Changes in the expression of P2X1 and P2X2 purinergic receptors in facial motoneurons after nerve lesions in rodents and correlation with motoneuron degeneration

Kassa, Roman M.; Bentivoglio, Marina; Mariotti, Raffaella

doi:10.1016/j.nbd.2006.08.020

Cited by 22 publications

(15 citation statements)

References 43 publications

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“…In Western blot, this antibody recognizes a double band at the expected size of ϳ50 kDa in human platelet lysates (manufacturer's technical information). Similar bands were detected in mouse-brain extracts, and the antibody detected injured rat MNs by immunocytochemistry (Kassa et al, 2007). The P2X 2 antibody (cat.…”

Section: Immunohistochemical Proceduressupporting

confidence: 58%

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Strong P2X₄ purinergic receptor‐like immunoreactivity is selectively associated with degenerating neurons in transgenic rodent models of amyotrophic lateral sclerosis

Casanovas

Hernández

Tarabal

et al. 2007

J of Comparative Neurology

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The distribution of the P2X family of ATP receptors was analyzed in a rat model for amyotrophic lateral sclerosis (ALS) expressing mutated human superoxide dismutase (mSOD1(G93A)). We showed that strong P2X(4) immunoreactivity was selectively associated with degenerating motoneurons (MNs) in spinal cord ventral horn. Degenerating P2X(4)-positive MNs did not display apoptotic features such as chromatin condensation, positive TUNEL reaction, or active caspase 3 immunostaining. In contrast, these neurons showed other signs of abnormality, such as loss of the neuronal marker NeuN and recruitment of microglial cells with neuronophagic activity. Similar changes were observed in MNs from the cerebral cortex and brainstem in mSOD1(G93A) in both rat and mice. In addition, P2X(4) immunostaining demonstrated the existence of neuronal degeneration in the locus coeruleus, reticular formation, and Purkinje cells of the cerebellar cortex. It is suggested that abnormal trafficking and proteolytic processing of the P2X(4) receptor protein may underlie these changes.

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Section: Immunohistochemical Proceduressupporting

confidence: 58%

“…Changes in the expression of P2X 1 and P2X 2 subtypes of ATP receptors have been observed in axotomized facial MNs (Kassa et al, 2007). P2X 4 was not studied in this work but was found in increased concentrations in axotomized vagal MNs in another study (Atkinson et al, 2003).…”

Section: Discussionmentioning

confidence: 67%

Strong P2X₄ purinergic receptor‐like immunoreactivity is selectively associated with degenerating neurons in transgenic rodent models of amyotrophic lateral sclerosis

Casanovas

Hernández

Tarabal

et al. 2007

J of Comparative Neurology

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“…Thus, in this model, NO/P2XR signalling is not associated with evident influences on postlesional death mechanisms. With all data pooled together, NO/P2XR signalling has been associated with either neuronal survival (Viscomi et al, 2004) or neuronal death (Kassa et al, 2007) or with neither of them (present study). All in all, it can be argued that the effects of NO and P2XR signalling on neuronal survival vary in relation to the lesion mechanisms involved, and both neuroprotective and neurodegenerative phenomena can be activated.…”

Section: Discussionmentioning

confidence: 51%

“…In a remote cell death model, nNOS and P2X 1 R have been observed to be induced in the same cells, and their interaction has been hypothesized to favor neuronal survival (Viscomi et al, 2004). In contrast, NOS and P2X 1 R coexpression has been linked to decrease regenerative capacities after facial nerve lesion development (Kassa et al, 2007). In the present study, neuronal death after TMT intoxication occurs at a constant rate through the time frame analyzed (see Fig.…”

Section: Discussionmentioning

confidence: 53%

Trimethyltin intoxication up‐regulates nitric oxide synthase in neurons and purinergic ionotropic receptor 2 in astrocytes in the hippocampus

