Neonatal infraorbital nerve transection in the rat: Comparison of effects on substance P immunoreactive primary afferents and those recognized by the lectin <i>Bandierea simplicifolia</i>‐I

White, Fletcher A.; Bennett‐Clarke, Carol A.; MacDonald, Gordon J. F.; Enfiejian, Howard L.; Chiaia, Nicolas L.; Rhoades, Robert W.

doi:10.1002/cne.903000208

Cited by 29 publications

(14 citation statements)

References 54 publications

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“…They noted that V ganglion cells born late in gestation, on E-12.5 through E-14.5, were significantly more likely than early-born (E-9.5 through E-11.5) cells to survive neonatal axotomy. The combination of these results with those provided by Enfiejian et al (1989) and White et al (1990) suggested to us that ganglion cells with different phenotypes may have different distributions of birth dates, indicating that these differences might be related to differential survival after neonatal axotomy.…”

Section: Indexing Terms: Neurogenesis Cell Death Immunocytochemistrmentioning

confidence: 56%

Birth dates and survival after axotomy of neurochemically defined subsets of trigeminal ganglion cells

White

Chiaia

MacDonald

et al. 1995

J of Comparative Neurology

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Trigeminal (V) ganglion cells with different neurochemical phenotypes or different birth dates are affected differently by neonatal axonal transection. The aim of the present study was to determine if V ganglion cell birth date and neurochemical phenotype were correlated and if these two variables could be related to responses to neonatal axonal transection. Immunocytochemistry, histochemistry, and [3H]thymidine labelling were used to determine the birth dates of V ganglion cells recognized by antibodies directed against neurofilament protein (NF), calcitonin gene-related peptide (CGRP), and substance P (SP) and those that bound the lectin Bandierea simplicifolia-I (BS-I). All V ganglion cells were born between embryonic days (E-) 9.5 and 14.5. All ganglion cells were born between E-9.5 and E-14.5. In a normalized population (percentages normalized to equal 100%), over 90% of NF-positive V ganglion cells were born between E-10.5 and E-12.5. The majority of CGRP-positive and SP-positive ganglion cells (> 90%) were generated from E-13.5 to E-14.5 and E-12.5 through E-14.5, respectively. Almost 85% of BS-I-positive ganglion cells were generated on E-12.5 through E-14.5. Previous results and additional data from this study indicated that NF- and BS-I-positive ganglion cells are proportionally more likely to be lost after neonatal axotomy and that SP-positive cells are more likely to remain. The percentage of CGRP-positive cells in the V ganglion was not significantly altered by neonatal infraorbital nerve transection. Overall, these findings do not indicate a strong relationship between cell birth date and the probability of survival after neonatal axonal damage for all V ganglion cell phenotypes.

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Section: Indexing Terms: Neurogenesis Cell Death Immunocytochemistrmentioning

confidence: 56%

Birth dates and survival after axotomy of neurochemically defined subsets of trigeminal ganglion cells

White

Chiaia

MacDonald

et al. 1995

J of Comparative Neurology

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“…Neonatal and adult sensory neurons also differ in their responses to injury. IB4-binding neurons are selectively vulnerable to neonatal axotomy (49), and adult neurons are more resistant than neonatal neurons to apoptotic stimuli, including phosphatidylinositol 3-kinase (PI3K) inhibition and NGF withdrawal (47). Finally, although adult ganglionic neurons differ in size (both in vitro and in vivo), cultured neonatal neurons are homogeneous in size (19).…”

Section: Discussionmentioning

confidence: 99%

A5-Positive Primary Sensory Neurons Are Nonpermissive for Productive Infection with Herpes Simplex Virus 1 In Vitro

