Ganglionectomy

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Robert E Widdop - One of the best experts on this subject based on the ideXlab platform.

  • Minocycline treatment attenuates microglia activation and non-angiotensin II [125I] CGP42112 binding in brainstem following nodose Ganglionectomy.
    Neuroscience, 2005
    Co-Authors: Carli L. Roulston, Andrew J. Lawrence, Robert E Widdop, Bevyn Jarrott
    Abstract:

    We have previously shown that following unilateral nodose Ganglionectomy, [125I] CGP42112 binds to a non-angiotensin II (Ang II) related binding site in rat dorsal motor nucleus of the vagus nerve, ambiguus nucleus and nucleus of the solitary tract. Furthermore, this up-regulated binding site localizes with activated microglia. Given that some tetracyclines may inhibit microglia activation in brain, we examined the effect of minocycline treatment on the binding of [125I] CGP42112 and [3H] PK11195 (an established radioligand for microglia), as well as OX-42 immunoreactivity (an immunomarker for activated microglia), following nodose Ganglionectomy. Male Wistar Kyoto rats underwent unilateral nodose Ganglionectomy or sham operation and were treated with saline or minocycline (50 mg/kg i.p.) 12 h before surgery and twice daily after surgery (each 50mg/kg i.p.) for 3 days. Subsequent to nodose Ganglionectomy, [125I] CGP42112 binding (insensitive to PD123319 or Ang II) was increased approximately two-fold in the ipsilateral nucleus of the solitary tract and was also induced in the ipsilateral dorsal motor nucleus of the vagus nerve and ambiguus nucleus of saline-treated rats. Treatment with minocycline reduced this non-angiotensin II [125I] CGP42112 binding (40-50% reduction) in the nucleus of the solitary tract, dorsal motor nucleus of the vagus nerve and ambiguus nucleus. Analogous experiments using [3H] PK11195 also revealed up-regulated binding in the ipsilateral nucleus of the solitary tract ( approximately 205%), dorsal motor nucleus of the vagus nerve (approximately 80%) and ambiguus nucleus (approximately 210%) of saline-treated rats following nodose Ganglionectomy, which was reduced by 40-100% with minocycline treatment. Immunoreactivity to OX-42 confirmed an increase in microglia activation and accumulation of macrophages in these brain stem nuclei following nodose Ganglionectomy, which was also attenuated following treatment with minocycline. These data demonstrate that non-Ang II [125I] CGP42112 binding following nodose Ganglionectomy is attenuated by minocycline treatment. This minocycline-induced effect was associated with reduced activation of microglia and an apparent reduction in the number of macrophages in the abovementioned nuclei. This evidence suggests that a non-Ang II [125I] CGP42112 binding site is located on, or associated with, activated microglia and macrophages, providing a useful tool with which to quantitate the neuroprotective effects of centrally acting anti-inflammatory compounds.

  • non angiotensin ii 125i cgp42112 binding is a sensitive marker of neuronal injury in brainstem following unilateral nodose Ganglionectomy comparison with markers for activated microglia
    Neuroscience, 2004
    Co-Authors: Carli L. Roulston, Andrew J. Lawrence, Bevyn Jarrott, Robert E Widdop
    Abstract:

    Abstract Previously we reported that a non-angiotensin II [ 125 I] CGP42112 binding site is up-regulated in rat brainstem nuclei as a result of unilateral nodose Ganglionectomy. In the present study, we compared non-angiotensin II [ 125 I] CGP42112 binding with microglia/macrophage activation following nodose Ganglionectomy, using both in vitro autoradiography and immunohistochemistry. Specific [ 125 I] CGP42112 binding was observed in the nucleus of the solitary tract (NTS) and revealed an AT 2 receptor component as well as a non-angiotensin II receptor component. Subsequent to unilateral nodose Ganglionectomy, [ 125 I] CGP42112 binding in the ipsilateral NTS was increased approximately two-fold and was also induced in the ipsilateral dorsal motor nucleus (DMX) and the nucleus ambiguus (n.amb). This non-angiotensin II [ 125 I] CGP42112 binding site was displaced by CGP42112 but not other ligands. Increased [ 3 H] PK11195 binding (a known marker of reactive gliosis) was also observed in the same brainstem nuclei as non-angiotensin II [ 125 I] CGP42112 binding after nodose Ganglionectomy. The similarity in binding patterns between [ 125 I] CGP42112 and [ 3 H] PK11195 was shown to be primarily due to retrograde degeneration in the ipsilateral NTS, DMX and n.amb, as both radioligands were localized to similar cellular targets within the interstial space and over cellular debris. Immunohistochemical data confirmed reactive gliosis within the ipsilateral NTS, DMX and n.amb, following nodose Ganglionectomy, which was predominantly characterized by an increase in OX-42 immunoreactivity (a marker for activated microglia/macrophages), with only a small increase in glial fibrillary acidic protein immunoreactivity (a marker of astrogliosis) detected. These data demonstrate for the first time that non-angiotensin II [ 125 I] CGP42112 binding is associated with activated microglia, as well as macrophages, following unilateral nodose Ganglionectomy. Furthermore, these studies also demonstrate the potential use of non-angiotensin II [ 125 I] CGP42112 binding as a marker for quantitating inflammatory events which occur as a result of damage to the CNS.

