HI and had returned to basal levels by 24 h. HI induced an increase in tyrosine phosphorylation of NR2A in 21 day, but not in 7-day-old animals. The differential effects of HI on the NMDA receptor at different post-natal ages may contribute to changing sensitivity to hypoxia-ischemia.

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Section: Discussionsupporting

confidence: 90%

“…1997). Synaptic tyrosine kinase activity increases during post‐natal development (Gurd and Bissoon 1990; Cudmore and Gurd 1991) and developmentally related increases in tyrosine phosphorylation of the NMDA receptor have been reported (Jin et al . 1997; Nakazawa et al .…”

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confidence: 99%

Differential effects of hypoxia–ischemia on subunit expression and tyrosine phosphorylation of the NMDA receptor in 7‐ and 21‐day‐old rats

Gurd

Bissoon

Beesley

et al. 2002

Journal of Neurochemistry

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“…Tyrosine phosphorylation of NR2 subunits activates the receptor ion channel (Kohr et al, 1994;Wang and Salter, 1994) and can also impact on interactions with associated postsynaptic density (PSD) proteins and downstream signaling molecules (Gurd, 1997;Takagi et al, 1999). Increases in synaptic tyrosine kinase activity occur during normal cerebral maturation (Cudmore and Gurd, 1991;Gurd and Bissoon, 1990) and have been associated with developmentally related increases in tyrosine phosphorylation of the NMDA receptor (Gurd et al, 2002). Although levels of NR2A relative to P21 are low in the P7 rat, there is a higher level of basal phosphorylation, which would contribute to the increased excitability of the NMDA receptor supporting normal cerebral development at this stage but also render it more vulnerable to H/I damage (Gurd et al, 2002).…”

Section: Energy Metabolism and Nutrient Transport In The Immature Bramentioning

confidence: 99%

Hypoxia–ischemia in the immature brain

Vannucci

Hagberg²

2004

Journal of Experimental Biology

398

284

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The immature brain has long been considered to be resistant to the damaging effects of hypoxia and hypoxia-ischemia (H/I). However, it is now appreciated that there are specific periods of increased vulnerability, which relate to the developmental stage at the time of the insult. Although much of our knowledge of the pathophysiology of cerebral H/I is based on extensive experimental studies in adult animal models, it is important to appreciate the major differences in the immature brain that impact on its response to, and recovery from, H/I. Normal maturation of the mammalian brain is characterized by periods of limitations in glucose transport capacity and increased use of alternative cerebral metabolic fuels such as lactate and ketone bodies, all of which are important during H/I and influence the development of energy failure. Cell death following H/I is mediated by glutamate excitotoxicity and oxidative stress, as well as other events that lead to delayed apoptotic death. The immature brain differs from the adult in its sensitivity to all of these processes. Finally, the ultimate outcome of H/I in the immature brain is determined by the impact on the ensuing cerebral maturation. A hypoxic-ischemic insult of insufficient severity to result in rapid cell death and infarction can lead to prolonged evolution of tissue damage.

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“…Samples were diluted to 0.1% SDS with water and glycoproteins isolated by binding to con A-agarose (Sigma Chemical Company, St. Louis, MO) using a batch procedure as described elsewhere (Gurd and Bissoon, 1990).…”

Section: Isolation and Digestion Of Concanavalin A (Con A)-binding Glmentioning

confidence: 99%

Tyrosine phosphorylation of glycoproteins in the adult and developing rat brain

Soulliere

Bissoon

Khurgel

et al. 1994

J of Neuroscience Research

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The tyrosine phosphorylation of glycoproteins in the adult and developing rat brain was investigated. Immunoblotting with anti-tyr(P) antibodies identified a glycoprotein with an apparent Mr of 180,000 (GP180) as the major tyrosine-phosphorylated protein in the concanavalin A (con A)-binding fraction prepared from forebrain homogenates. This glycoprotein had the same electrophoretic mobility as the postsynaptic density (PSD)-associated glycoprotein PSD-GP180. Tyrosine-phosphorylated GP180 was enriched 24-fold in isolated PSDs relative to homogenates. Digestion with endoglycosidase F/N-glycosidase F demonstrated that GP180 present in total homogenates and PSD-GP180 present in isolated PSDs contained similar amounts of N-linked oligosaccharide suggesting that they are the same glycoprotein. The tyrosine phosphorylation of GP180 in homogenates varied between brain regions with the highest levels occurring in cortical areas and the amygdala and low or undetectable amounts being present in hindbrain regions. Incubation of homogenates with adenosine triphosphate (ATP) resulted in the tyrosine phosphorylation of GP180 in all regions examined except the cerebellum and identified a second con A-binding glycoprotein, GP110, which was phosphorylated on tyrosine. GP180 was not phosphorylated on tyrosine following the incubation of cerebellar homogenate, synaptic membranes, or PSDs and ATP. Tyr(P)-GP180 was not detected prior to the onset of synaptogenesis, increased in parallel with the formation of synapses during the first 4 weeks of postnatal development of the frontal cortex and hippocampus, and then decreased 50-60% to adult levels. The results suggest that GP180 corresponds to the PSD glycoprotein PSD-GP180 and are consistent with a role for this glycoprotein in synaptic development and signal transduction at the synapse.

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Phosphorylation of proteins of the postsynaptic density: Effect of development on protein tyrosine kinase and phosphorylation of the postsynaptic density glycoprotein, PSD‐GP180

Cited by 19 publications

References 57 publications

Differential effects of hypoxia–ischemia on subunit expression and tyrosine phosphorylation of the NMDA receptor in 7‐ and 21‐day‐old rats

Differential effects of hypoxia–ischemia on subunit expression and tyrosine phosphorylation of the NMDA receptor in 7‐ and 21‐day‐old rats

Hypoxia–ischemia in the immature brain

Tyrosine phosphorylation of glycoproteins in the adult and developing rat brain

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