6 results on '"Basille M"'
Search Results
2. PACAP protects cerebellar granule neurons against oxidative stress-induced apoptosis
- Author
-
Vaudry, D., Pamantung, T. F., Basille, M., Rousselle, C., Fournier, A., Vaudry, H., Beauvillain, J. C., and Gonzalez, B. J.
- Published
- 2002
3. Long-term enhancement of REM sleep by the pituitary adenylyl cyclase-activating polypeptide (PACAP) in the pontine reticular formation of the rat
- Author
-
Ahnaou, A., primary, Basille, M., additional, Gonzalez, B., additional, Vaudry, H., additional, Hamon, M., additional, Adrien, J., additional, and Bourgin, P., additional
- Published
- 1999
- Full Text
- View/download PDF
4. PACAP inhibits delayed rectifier potassium current via a cAMP/PKA transduction pathway: evidence for the involvement of IK in the anti-apoptotic action of PACAP.
- Author
-
Mei, Y. A., Vaudry, D., Basille, M., Castel, H., Fournier, A., Vaudry, H., and Gonzalez, B. J.
- Subjects
POTASSIUM channels ,PEPTIDES ,GROWTH factors ,CELL death ,PHOSPHOTRANSFERASES ,LYASES - Abstract
Activation of potassium (K
+ ) currents plays a critical role in the control of programmed cell death. Because pituitary adenylate cyclase-activating polypeptide (PACAP) has been shown to inhibit the apoptotic cascade in the cerebellar cortex during development, we have investigated the effect of PACAP on K+ currents in cultured cerebellar granule cells using the patch-clamp technique in the whole-cell configuration. Two types of outward K+ currents, a transient K+ current ( IA ) and a delayed rectifier K+ current ( IK ) were characterized using two different voltage protocols and specific inhibitors of K+ channels. Application of PACAP induced a reversible reduction of the IK amplitude, but did not affect IA , while the PACAP-related peptide vasoactive intestinal polypeptide had no effect on either types of K+ currents. Repeated applications of PACAP induced gradual attenuation of the electrophysiological response. In the presence of guanosine 5′-[γthio]triphosphate (GTPγS), PACAP provoked a marked and irreversible IK depression, whereas cell dialysis with guanosine 5′-[βthio]diphosphate GDPβS totally abolished the effect of PACAP. Pre-treatment of the cells with pertussis toxin did not modify the effect of PACAP on IK . In contrast, cholera toxin suppressed the PACAP-induced inhibition of IK . Exposure of granule cells to dibutyryl cyclic adenosine monophosphate (dbcAMP) mimicked the inhibitory effect of PACAP on IK . Addition of the specific protein kinase A inhibitor H89 in the patch pipette solution prevented the reduction of IK induced by both PACAP and dbcAMP. PACAP provoked a sustained increase of the resting membrane potential in cerebellar granule cells cultured either in high or low KCl-containing medium, and this long-term depolarizing effect of PACAP was mimicked by the IK specific blocker tetraethylammonium chloride (TEA). In addition, pre-incubation of granule cells with TEA suppressed the effect of PACAP on resting membrane potential. TEA mimicked the neuroprotective effect of PACAP against ethanol-induced apoptotic cell death, and the increase of caspase-3 activity observed after exposure of granule cells to ethanol was also significantly inhibited by TEA. Taken together, the present results demonstrate that, in rat cerebellar granule cells, PACAP reduces the delayed outward rectifier K+ current by activating a type 1 PACAP (PAC1) receptor coupled to the adenylyl cyclase/protein kinase A pathway through a cholera toxin-sensitive Gs protein. Our data also show that PACAP and TEA induce long-term depolarization of the resting membrane potential, promote cell survival and inhibit caspase-3 activity, suggesting that PACAP-evoked inhibition of IK contributes to the anti-apoptotic effect of the peptide on cerebellar granule cells. [ABSTRACT FROM AUTHOR]- Published
- 2004
- Full Text
- View/download PDF
5. Altered cerebellar development in mice lacking pituitary adenylate cyclase-activating polypeptide.
- Author
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Allais A, Burel D, Isaac ER, Gray SL, Basille M, Ravni A, Sherwood NM, Vaudry H, and Gonzalez BJ
- Subjects
- Animals, Animals, Newborn, Biomarkers metabolism, Caspase 3 metabolism, Cell Death genetics, Cell Differentiation genetics, Cerebellum metabolism, Cyclic AMP metabolism, Enzyme Activation physiology, Intermediate Filament Proteins metabolism, Mice, Mice, Inbred C57BL, Mice, Knockout, Nerve Tissue Proteins metabolism, Nervous System Malformations genetics, Nervous System Malformations metabolism, Nervous System Malformations physiopathology, Nestin, Neurons cytology, Stem Cells cytology, Synaptophysin metabolism, Cerebellum abnormalities, Cerebellum growth & development, Gene Expression Regulation, Developmental genetics, Neurons metabolism, Pituitary Adenylate Cyclase-Activating Polypeptide genetics, Stem Cells metabolism
- Abstract
Previous studies have demonstrated that pituitary adenylate cyclase-activating polypeptide (PACAP) exerts trophic effects during neurodevelopment. In particular, the occurrence of PACAP and its receptors in the cerebellum during pre- and postnatal periods suggests that it could play a crucial role in ontogenesis of this structure. To test this hypothesis, we compared the histogenesis of cerebellar cortex in wild-type and PACAP-knockout (PACAP-/-) mice at postnatal days (P)4 and 7. Morphometric analysis of PACAP-/- mice revealed a significant reduction in the thickness of the external granule cell layer at P4 and of the internal granule cell layer at P7. Expression of nestin, a neural precursor marker, and synaptophysin, a mature neuronal marker, was quantified by real-time PCR and Western blot. No modification of nestin expression was noticed between wild-type and PACAP-/- mice, but a substantial decrease in synaptophysin expression was observed in PACAP-/- mice at P4 and P7. Immunohistochemistry revealed a reduction in synaptophysin labelling in the molecular and internal granule cell layers of PACAP-/- mice at P7. Caspase-3 activation was significantly increased in PACAP-/- mice at P4 and P7. Autoradiographic studies revealed no difference in PACAP binding site distributions and PACAP was effective at stimulating cAMP production in both wild-type and PACAP-/- cultured granule cells. This study demonstrates that disruption of the PACAP gene induces alteration of the immature cerebellum. Neuronal differentiation of granule cells was delayed whereas cell death that naturally occurs during ontogeny was increased in PACAP-/- mice. These data provide the first evidence of a physiological role for PACAP during cerebellar development.