  • localization of at2 receptors in the nucleus of the solitary tract of spontaneously hypertensive and wistar kyoto rats using 125i cgp42112 upregulation of a non angiotensin ii binding site following unilateral nodose Ganglionectomy
    Brain Research, 2003
    Co-Authors: Carli L. Roulston, Andrew J. Lawrence, Bevyn Jarrott, Robert E Widdop
    Abstract:

    Abstract We have examined the binding distribution of a selective AT 2 receptor ligand [ 125 I] CGP42112 in the brain of adult Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). AT 2 receptor localization was also examined in the rat brainstem following unilateral nodose Ganglionectomy. Specific [ 125 I] CGP42112 binding was observed in discrete brain regions from both rat strains, including the nucleus of the solitary tract (NTS), and did not differ between WKY and SHR. [ 125 I] CGP42112 binding in the NTS revealed an AT 2 receptor component that was displaceable by PD 123319 and Ang II (50–58%), as well as a non-angiotensin II receptor component (42–49%). Following unilateral nodose Ganglionectomy, [ 125 I] CGP42112 binding density on the denervated side of the NTS was increased approximately two-fold in both WKY and SHR. This increased [ 125 I] CGP42112 binding density in the ipsilateral NTS was comprised of a greater non-angiotensin II component than that observed in the sham groups, since only ∼30% was displaced by PD123319 and angiotensin II. Furthermore, [ 125 I] CGP42112 also revealed high binding density on the denervated side in the dorsal motor nucleus and the nucleus ambiguus in both WKY and SHR. AT 2 receptor immunoreactivity was also visualised in the NTS of sham operated rats, but was not observed in the dorsal motor nucleus or the nucleus ambiguus, nor was it up-regulated following nodose Ganglionectomy. These results demonstrate, for the first time, an AT 2 receptor binding site in the NTS, as well as a non-angiotensin II [ 125 I] CGP42112 binding site. These studies also demonstrate that nodose Ganglionectomy represents a useful model in which to study a non-angiotensin II [ 125 I] CGP42112 binding site that is up-regulated following degeneration of afferent vagal nerves.

Deeptankar Demazumder - One of the best experts on this subject based on the ideXlab platform.

Carli L. Roulston - One of the best experts on this subject based on the ideXlab platform.

  • Minocycline treatment attenuates microglia activation and non-angiotensin II [125I] CGP42112 binding in brainstem following nodose Ganglionectomy.
    Neuroscience, 2005
    Co-Authors: Carli L. Roulston, Andrew J. Lawrence, Robert E Widdop, Bevyn Jarrott
    Abstract:

