Effects of PACAP and VIP on cyclic AMP formation in rat neuronal and astrocyte cultures under normoxic and hypoxic condition

Nowak, Jerzy Z.; Jóźwiak-Bębenista, Marta; Bednarek, Katarzyna

doi:10.1016/j.peptides.2007.04.007

Cited by 19 publications

(18 citation statements)

References 39 publications

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“…Actions on Glial Cells. Consistent with the occurrence of the PAC1-R-short and -hop splice variants in astroglial cells , PACAP has been shown to stimulate cAMP production Masmoudi et al, 2003;Nowak et al, 2007), to promote polyphosphoinositide turnover (Masmoudi et al, 2003;Dejda et al, 2006), to mobilize intracellular calcium stores , and to activate a quinine-sensitive potassium outward current (Ichinose et al, 1998) in rat astrocytes. The effect of PACAP on cAMP production involves neurofibromin, a protein controlling astrocyte proliferation (Dasgupta et al, 2003).…”

Section: Kip2mentioning

confidence: 68%

Pituitary Adenylate Cyclase-Activating Polypeptide and Its Receptors: 20 Years after the Discovery

et al. 2009

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Section: Kip2mentioning

confidence: 68%

Pituitary Adenylate Cyclase-Activating Polypeptide and Its Receptors: 20 Years after the Discovery

et al. 2009

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“…The formation of [3H]cAMP was measured in [3H]adenine prelabeled T98G cells as previously described in detail by Jozwiak-Bebenista et al [23] and Nowak et al [24]. …”

Section: Methodsmentioning

confidence: 99%

Neuroleptic Drugs and PACAP Differentially Affect the mRNA Expression of Genes Encoding PAC1/VPAC Type Receptors

Jóźwiak-Bębenista

Kowalczyk

2016

Neurochem Res

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Several lines of evidence suggest that pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide playing an important role as a neuromodulator. It has been indicated that PACAP is associated with mental diseases, and that regulation of the PACAPergic signals could be a potential target for the treatment of such psychiatric states as schizophrenia. Recent studies have suggested that action of neuroleptic drugs is mediated not only by dopaminergic and serotonergic neurotransmission, but also via neuropeptides which may act both as neurotransmitters and as neuromodulators. The present study examines whether currently-used neuroleptics influence the action of PACAP receptors, whose expression is altered in a schizophrenic patient. Real-time polymerase chain reaction (PCR) was used to examine the effects of haloperidol, olanzapine and amisulpride on the expression of genes coding PAC1/VPAC type receptors in the T98G glioblastoma cell line, as an example of an in vitro model of glial cells. PAC1 mRNA expression fell after 24-h incubation with haloperidol or olanzapine; however the effect was not maintained after 72 h, and haloperidol even up-regulated PAC1 mRNA expression in a dose-dependent manner. All the examined drugs decreased VPAC2 mRNA expression, especially after 72-h incubation. Haloperidol (typical neuroleptic) was distinctly more potent than atypical neuroleptic drugs (olanzapine and amisulpride). In addition, PACAP increased PAC1 and VPAC2 mRNA expression. In conclusion, our findings suggest PACAP receptors may be involved in the mechanism of typical and atypical neuroleptic drugs.

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“…PACAP is also protective in other neurodegenerative conditions, e.g., in association with Parkinson’s (Reglodi et al, 2004; Reglodi et al, 2006) and Alzheimer’s disease (Kojro et al, 2006; Rat et al, 2011). In cell culture, PACAP promotes the survival of cultured cortical neurons under hypoxic/ischemic and excitotoxic conditions (Morio et al, 1996; Pellegri et al, 1998; Said et al, 1998; Frechilla et al, 2001; Shintani et al, 2005; Nowak et al, 2007; Stumm et al, 2007). Multiple other cell types are protected by PACAP under a variety of conditions that promote apoptosis.…”

Section: Introductionmentioning

confidence: 99%

STC1 Induction by PACAP is Mediated Through cAMP and ERK1/2 but not PKA in Cultured Cortical Neurons

2011

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The neuroprotective actions of PACAP (pituitary adenylate cyclase-activating polypeptide) in vitro and in vivo suggest that activation of its cognate G protein-coupled receptor PAC1 or downstream signaling molecules, and thus activation of PACAP target genes, could be of therapeutic benefit. Here we show, that cultured rat cortical neurons predominantly expressed the PAC1hop and null variants, activation of which resulted in elevation of the two second messengers cAMP and Ca2+ and expression of the putative neuroprotectant stanniocalcin 1 (STC1). PACAP signaling to the STC1 gene proceeded through the extracellular signal-regulated kinases 1 and 2 (ERK1/2), but not through the cAMP dependent protein kinase (PKA), and was mimicked by the adenylate cyclase activator forskolin. PACAP- and forskolin-mediated activation of ERK1/2 occurred through cAMP, but not PKA. These results suggest that STC1 gene induction proceeds through cAMP and ERK1/2, independently of PKA, the canonical cAMP effector. In contrast, PACAP signaling to the BDNF gene proceeded through PKA, suggesting that two different neuroprotective cAMP pathways co-exist in differentiated cortical neurons. The selective activation of a potentially neuroprotective cAMP dependent pathway different from the canonical cAMP pathway used in many physiological processes, such as memory storage, has implications for pharmacological activation of neuroprotection in vivo.

show abstract

Effects of PACAP and VIP on cyclic AMP formation in rat neuronal and astrocyte cultures under normoxic and hypoxic condition

Cited by 19 publications

References 39 publications

Pituitary Adenylate Cyclase-Activating Polypeptide and Its Receptors: 20 Years after the Discovery

Pituitary Adenylate Cyclase-Activating Polypeptide and Its Receptors: 20 Years after the Discovery

Neuroleptic Drugs and PACAP Differentially Affect the mRNA Expression of Genes Encoding PAC1/VPAC Type Receptors

STC1 Induction by PACAP is Mediated Through cAMP and ERK1/2 but not PKA in Cultured Cortical Neurons

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