- Published
- 2007
- Full Text
- View/download PDF
6. PACAP inhibits delayed rectifier potassium current via a cAMP/PKA transduction pathway: evidence for the involvement of I k in the anti-apoptotic action of PACAP.
- Author
-
Mei YA, Vaudry D, Basille M, Castel H, Fournier A, Vaudry H, and Gonzalez BJ
- Subjects
- 4-Aminopyridine pharmacology, Animals, Animals, Newborn, Caspase 3, Caspases metabolism, Cell Survival drug effects, Cells, Cultured, Central Nervous System Depressants pharmacology, Cerebellum cytology, Cholera Toxin pharmacology, Cyclic AMP physiology, Cyclic AMP-Dependent Protein Kinases physiology, Delayed Rectifier Potassium Channels, Drug Interactions, Electric Conductivity, Enzyme Inhibitors pharmacology, Ethanol pharmacology, Guanosine 5'-O-(3-Thiotriphosphate) pharmacology, Guanosine Diphosphate pharmacology, Isoquinolines pharmacology, Membrane Potentials drug effects, Models, Neurological, Neural Inhibition drug effects, Neurons drug effects, Patch-Clamp Techniques methods, Peptide Fragments pharmacology, Pertussis Toxin pharmacology, Pituitary Adenylate Cyclase-Activating Polypeptide, Potassium Channel Blockers pharmacology, Rats, Rats, Wistar, Tetraethylammonium pharmacology, Tetrodotoxin pharmacology, Thionucleotides pharmacology, Time Factors, Vasoactive Intestinal Peptide pharmacology, Apoptosis drug effects, Cyclic AMP metabolism, Cyclic AMP-Dependent Protein Kinases metabolism, Guanosine Diphosphate analogs & derivatives, Neuropeptides pharmacology, Potassium Channels drug effects, Potassium Channels, Voltage-Gated, Signal Transduction drug effects, Sulfonamides
- Abstract
Abstract Activation of potassium (K(+)) currents plays a critical role in the control of programmed cell death. Because pituitary adenylate cyclase-activating polypeptide (PACAP) has been shown to inhibit the apoptotic cascade in the cerebellar cortex during development, we have investigated the effect of PACAP on K(+) currents in cultured cerebellar granule cells using the patch-clamp technique in the whole-cell configuration. Two types of outward K(+) currents, a transient K(+) current (I(A)) and a delayed rectifier K(+) current (I(K)) were characterized using two different voltage protocols and specific inhibitors of K(+) channels. Application of PACAP induced a reversible reduction of the I(K) amplitude, but did not affect I(A), while the PACAP-related peptide vasoactive intestinal polypeptide had no effect on either types of K(+) currents. Repeated applications of PACAP induced gradual attenuation of the electrophysiological response. In the presence of guanosine 5'-[gammathio]triphosphate (GTPgammaS), PACAP provoked a marked and irreversible I(K) depression, whereas cell dialysis with guanosine 5'-[betathio]diphosphate GDPbetaS totally abolished the effect of PACAP. Pre-treatment of the cells with pertussis toxin did not modify the effect of PACAP on I(K). In contrast, cholera toxin suppressed the PACAP-induced inhibition of I(K). Exposure of granule cells to dibutyryl cyclic adenosine monophosphate (dbcAMP) mimicked the inhibitory effect of PACAP on I(K). Addition of the specific protein kinase A inhibitor H89 in the patch pipette solution prevented the reduction of I(K) induced by both PACAP and dbcAMP. PACAP provoked a sustained increase of the resting membrane potential in cerebellar granule cells cultured either in high or low KCl-containing medium, and this long-term depolarizing effect of PACAP was mimicked by the I(K) specific blocker tetraethylammonium chloride (TEA). In addition, pre-incubation of granule cells with TEA suppressed the effect of PACAP on resting membrane potential. TEA mimicked the neuroprotective effect of PACAP against ethanol-induced apoptotic cell death, and the increase of caspase-3 activity observed after exposure of granule cells to ethanol was also significantly inhibited by TEA. Taken together, the present results demonstrate that, in rat cerebellar granule cells, PACAP reduces the delayed outward rectifier K(+) current by activating a type 1 PACAP (PAC1) receptor coupled to the adenylyl cyclase/protein kinase A pathway through a cholera toxin-sensitive Gs protein. Our data also show that PACAP and TEA induce long-term depolarization of the resting membrane potential, promote cell survival and inhibit caspase-3 activity, suggesting that PACAP-evoked inhibition of I(K) contributes to the anti-apoptotic effect of the peptide on cerebellar granule cells.
- Published
- 2004
- Full Text
- View/download PDF
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