Urea enhances the nerve growth factor-induced neuroprotective effect on cholinergic neurons in organotypic rat brain slices

  title={Urea enhances the nerve growth factor-induced neuroprotective effect on cholinergic neurons in organotypic rat brain slices},
  author={Birgit Zassler and Georg Dechant and Christian Humpel},

S100b Counteracts Neurodegeneration of Rat Cholinergic Neurons in Brain Slices after Oxygen-Glucose Deprivation

It is concluded that S100b is a potent neuroprotective factor for cholinergic neurons during ischemic events.

The pro-apoptotic substance thapsigargin selectively stimulates re-growth of brain capillaries.

The induced cell death of cholinergic and dopaminergic neurons may be accompanied by enhanced angiogenic activity and selectively stimulated the laminin-positive capillary growth between the nBM and Ctx.

Microcontact Printing of Cholinergic Neurons in Organotypic Brain Slices

A novel innovative microcontact printing technique on semipermeable membranes which can be coupled with brain slices is provided and is provided to characterize neuronal survival and axonal growth in Alzheimer's disease.

Rotenone Induces Cell Death of Cholinergic Neurons in an Organotypic Co-Culture Brain Slice Model

In summary, inhibition of complex I of the electron transport chain may play a role in neurodegeneration of cholinergic neurons in an organotypic in vitro brain co-slice model.



Nerve growth factor and cholinergic CNS neurons studied in organotypic brain slices. Implication in Alzheimer's disease?

In conclusion, NGF is the most potent growth factor for cholinergic neurons and is a promising candidate for treating Alzheimers disease, however, the delivery of NGF to the brain must the solved.

Death of developing septal cholinergic neurons following NGF withdrawal in vitro: protection by protein synthesis inhibition

It is suggested that septal cholinergic neurons are dependent on NGF for survival only during a critical period of development and that growth factor-regulated developmental cell death may occur in CNS neurons by activation of programmed cell death requiring protein synthesis.

Nerve growth factor rapidly suppresses basal, NMDA-evoked, and AMPA-evoked nitric oxide synthase activity in rat hippocampus in vivo.

Rapid suppression by NGF of basal and glutamate-stimulated NOS activity may regulate neuromodulatory functions of NO or protect neurons from NO toxicity and suggests a novel mechanism for rapidly mediating functions of NGF and other neurotrophins.

NOS induction by NGF in basal forebrain cholinergic neurones: evidence for regulation of brain NOS by a neurotrophin

The results indicate that brain NOS can be regulated by a neurotrophic factor and suggest that NGF influences forebrain function by regulating production of nitric oxide as well as acetylcholine.

Molecualr mechanisms regulating NGF-mediated enhancement of cholinergic neuronal phenotype: c-Fos trans-activation of the choline acetyltransferase gene

Treatment of cultured rat embryonic basal forebrain neurons with anti-c-fos, prior to administering NGF, blocked NGF-mediated increases in ChAT activity by 67%; basal Chat activity was not affected by the antisense oligonucleotide treatment, and Reverse transcription-polymerase chain reaction revealed that anti- c- fos treatment resulted in not only blockade but enhancement of steady-state ChAT mRNA at different time points.