Dye coupling among satellite glial cells in mammalian dorsal root ganglia

Huang, Tian-Ying; Cherkas, Pavel; Rosenthal, David W.; Hanani, Menachem

doi:10.1016/j.brainres.2004.12.021

Cited by 76 publications

(70 citation statements)

References 45 publications

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“…In a manner analogous to that already shown for astrocytes, an increased ability of gap junctions to diffuse metabolites may be beneficial to the neuron (Andrade-Rozental et al, 2000;Farahani et al, 2005;Goldberg et al, 1999). Increased coupling by SGCs in sensory ganglia also appears to be involved in a variety of neuropathic pain states (Dublin and Hanani, 2007;Warwick and Hanani, 2013;Zhang et al, 2010) and may be linked to altered buffering of ionic currents, including potassium, amongst SGCs (Huang et al, 2005;Konishi, 1996). Further, the reduced expression of an inward rectifying potassium channel, K ir 4.1, expression in SGCs associated with axotomized sensory neurons also impacts these pain states (Tang et al, 2010).…”

mentioning

confidence: 79%

Induction of a reactive state in perineuronal satellite glial cells akin to that produced by nerve injury is linked to the level of p75NTR expression in adult sensory neurons

Nadeau

Wilson-Gerwing

Verge

2014

Glia

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Satellite glial cells (SGCs) surrounding primary sensory neurons are similar to astrocytes of the central nervous system in that they buffer the extracellular environment via potassium and calcium channels and express the intermediate filament glial fibrillary acidic protein (GFAP). Peripheral nerve injury induces a reactive state in SGCs that includes SGC proliferation, increased SGC/SGC coupling via gap junctions, decreased inward rectifying potassium channel 4.1 (Kir 4.1) expression and increased expression of GFAP and the common neurotrophin receptor, p75NTR. In contrast, neuronal p75NTR expression, normally detected in ∼80% of adult rat sensory neurons, decreases in response to peripheral axotomy. Given the differential regulation of p75NTR expression in neurons versus SGCs with injury, we hypothesized that reduced signaling via neuronal p75NTR contributes to the induction of a reactive state in SGCs. We found that reducing neuronal p75NTR protein expression in uninjured sensory neurons by intrathecal subarachnoid infusion of p75NTR-selective anti-sense oligodeoxynucleotides for one week was sufficient to induce a "reactive-like" state in the perineuronal SGCs akin to that normally observed following peripheral nerve injury. This reactive state included significantly increased SGC p75NTR, GFAP and gap junction protein connexin-43 protein expression, increased numbers of SGCs surrounding individual sensory neurons and decreased SGC Kir 4.1 channel expression. Collectively, this supports the tenet that reductions in target-derived trophic support leading to, or as a consequence of, reduced neuronal p75NTR expression plays a critical role in switching the SGC to a reactive state.

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mentioning

confidence: 79%

Induction of a reactive state in perineuronal satellite glial cells akin to that produced by nerve injury is linked to the level of p75NTR expression in adult sensory neurons

Nadeau

Wilson-Gerwing

Verge

2014

Glia

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“…A glass electrode was filled with 4% Lucifer Yellow, which was then injected for 5 min using Axopatch 200B (Axon Instruments, Foster City, CA, USA). With this process, approximately five neurons within a 100-200 mm depth from the surface of a slice were injected (Huang et al 2005, Hanani 2012). …”

Section: Current Injection Of Neurons By Lucifer Yellowmentioning

confidence: 99%

Hippocampal spine changes across the sleep–wake cycle: corticosterone and kinases

Ikeda¹,

Hojo²,

Komatsuzaki³

et al. 2015

Journal of Endocrinology

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The corticosterone (CORT) level changes along the circadian rhythm. Hippocampus is sensitive to CORT, since glucocorticoid receptors are highly expressed. In rat hippocampus fixed in a living state every 3 h, we found that the dendritic spine density of CA1 pyramidal neurons increased upon waking (within 3 h), as compared with the spine density in the sleep state. Particularly, the large-head spines increased. The observed change in the spine density may be due to the change in the hippocampal CORT level, since the CORT level at awake state (w30 nM) in cerebrospinal fluid was higher than that at sleep state (w3 nM), as observed from our earlier study. In adrenalectomized (ADX) rats, such a wake-induced increase of the spine density disappeared. S.c. administration of CORT into ADX rats rescued the decreased spine density. By using isolated hippocampal slices, we found that the application of 30 nM CORT increased the spine density within 1 h and that the spine increase was mediated via PKA, PKC, ERK MAPK, and LIMK signaling pathways. These findings suggest that the moderately rapid increase of the spine density on waking might mainly be caused by the CORT-driven kinase networks.

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“…The permeability of gap junctions in non-nervous tissues [9,34,36], in the central nervous system [31], and in spinal ganglia [15] is regulated by a number of conditions. In the absence of data on the gap junction permeability in satellite cells of various ages, it is not clear what influence the age changes in number and density of gap junctions have on the functions of perineuronal satellite cells.…”

Section: Discussionmentioning

confidence: 99%

Increase in number of the gap junctions between satellite neuroglial cells during lifetime: An ultrastructural study in rabbit spinal ganglia from youth to extremely advanced age

Martinelli

Sartori

Palo

et al. 2005

Brain Research Bulletin

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Dye coupling among satellite glial cells in mammalian dorsal root ganglia

Cited by 76 publications

References 45 publications

Induction of a reactive state in perineuronal satellite glial cells akin to that produced by nerve injury is linked to the level of p75NTR expression in adult sensory neurons

Induction of a reactive state in perineuronal satellite glial cells akin to that produced by nerve injury is linked to the level of p75NTR expression in adult sensory neurons

Hippocampal spine changes across the sleep–wake cycle: corticosterone and kinases

Increase in number of the gap junctions between satellite neuroglial cells during lifetime: An ultrastructural study in rabbit spinal ganglia from youth to extremely advanced age

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