CXC chemokines interleukin-8 (IL-8) and growth-related gene product α (GROα) modulate Purkinje neuron activity in mouse cerebellum

Giovannelli, Alessandro; Limatola, Cristina; Ragozzino, Davide; Mileo, Anna Maria; Ruggieri, Alessandro; Ciotti, Maria Teresa; Mercanti, Delio; Santoni, Angela; Eusebi, Fabrizio

doi:10.1016/s0165-5728(98)00192-1

Cited by 143 publications

(86 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several studies have demonstrated that chemokines CXCL1, CXCL8, or CXCL12 regulate neurotransmitter release or modulate ion channel activity at both the presynaptic and postsynaptic levels. 36,37 Moreover, a recent study has reported that CX3CL1, a chemokine constitutively expressed in the CNS (along with CXCL12 and CXCL14), is a potent neuromodulator of evoked excitatory synaptic transmission. 38 Beyond their role in the CNS under physiological conditions, chemokines and chemokine receptors are studied primarily as mediators of CNS pathologies, especially those with an inflammatory component such as multiple sclerosis (MS).…”

Section: Chemokines and Chemokine Receptors In The Central Nervous Symentioning

confidence: 99%

Chemokines and Chemokine Receptors in Neurological Disease: Raise, Retain, or Reduce?

Savarin-Vuaillat¹,

Ransohoff²

2007

Neurotherapeutics

155

126

View full text Add to dashboard Cite

Summary:Chemokines and chemokine receptors comprise a large number of molecules implicated in a wide range of physiological and pathological functions. Numerous studies have demonstrated the roles of chemokines and chemokine receptors: 1) during development, by regulating hematopoiesis, cardiogenesis, and vascular and cerebellar development; 2) during tumor biology, by controlling cell proliferation, angiogenesis, and metastasis; and 3), especially during leukocyte migration, by acting on firm adhesion, locomotion, diapedesis, and chemotaxis. This review focuses on chemokine and chemokine receptor involvement in diverse neurological diseases and their therapeutic potentials. Because of its induction or upregulation during CNS pathologies, members of the chemokine system can be used as biological markers. CXCR4 and CXCL12, by the correlation between their expression and the glioblastoma tumor progression, could be a marker to grade this type of CNS tumor. CCR1, by virtue of specific expression in A␤ plaques, may be a marker for Alzheimer pathology. Downregulation of CCL2 in cerebrospinal fluid may be a candidate to characterize multiple sclerosis (MS), but needs additional investigation. Moreover, chemokines and chemokine receptors represent interesting therapeutic targets. Using chemokine receptor antagonists, several studies provided exciting findings for potential neurological disease treatment. Chemokine receptor antagonists reduce disease severity in animal models of MS. In glioblastoma, a CXCR4 antagonist (AMD3100) showed an inhibition of tumor growth. Inhibition of chemokine receptor signaling is not the only therapeutic strategy: for example, CXCR4 -CXCL12 has anti-inflammatory properties and CX3CL1-CX3CR1 controls neurotoxicity. Thus, chemokine biology suggests several approaches for treating neurological disease.

show abstract

Section: Chemokines and Chemokine Receptors In The Central Nervous Symentioning

confidence: 99%

Chemokines and Chemokine Receptors in Neurological Disease: Raise, Retain, or Reduce?

Savarin-Vuaillat¹,

Ransohoff²

2007

Neurotherapeutics

155

126

View full text Add to dashboard Cite

show abstract

“…Slices were placed in a slice incubation chamber at room temperature with oxygenated ACSF and transferred to a recording chamber within 2-24 h after slice preparation. Whole-cell patch-clamp recordings were performed at 24-25°C, as described for pyramidal neurons (10,18). Membrane currents were recorded by using glass electrodes (3-4 M⍀) filled with 130 mM CsCl, 10 mM Hepes, 5 mM 1,2-bis(2-aminophenoxy)ethane-N,N,NЈ,NЈ-tetraacetate, and 2 mM Mg-ATP (pH 7.3, with CsOH).…”

Section: Membrane Preparation Injection Procedure and Electrophysiomentioning

confidence: 99%

Rundown of GABA type A receptors is a dysfunction associated with human drug-resistant mesial temporal lobe epilepsy