    We have previously shown that following unilateral nodose Ganglionectomy, [125I] CGP42112 binds to a non-angiotensin II (Ang II) related binding site in rat dorsal motor nucleus of the vagus nerve, ambiguus nucleus and nucleus of the solitary tract. Furthermore, this up-regulated binding site localizes with activated microglia. Given that some tetracyclines may inhibit microglia activation in brain, we examined the effect of minocycline treatment on the binding of [125I] CGP42112 and [3H] PK11195 (an established radioligand for microglia), as well as OX-42 immunoreactivity (an immunomarker for activated microglia), following nodose Ganglionectomy. Male Wistar Kyoto rats underwent unilateral nodose Ganglionectomy or sham operation and were treated with saline or minocycline (50 mg/kg i.p.) 12 h before surgery and twice daily after surgery (each 50mg/kg i.p.) for 3 days. Subsequent to nodose Ganglionectomy, [125I] CGP42112 binding (insensitive to PD123319 or Ang II) was increased approximately two-fold in the ipsilateral nucleus of the solitary tract and was also induced in the ipsilateral dorsal motor nucleus of the vagus nerve and ambiguus nucleus of saline-treated rats. Treatment with minocycline reduced this non-angiotensin II [125I] CGP42112 binding (40-50% reduction) in the nucleus of the solitary tract, dorsal motor nucleus of the vagus nerve and ambiguus nucleus. Analogous experiments using [3H] PK11195 also revealed up-regulated binding in the ipsilateral nucleus of the solitary tract ( approximately 205%), dorsal motor nucleus of the vagus nerve (approximately 80%) and ambiguus nucleus (approximately 210%) of saline-treated rats following nodose Ganglionectomy, which was reduced by 40-100% with minocycline treatment. Immunoreactivity to OX-42 confirmed an increase in microglia activation and accumulation of macrophages in these brain stem nuclei following nodose Ganglionectomy, which was also attenuated following treatment with minocycline. These data demonstrate that non-Ang II [125I] CGP42112 binding following nodose Ganglionectomy is attenuated by minocycline treatment. This minocycline-induced effect was associated with reduced activation of microglia and an apparent reduction in the number of macrophages in the abovementioned nuclei. This evidence suggests that a non-Ang II [125I] CGP42112 binding site is located on, or associated with, activated microglia and macrophages, providing a useful tool with which to quantitate the neuroprotective effects of centrally acting anti-inflammatory compounds.

  • non angiotensin ii 125i cgp42112 binding is a sensitive marker of neuronal injury in brainstem following unilateral nodose Ganglionectomy comparison with markers for activated microglia
    Neuroscience, 2004
    Co-Authors: Carli L. Roulston, Andrew J. Lawrence, Bevyn Jarrott, Robert E Widdop
    Abstract:

    Abstract Previously we reported that a non-angiotensin II [ 125 I] CGP42112 binding site is up-regulated in rat brainstem nuclei as a result of unilateral nodose Ganglionectomy. In the present study, we compared non-angiotensin II [ 125 I] CGP42112 binding with microglia/macrophage activation following nodose Ganglionectomy, using both in vitro autoradiography and immunohistochemistry. Specific [ 125 I] CGP42112 binding was observed in the nucleus of the solitary tract (NTS) and revealed an AT 2 receptor component as well as a non-angiotensin II receptor component. Subsequent to unilateral nodose Ganglionectomy, [ 125 I] CGP42112 binding in the ipsilateral NTS was increased approximately two-fold and was also induced in the ipsilateral dorsal motor nucleus (DMX) and the nucleus ambiguus (n.amb). This non-angiotensin II [ 125 I] CGP42112 binding site was displaced by CGP42112 but not other ligands. Increased [ 3 H] PK11195 binding (a known marker of reactive gliosis) was also observed in the same brainstem nuclei as non-angiotensin II [ 125 I] CGP42112 binding after nodose Ganglionectomy. The similarity in binding patterns between [ 125 I] CGP42112 and [ 3 H] PK11195 was shown to be primarily due to retrograde degeneration in the ipsilateral NTS, DMX and n.amb, as both radioligands were localized to similar cellular targets within the interstial space and over cellular debris. Immunohistochemical data confirmed reactive gliosis within the ipsilateral NTS, DMX and n.amb, following nodose Ganglionectomy, which was predominantly characterized by an increase in OX-42 immunoreactivity (a marker for activated microglia/macrophages), with only a small increase in glial fibrillary acidic protein immunoreactivity (a marker of astrogliosis) detected. These data demonstrate for the first time that non-angiotensin II [ 125 I] CGP42112 binding is associated with activated microglia, as well as macrophages, following unilateral nodose Ganglionectomy. Furthermore, these studies also demonstrate the potential use of non-angiotensin II [ 125 I] CGP42112 binding as a marker for quantitating inflammatory events which occur as a result of damage to the CNS.

