p38 Mitogen-Activated Protein Kinase Contributes to Adenosine A<sub>1</sub>Receptor-Mediated Synaptic Depression in Area CA1 of the Rat Hippocampus

Brust, Tyson B.; Cayabyab, Francisco S.; Zhou, Ning; MacVicar, Brian A.

doi:10.1523/jneurosci.4052-06.2006

Cited by 45 publications

(43 citation statements)

References 105 publications

(106 reference statements)

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“…The signaling pathways required for proper synaptic transmission that are altered by IB2 disruption have not been determined. p38 MAP kinase signaling is a plausible candidate pathway, as IB2 preferentially associates with the p38 subclass of MAP kinases (Schoorlemmer and Goldfarb, 2001; Buchsbaum et al, 2002; Schoorlemmer and Goldfarb, 2002; Robidoux et al, 2005), and both presynaptic and postsynaptic p38 signaling are known to regulate synaptic transmission (Derkinderen et al, 2001; Huang et al, 2004; Krapivinsky et al, 2004; Brust et al, 2006; Li et al, 2006). Other possible mechanisms of IB2 action include modulation of src-like kinase activity (Kennedy et al, 2007) or control of macromolecular transport through IB2 association with kinesin (Verhey et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Behavioral and Cerebellar Transmission Deficits in Mice Lacking the Autism-Linked Gene Islet Brain-2

Giza¹,

Urbanski²,

Prestori³

et al. 2010

J. Neurosci.

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Deletion of the human SHANK3 gene near the terminus of chromosome 22q is associated with Phelan-McDermid syndrome and autism spectrum disorders. Nearly all such deletions also span the tightly linked IB2 gene. We show here that IB2 protein is broadly expressed in the brain and is highly enriched within postsynaptic densities. Experimental disruption of the IB2 gene in mice reduces AMPA and enhances NMDA receptor-mediated glutamatergic transmission in cerebellum, changes the morphology of Purkinje cell dendritic arbors, and induces motor and cognitive deficits suggesting an autism phenotype. These findings support a role for human IB2 mutation as a contributing genetic factor in Chr22qter-associated cognitive disorders.

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Section: Discussionmentioning

confidence: 99%

Behavioral and Cerebellar Transmission Deficits in Mice Lacking the Autism-Linked Gene Islet Brain-2

Giza¹,

Urbanski²,

Prestori³

et al. 2010

J. Neurosci.

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“…It is unknown if the increase in p38 MAPK observed in our studies played a role in the CCL2-induced increase in synaptic network activity. Both p38 MAPK and CREB have been shown to play a key regulatory role in synaptic transmission, synaptic plasticity and memory mechanisms (Alonso et al, 2003;Brust et al, 2006;Butler et al, 2004;Josselyn and Nguyen, 2005;Rossato et al, 2006;Wang et al, 2007). Thus, these hippocampal synaptic functions may be an important target of CCL2 in the normal brain or during conditions associated with neuroinflammation and p38 MAPK may play a central role in the effects of CCL2 on these functions.…”

Section: Discussionmentioning

confidence: 99%

The chemokine CCL2 activates p38 mitogen-activated protein kinase pathway in cultured rat hippocampal cells

Cho

Gruol

2008

Journal of Neuroimmunology

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Emerging evidence indicates that chemokines can regulate both the physiology and biochemistry of CNS neurons and glia. In the current study, Western blot analysis showed that in rat hippocampal neuronal/glial cultures the signal transduction pathway activated by CCL2, a chemokine expressed in the normal brain and at elevated levels during neuroinflammation, involves a G-protein coupled receptor, p38 MAPK as well as its immediate upstream kinase MKK3/6, and the downstream transcription factor CREB. ERK 1/2 and the transcription factors STAT1 and STAT3 do not play a prominent role. CCL2 also altered Ca 2+ influx and synaptic network activity in the hippocampal neurons. These results suggest an important role for p38 MAPK and CREB in hippocampal actions of CCL2.

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“…Adenosine also affects both brain neuronal and astrocytic intermediary metabolism [63,[172][173][174][175][176]. In particular, A 1 R can affect AMPK [177], p38 MAPK [178][179][180][181] or preserve mitochondria function through control of K ATP channels [182][183][184][185][186]; these are all pathways known to coordinate primary metabolism and to have a profound impact on neuronal function and viability [187][188][189]. However, an integrative picture relating A 1 R activation and the putative recruitment of each of these candidate transducing pathways in the realm of neuroprotection has still not been put forward.…”

Section: B Possible Mechanisms Operated By a 1 Receptors To Managementioning

confidence: 99%

Role of The Purinergic Neuromodulation System in Epilepsy

Tomé¹,

Silva²,

Cunha³

2010

TONEURJ

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Adenosine has long been considered an endogenous anti-epileptic compound. This concept was based on the widespread distribution of adenosine A 1 receptors (A 1 R), which are mostly located in excitatory synapses; here, A 1 R inhibit glutamate release, decrease glutamatergic responsiveness and hyperpolarise neurons. However, the combined observation that synaptic A 1 R undergo desensitisation in chronic noxious situations whereas the activation of A 1 R still prevents seizure activity suggests that the A 1 R anti-epileptic action may involve non-synaptic mechanisms. Two alternative mechanisms can be considered to explain the ability of A 1 R to control seizure activity and resulting neurodegeneration: 1) the possible role of A 1 R-mediated control of metabolism; 2) the A 1 R-mediated preconditioning involving a coordinated control of neuron-glia communication. However, purinergic modulation of seizure activity is likely to involve other systems apart from A 1 R. Thus, the blockade of adenosine A 2A receptors (A 2A R), which density increases in animal models of epilepsy, can attenuate seizure activity and prevent seizure-induced neurodegeneration. Furthermore, ATP, which is the main source of the endogenous adenosine activating A 2A R, also act as a general danger signal and may also directly control seizure activity through P 2 receptors (P 2 R). Therefore, the purinergic control of epilepsy may actually involve different parallel signalling arms, some beneficial and others deleterious, probably acting at different sites (in epileptic foci and in their neighbourhood) and at different times. It is likely that combined targeting of different purinergic receptors may be the most efficacious way to control seizure activity, its spreading and the resulting neurodegeneration.

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p38 Mitogen-Activated Protein Kinase Contributes to Adenosine A₁Receptor-Mediated Synaptic Depression in Area CA1 of the Rat Hippocampus

Cited by 45 publications

References 105 publications

Behavioral and Cerebellar Transmission Deficits in Mice Lacking the Autism-Linked Gene Islet Brain-2

Behavioral and Cerebellar Transmission Deficits in Mice Lacking the Autism-Linked Gene Islet Brain-2

The chemokine CCL2 activates p38 mitogen-activated protein kinase pathway in cultured rat hippocampal cells

Role of The Purinergic Neuromodulation System in Epilepsy

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p38 Mitogen-Activated Protein Kinase Contributes to Adenosine A1Receptor-Mediated Synaptic Depression in Area CA1 of the Rat Hippocampus

Cited by 45 publications

References 105 publications

Behavioral and Cerebellar Transmission Deficits in Mice Lacking the Autism-Linked Gene Islet Brain-2

Behavioral and Cerebellar Transmission Deficits in Mice Lacking the Autism-Linked Gene Islet Brain-2

The chemokine CCL2 activates p38 mitogen-activated protein kinase pathway in cultured rat hippocampal cells

Role of The Purinergic Neuromodulation System in Epilepsy

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Product

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About

p38 Mitogen-Activated Protein Kinase Contributes to Adenosine A₁Receptor-Mediated Synaptic Depression in Area CA1 of the Rat Hippocampus