The protective effect of L-threo-3,4-dihydroxyphenylserine on ischemic hippocampal neuronal death in gerbils.

Lee, Tsong Hai; Abe, Kōji; Akiyama, Masashi; Nakamura, Mitsutaka; Kogure, Kyuya; Itoyama, Yasuto

doi:10.1161/01.str.25.7.1425

Cited by 32 publications

(21 citation statements)

References 43 publications

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“…Immunostaining against NGF, [25][26][27] trkA, GFAP, and HSP70 in fresh-frozen brain sections was performed by the avidin-biotin peroxidase (ABC) method using a kit (PK-6101 for NGF and trkA and PK-6102 for GFAP and HSP70; Vector Labs). First, fresh-frozen sections were fixed in ice-cold acetone for 30 minutes and air-dried.…”

Section: Methodsmentioning

confidence: 99%

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Expression of Nerve Growth Factor and trkA After Transient Focal Cerebral Ischemia in Rats

Lee

Kato

Chen

et al. 1998

Stroke

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Background and Purpose-In vitro studies have shown that nerve growth factor (NGF) is protective to cortical neurons against various insults. However, the role of NGF in relation to its high-affinity trkA receptor in the cortical neurons has not been well discussed. In this experiment, we studied the possible involvement of the NGF/receptor system in the ischemic injury of cortical neurons after focal cerebral ischemia in rats. Methods-Male Wistar rats received right middle cerebral artery occlusion of 90 minutes' duration. The rats were decapitated at different reperfusion time points: hour 4 and days 1, 3, 7, and 14 of recirculation. Brain sections at the level of striatum were immunostained against NGF, trkA, glial fibrillary acidic protein (GFAP), and stress protein HSP70. Double immunostaining against NGF and GFAP was also performed. Optical density of NGF immunoreactivity in the ischemic and nonischemic cortexes was compared between sham-control and ischemic animals. Results-In the sham-control rats, NGF immunoreactivity was present in the cortical and striatal neurons. However, beginning at hour 4 after recirculation, there was a significant decrease of NGF in the ischemic cortex and striatum. Beginning at day 1, NGF was absent completely in the infarcted striatum and cortex. However, in the peri-infarct penumbra area, despite a decrease in NGF at hour 4 and day 1, NGF recovered beginning at day 3 and returned almost to the sham-control level at day 14. In the nonischemic cortex, NGF increased beginning at hour 4, peaked at day 7, and returned almost to the sham-control level at day 14. The trkA and HSP70 immunoreactivities were not present in the sham-control cortex. However, trkA was induced at hour 4 in the ischemic cortex and at days 1 and 3 in the peri-infarct penumbra cortex. The HSP70 was induced at days 1 and 3 in the peri-infarct penumbra area. Double immunostaining showed that the number of GFAP-positive cells increased gradually, and NGF immunoreactivity in the GFAP-positive cells became gradually intense after ischemia. Conclusions-Our study demonstrated a temporal profile of NGF and trkA in the ischemic cortex and NGF expression by reactive astrocytes. Our data suggest that the NGF/receptor system may play a role in the astrocyte/neuron interaction under certain pathological conditions, such as focal cerebral ischemia. (Stroke. 1998;29:1687-1697.)

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Section: Methodsmentioning

confidence: 99%

“…25 The background density was detected on the sections immunostained without the primary antibody. The data between the sham-control and ischemic animals at each time point in the ischemic and nonischemic cortex were statistically compared.…”

Section: Methodsmentioning

confidence: 99%

Expression of Nerve Growth Factor and trkA After Transient Focal Cerebral Ischemia in Rats

Lee

Kato

Chen

et al. 1998

Stroke

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“…The right MCA was occluded by the insertion of a nylon thread through the common carotid artery according to the technique used in a previous report. 23 Body temperature was maintained at 37Ϯ0.3°C during surgical procedure for MCA occlusion. Immediately after the MCAO, a part of the dura mater was carefully removed (diameter 2.0 mm) through the drilling hole.…”

Section: Permanent Mcaomentioning

confidence: 99%

“…Water contents were then measured by the dry-weight method we reported previously. 23 Sham control cerebral cortexes (nϭ6) were also dissected immediately after the sham operation without MCAO. Statistical analyses were performed using Student's t tests.…”

Section: Estimation Of Infarct Area and Brain Edema After Permanent Mcaomentioning

confidence: 99%

Reduction of Ischemic Brain Injury by Topical Application of Glial Cell Line–Derived Neurotrophic Factor After Permanent Middle Cerebral Artery Occlusion in Rats