Latini

Geloso²,

Corvino³

et al. 2009

J of Neuroscience Research

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Nitric oxide (NO) and purinergic ionotropic receptors (P2X) mediate cellular events in the central nervous system (CNS) under physiological conditions as well as during pathological events, and they have been recently proposed to interact in mediating CNS response to injury (Viscomi et al. [2004] Neuroscience 123:393-404; Florenzano et al. [2008] Pflugers Arch. 452:622-644). Trimethyltin (TMT) is an organotin compound that generates neurotoxic effects, and it has been used in a model of neurodegenerative disease and memory dysfunction. TMT causes neuronal death and reactive gliosis primarily in the hippocampus and other limbic regions. In the present study, we examined the degenerative events and the expression of nitric oxide synthase (NOS) and P2X receptor subtypes (P2X(1,2,4,7)Rs) that were induced by TMT administration at different time points (3, 7, 14, and 21 days) by conventional and confocal microscopy and Western blotting. Massive glial activation and neuronal death in the CA1 and CA3 regions were observed after TMT treatment. In these areas, astrocytic P2X(2)R and neuronal NOS were temporarily enhanced in association with the progression of neuronal death. In the hippocampus, the physiological expression of P2X(1)R, P2X(4)R, and P2X(7)R was not modified by TMT. The present data demonstrate that, as in other neurodegenerative models, TMT-induced hippocampal degeneration is associated with nitrergic and purinergic activations. Nevertheless, at odds with previous data, in this model the two systems are active in segregated cell populations, namely, P2XR in astrocytes and NOS in neurons. Finally, the temporal relations between P2XR and NOS expression and neuronal degeneration suggest interactions between P2XR/NO signaling and cell survival.

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“…The zero value of uncalibrated optical density was assigned to the background in each section, evaluated in tissue devoid of specific labeling according to a standardized previously adopted protocol (27). The data (mean value of optical density units per animal T standard deviation) were statistically evaluated with the independent sample t-test; significance was set at p G 0.05.…”

Section: Densitometric Analysis Of Glia Immunosignalmentioning

confidence: 99%

Gene, Cell, and Axon Changes in the Familial Amyotrophic Lateral Sclerosis Mouse Sensorimotor Cortex

Kassa¹,

Mariotti²,

Bonaconsa³

et al. 2009

J Neuropathol Exp Neurol

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Lower motoneuron abnormalities have been extensively documented in the murine model of familial amyotrophic lateral sclerosis, whereas information on corticospinal neurons in these mice is very limited. We investigated 1) mRNA levels of inflammation-related molecules in the deep layers in which corticospinal neurons reside, 2) corticospinal neurons labeled from tracer injections in the corticospinal tract at the cervical level, 3) axonal damage revealed by A-amyloid precursor protein accumulation, and 4) glial cell activation in the sensorimotor cortex of presymptomatic and endstage superoxide dismutase (SOD)-1 (G93A) mice. We demonstrated induction of inflammatory gene transcripts in the deep layers, early and progressive shrinkage of corticospinal cell bodies and activation of surrounding astrocytes and microglia with upregulation of major histocompatibility complex class I antigen. Accumulation of A-amyloid precursor protein in proximal axonal swellings indicating axonal injury was also evident at the terminal stage in the motor cortex and internal capsule. Glial and axon changes were not observed elsewhere in the cortex. These data reveal that the entire motor circuit is affected in this murine amyotrophic lateral sclerosis model as it is in human amyotrophic lateral sclerosis. Sensorimotor cortical inflammation and progressive corticospinal cell body and fiber damage may reflect transsynaptic signaling of damage from lower motoneurons.

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Changes in the expression of P2X1 and P2X2 purinergic receptors in facial motoneurons after nerve lesions in rodents and correlation with motoneuron degeneration

Cited by 22 publications

References 43 publications

Strong P2X₄ purinergic receptor‐like immunoreactivity is selectively associated with degenerating neurons in transgenic rodent models of amyotrophic lateral sclerosis

Strong P2X₄ purinergic receptor‐like immunoreactivity is selectively associated with degenerating neurons in transgenic rodent models of amyotrophic lateral sclerosis

Trimethyltin intoxication up‐regulates nitric oxide synthase in neurons and purinergic ionotropic receptor 2 in astrocytes in the hippocampus

Gene, Cell, and Axon Changes in the Familial Amyotrophic Lateral Sclerosis Mouse Sensorimotor Cortex

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Changes in the expression of P2X1 and P2X2 purinergic receptors in facial motoneurons after nerve lesions in rodents and correlation with motoneuron degeneration

Cited by 22 publications

References 43 publications

Strong P2X4 purinergic receptor‐like immunoreactivity is selectively associated with degenerating neurons in transgenic rodent models of amyotrophic lateral sclerosis

Strong P2X4 purinergic receptor‐like immunoreactivity is selectively associated with degenerating neurons in transgenic rodent models of amyotrophic lateral sclerosis

Trimethyltin intoxication up‐regulates nitric oxide synthase in neurons and purinergic ionotropic receptor 2 in astrocytes in the hippocampus

Gene, Cell, and Axon Changes in the Familial Amyotrophic Lateral Sclerosis Mouse Sensorimotor Cortex

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Strong P2X₄ purinergic receptor‐like immunoreactivity is selectively associated with degenerating neurons in transgenic rodent models of amyotrophic lateral sclerosis

Strong P2X₄ purinergic receptor‐like immunoreactivity is selectively associated with degenerating neurons in transgenic rodent models of amyotrophic lateral sclerosis