Bertke

Swanson

Chen

et al. 2011

J Virol

120

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Herpes simplex viruses 1 and 2 (HSV-1 and HSV-2) establish latency and express the latency-associated transcript (LAT) preferentially in different murine sensory neuron populations, with most HSV-1 LAT expression in A5؉ neurons and most HSV-2 LAT expression in KH10 ؉ neurons. To study the mechanisms regulating the establishment of HSV latency in specific subtypes of neurons, cultured dissociated adult murine trigeminal ganglion (TG) neurons were assessed for relative permissiveness for productive infection. In contrast to that for neonatal TG, the relative distribution of A5 ؉ and KH10 ؉ neurons in cultured adult TG was similar to that seen in vivo. Productive infection with HSV was restricted, and only 45% of cultured neurons could be productively infected with either HSV-1 or HSV-2. A5؉ neurons supported productive infection with HSV-2 but were selectively nonpermissive for productive infection with HSV-1, a phenomenon that was not due to restricted viral entry or DNA uncoating, since HSV-1 expressing ␤-galactosidase under the control of the neurofilament promoter was detected in ϳ90% of cultured neurons, with no preference for any neuronal subtype. Infection with HSV-1 reporter viruses expressing enhanced green fluorescent protein (EGFP) from immediate early (IE), early, and late gene promoters indicated that the block to productive infection occurred before IE gene expression. Trichostatin A treatment of quiescently infected neurons induced productive infection preferentially from non-A5 ؉ neurons, demonstrating that the nonpermissive neuronal subtype is also nonpermissive for reactivation. Thus, HSV-1 is capable of entering the majority of sensory neurons in vitro; productive infection occurs within a subset of these neurons; and this differential distribution of productive infection is determined at or before the expression of the viral IE genes.Herpes simplex virus 1 and 2 (HSV-1 and HSV-2) replication at the periphery is accompanied by infection of neuronal axons and subsequent retrograde axonal transport to cell bodies of primary sensory neurons, where infection may follow either a productive or a latent pathway. For some neurons, lytic gene expression and progeny virus production are thought to result in cell death, while in other neurons, the productive cycle fails and the virus establishes a latent infection. The factors that determine whether HSV progresses through a productive cycle or establishes latency are not clear. It is suspected that different neuronal subtypes and/or the presence or absence of certain host factors may be critical in determining the outcome of infection.Primary sensory neurons are a diverse population of cells that are classified according to cellular morphology, physiological response properties, and patterns of gene expression. We have demonstrated previously that HSV-1 and HSV-2 preferentially establish latency and express the latency-associated transcript (LAT) in different populations of neurons, identified by the A5 and KH10 markers, within sensory ganglia (21,28,52). ...

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“…During embryonic development, this neuron population appears to depend on NGF for survival initially but downregulates trkA during early postnatal life and thereafter becomes dependent on GDNF , but the reasons for these changes in trophic dependence and their physiological significance are uncertain. In adult animals, it is well established that projections of IB4-labeled neurons in the dorsal horn regress after PNS lesions (White et al, 1990;Bennett et al, 1998;Bailey and Ribeiro-daSilva, 2006), although projections of CGRP-positive neurons appear less affected. One consequence of the regression of the IB4-labeled axonal projection is that it might allow sprouting of other classes of axons into the denervated territory, which could contribute to hyperalgesia associated with nerve lesions (Doubell et al, 1997), although this hypothesis has been challenged (Bao et al, 2002;Hughes et al, 2003;Shehab et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Impaired Axonal Regeneration by Isolectin B4-Binding Dorsal Root Ganglion NeuronsIn Vitro

Leclere¹,

Norman²,

Groutsi³

et al. 2007

J. Neurosci.

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The subpopulation of dorsal root ganglion (DRG) neurons recognized by Griffonia simplicifolia isolectin B4 (IB4) differ from other neurons by expressing receptors for glial cell line-derived neurotrophic factor (GDNF) rather than neurotrophins. Additionally, IB4-labeled neurons do not express the laminin receptor, ␣7-integrin (Gardiner et al., 2005), necessary for optimal axonal regeneration in the peripheral nervous system. In cultures of dissociated DRG neurons of adult mice on laminin, robust spontaneous neurite outgrowth from IB4-negative neurons occurs and is strongly enhanced by previous axotomy. In contrast, IB4-labeled neurons show little neurite outgrowth and do not express GAP 43, even after axotomy or culture with GDNF. Moreover, growth of their axons through collagen gels is impaired compared with other DRG neurons. To determine whether the sparse neurite outgrowth of IB4-labeled neurons is attributable to lack of integrin expression, DRG cultures were infected with a herpes simplex 1 vector encoding ␣7-integrin, but its forced expression failed to promote neurite outgrowth in either IB4-labeled or other DRG neurons or in cultured adult retinal ganglion cells. Forced coexpression of both ␣7-integrin and GAP 43 also failed to promote neurite outgrowth in IB4-labeled neurons. In addition, cultured sciatic nerve segments were found to release much lower levels of GDNF, demonstrated by ELISA, than nerve growth factor. These findings together with their impaired intrinsic axonal regeneration capacity may contribute to the known vulnerability of the IB4-labeled population of DRG neurons to peripheral nerve injury.

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Neonatal infraorbital nerve transection in the rat: Comparison of effects on substance P immunoreactive primary afferents and those recognized by the lectin Bandierea simplicifolia‐I

Cited by 29 publications

References 54 publications

Birth dates and survival after axotomy of neurochemically defined subsets of trigeminal ganglion cells

Birth dates and survival after axotomy of neurochemically defined subsets of trigeminal ganglion cells

A5-Positive Primary Sensory Neurons Are Nonpermissive for Productive Infection with Herpes Simplex Virus 1 In Vitro

Impaired Axonal Regeneration by Isolectin B4-Binding Dorsal Root Ganglion NeuronsIn Vitro

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