Ragozzino

Palma

Angelantonio

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Pharmacotherapeutic strategies have been difficult to develop for several forms of temporal lobe epilepsy, which are consequently treated by surgical resection. To examine this problem, we have studied the properties of transmitter receptors of tissues removed during surgical treatment. We find that when cell membranes, isolated from the temporal neocortex of patients afflicted with drug-resistant mesial temporal lobe epilepsy (TLE), are injected into frog oocytes they acquire GABA type A receptors (GABA A-receptors) that display a marked rundown during repetitive applications of GABA. In contrast, GABA A-receptor function is stable in oocytes injected with cell membranes isolated from the temporal lobe of TLE patients afflicted with neoplastic, dysgenetic, traumatic, or ischemic temporal lesions (lesional TLE, LTLE). Use-dependent GABA A-receptor rundown is also found in the pyramidal neurons of TLE neocortical slices and is antagonized by BDNF. Pyramidal neurons in cortical slices of a traumatic LTLE patient did not show GABA A-receptor rundown. However, the apparent affinity of GABA A-receptor in oocytes microtransplanted with membranes from all of the epileptic patients studied was smaller than the affinity of receptors transplanted from the nonepileptic brain. We conclude that the use-dependent rundown of neocortical GABA Areceptor represents a TLE-specific dysfunction, whereas the reduced affinity may be a general feature of brains of both TLE and LTLE patients, and we speculate that our findings may help to develop new treatments for TLE and LTLE.human slices ͉ Xenopus oocytes

show abstract

“…Our hypothesis was that activating CXCR2, which is known to raise intracellular Ca 2ϩ (7), could lead to release of glutamate. Previously we have shown that GRO␤ modulates the spontaneous release from GABAergic nerve terminals making contacts with Purkinje neurons in cerebellar slices (17,27). To address this issue, we performed both release experiments, prelabeling the intracellular pool of glutamate, and whole-cell patch-clamp recordings from cultured granule neurons acutely exposed to GRO␤.…”

Section: The Neuroprotective Effect Of Gro␤ Is Blocked By Ampa Receptormentioning

confidence: 99%

The chemokine growth-related gene product β protects rat cerebellar granule cells from apoptotic cell death through α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors

Limatola¹,

Ciotti²,

Mercanti³

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

View full text Add to dashboard Cite

Cultured cerebellar granule neurons are widely used as a cellular model to study mechanisms of neuronal cell death because they undergo programmed cell death when switched from a culture medium containing 25 mM to one containing 5 mM K ؉ . We have found that the growth-related gene product ␤ (GRO␤) partially prevents the K ؉ -depletion-induced cell death, and that the neuroprotective action of GRO␤ on granule cells is mediated through the ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) type of ionotropic glutamate receptors. GRO␤-induced survival was suppressed by 6-cyano-7-nitroquinoxaline-2,3-dione, which is a specific antagonist of AMPA͞kainate receptors; it was not affected by the inhibitor of N-methyl-D-aspartate receptors, 2-amino-5-phosphonopentanoic acid, and was comparable to the survival of granule cells induced by AMPA (10 M) treatment. Moreover, GRO␤-induced neuroprotection was abolished when granule cells were treated with antisense oligonucleotides specific for the AMPA receptor subunits, which significantly reduced receptor expression, as verified by Western blot analysis with subunitspecific antibodies and by granule cell electrophysiological sensitivity to AMPA. Our data demonstrate that GRO␤ is neurotrophic for cerebellar granule cells, and that this activity depends on AMPA receptors.chemokines ͉ apoptosis ͉ cerebellar granule neurons ͉ glutamate receptors

show abstract

CXC chemokines interleukin-8 (IL-8) and growth-related gene product α (GROα) modulate Purkinje neuron activity in mouse cerebellum

Cited by 143 publications

References 39 publications

Chemokines and Chemokine Receptors in Neurological Disease: Raise, Retain, or Reduce?

Chemokines and Chemokine Receptors in Neurological Disease: Raise, Retain, or Reduce?

Rundown of GABA type A receptors is a dysfunction associated with human drug-resistant mesial temporal lobe epilepsy

The chemokine growth-related gene product β protects rat cerebellar granule cells from apoptotic cell death through α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors

Contact Info

Product

Resources

About