Kitagawa

Hayashi

Mitsumoto

et al. 1998

Stroke

183

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Background and Purpose-Glial cell line-derived neurotrophic factor (GDNF) plays important roles in the survival and recovery of some mature neurons under pathological conditions. However, the effect of GDNF in ameliorating ischemic brain injury has not been well documented. Therefore, we investigated a possible effect of GDNF on the changes of infarct size, brain edema, DNA fragmentation, and immunoreactivities for caspases after permanent middle cerebral artery occlusion (MCAO) in rats. Methods-For the estimation of ischemic brain injury, we calculated the infarct size of MCA region and also measured the brain water content as edema formation at 24 hours after the MCAO. Terminal deoxynucleotidyl transferasemediated dUTP-biotin in situ nick labeling (TUNEL) staining was performed for the detection of DNA fragmentation.Immunoreactivities for caspase-1 (ICE), caspase-2 (Nedd-2), and caspase-3 (CPP32) were stained. Results-Both infarct size and brain edema after permanent MCAO were significantly reduced by topical application of GDNF (48% and 30% decreases, Pϭ0.01). TUNEL staining and immunoreactivities for caspases were markedly induced at 12 hours after permanent MCAO in the vehicle-treated animals. However, the spatial distribution of those immunohistochemically positive cells was dissociative in each caspase. Induction of TUNEL staining and immunoreactivities for caspases-1 and -3 was greatly reduced with GDNF treatment, whereas the reduction of caspase-2 staining was only minimum. Conclusions-These data suggest that the reduction of infarct size and brain edema by GDNF was greatly associated with the reduction of DNA fragmentation and apoptotic signals predominantly through caspases-1 and -3 cascades. (Stroke.

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“…In addition to these classic transmitter signaling functions, NA is thought to play a key role in neuronal survival, differentiation and plasticity, and to participate in brain repair mechanisms. For instance, compounds that mimic or increase LC output, including NA itself, its precursor L-threo-3,4-dihydroxyphenylserine, and amphetamine, improve behavioral recovery (Feeney, 1998), stimulate neural sprouting and synaptogenesis (Lee et al, 1994;Stroemer et al, 1998) and limit neuronal death in experimental models of cerebral ischemia (Lee et al, 1994). Another class of molecules that elevates extracellular levels of NA (i.e., ␣ 2 adrenoceptor antagonists) is effective in protecting brain cholinergic neurons against cortical devascularization (Debeir et al, 2001) and excitotoxin-induced lesioning (Martel et al, 1998).…”

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confidence: 99%

Activation of the Mitogen-Activated Protein Kinase (ERK1/2) Signaling Pathway by Cyclic AMP Potentiates the Neuroprotective Effect of the Neurotransmitter Noradrenaline on Dopaminergic Neurons

Troadec

Marien²,

Mourlevat³

et al. 2002

Molecular Pharmacology

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We have shown previously that low concentrations of noradrenaline (NA) confer long-term but partial protection to tyrosine hydroxylase (TH ϩ ) dopaminergic neurons by reducing spontaneously occurring oxidative stress. We demonstrate here that the effect of NA is strongly enhanced by cAMPelevating agents, in particular forskolin (FK), through a mechanism that does not involve activation of adrenoceptors. FK also enhanced the neuroprotective action of antioxidants that mimic the trophic effects of NA, such as trolox and pyrocatechol, but was totally ineffective by itself, suggesting that inhibition of oxidative stress was a required step to reveal the cAMP-dependent mechanism. Neuroprotection afforded by FK was rapidly reversible, optimal when the treatment was initiated in the early phase of the culture and exquisitely specific to dopaminergic neurons. FK stimulated the phosphorylation of extracellular signal-activated kinases (ERK) 1/2 in a subpopulation of dopaminergic neurons, suggesting that the mitogen-activated protein kinase (MAPK) pathway was involved in the effects of cAMP-elevating agents. Accordingly, inhibition of the upstream kinases of ERK 1/2 by 2Ј-amino-3Ј-methoxyflavone (PD98059) not only suppressed MAPK activation caused by FK but also abolished the survival promoting activity that this compound exerts on TH ϩ neurons. PD98059 did not reduce, however, the trophic effects provided by NA alone. Surprisingly, the archetypal cAMP-dependent protein kinase was apparently not responsible for ERK 1/2 activation. The data suggest that the MAPK signaling pathway plays a key role in the trophic effects that cAMP elevating agents and NA cooperatively exert on TH ϩ neurons.

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The protective effect of L-threo-3,4-dihydroxyphenylserine on ischemic hippocampal neuronal death in gerbils.

Cited by 32 publications

References 43 publications

Expression of Nerve Growth Factor and trkA After Transient Focal Cerebral Ischemia in Rats

Expression of Nerve Growth Factor and trkA After Transient Focal Cerebral Ischemia in Rats

Reduction of Ischemic Brain Injury by Topical Application of Glial Cell Line–Derived Neurotrophic Factor After Permanent Middle Cerebral Artery Occlusion in Rats

Activation of the Mitogen-Activated Protein Kinase (ERK1/2) Signaling Pathway by Cyclic AMP Potentiates the Neuroprotective Effect of the Neurotransmitter Noradrenaline on Dopaminergic Neurons

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