  • localization of at2 receptors in the nucleus of the solitary tract of spontaneously hypertensive and wistar kyoto rats using 125i cgp42112 upregulation of a non angiotensin ii binding site following unilateral nodose Ganglionectomy
    Brain Research, 2003
    Co-Authors: Carli L. Roulston, Andrew J. Lawrence, Bevyn Jarrott, Robert E Widdop
    Abstract:

    Abstract We have examined the binding distribution of a selective AT 2 receptor ligand [ 125 I] CGP42112 in the brain of adult Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). AT 2 receptor localization was also examined in the rat brainstem following unilateral nodose Ganglionectomy. Specific [ 125 I] CGP42112 binding was observed in discrete brain regions from both rat strains, including the nucleus of the solitary tract (NTS), and did not differ between WKY and SHR. [ 125 I] CGP42112 binding in the NTS revealed an AT 2 receptor component that was displaceable by PD 123319 and Ang II (50–58%), as well as a non-angiotensin II receptor component (42–49%). Following unilateral nodose Ganglionectomy, [ 125 I] CGP42112 binding density on the denervated side of the NTS was increased approximately two-fold in both WKY and SHR. This increased [ 125 I] CGP42112 binding density in the ipsilateral NTS was comprised of a greater non-angiotensin II component than that observed in the sham groups, since only ∼30% was displaced by PD123319 and angiotensin II. Furthermore, [ 125 I] CGP42112 also revealed high binding density on the denervated side in the dorsal motor nucleus and the nucleus ambiguus in both WKY and SHR. AT 2 receptor immunoreactivity was also visualised in the NTS of sham operated rats, but was not observed in the dorsal motor nucleus or the nucleus ambiguus, nor was it up-regulated following nodose Ganglionectomy. These results demonstrate, for the first time, an AT 2 receptor binding site in the NTS, as well as a non-angiotensin II [ 125 I] CGP42112 binding site. These studies also demonstrate that nodose Ganglionectomy represents a useful model in which to study a non-angiotensin II [ 125 I] CGP42112 binding site that is up-regulated following degeneration of afferent vagal nerves.

Bevyn Jarrott - One of the best experts on this subject based on the ideXlab platform.

  • Minocycline treatment attenuates microglia activation and non-angiotensin II [125I] CGP42112 binding in brainstem following nodose Ganglionectomy.
    Neuroscience, 2005
    Co-Authors: Carli L. Roulston, Andrew J. Lawrence, Robert E Widdop, Bevyn Jarrott
    Abstract:

    We have previously shown that following unilateral nodose Ganglionectomy, [125I] CGP42112 binds to a non-angiotensin II (Ang II) related binding site in rat dorsal motor nucleus of the vagus nerve, ambiguus nucleus and nucleus of the solitary tract. Furthermore, this up-regulated binding site localizes with activated microglia. Given that some tetracyclines may inhibit microglia activation in brain, we examined the effect of minocycline treatment on the binding of [125I] CGP42112 and [3H] PK11195 (an established radioligand for microglia), as well as OX-42 immunoreactivity (an immunomarker for activated microglia), following nodose Ganglionectomy. Male Wistar Kyoto rats underwent unilateral nodose Ganglionectomy or sham operation and were treated with saline or minocycline (50 mg/kg i.p.) 12 h before surgery and twice daily after surgery (each 50mg/kg i.p.) for 3 days. Subsequent to nodose Ganglionectomy, [125I] CGP42112 binding (insensitive to PD123319 or Ang II) was increased approximately two-fold in the ipsilateral nucleus of the solitary tract and was also induced in the ipsilateral dorsal motor nucleus of the vagus nerve and ambiguus nucleus of saline-treated rats. Treatment with minocycline reduced this non-angiotensin II [125I] CGP42112 binding (40-50% reduction) in the nucleus of the solitary tract, dorsal motor nucleus of the vagus nerve and ambiguus nucleus. Analogous experiments using [3H] PK11195 also revealed up-regulated binding in the ipsilateral nucleus of the solitary tract ( approximately 205%), dorsal motor nucleus of the vagus nerve (approximately 80%) and ambiguus nucleus (approximately 210%) of saline-treated rats following nodose Ganglionectomy, which was reduced by 40-100% with minocycline treatment. Immunoreactivity to OX-42 confirmed an increase in microglia activation and accumulation of macrophages in these brain stem nuclei following nodose Ganglionectomy, which was also attenuated following treatment with minocycline. These data demonstrate that non-Ang II [125I] CGP42112 binding following nodose Ganglionectomy is attenuated by minocycline treatment. This minocycline-induced effect was associated with reduced activation of microglia and an apparent reduction in the number of macrophages in the abovementioned nuclei. This evidence suggests that a non-Ang II [125I] CGP42112 binding site is located on, or associated with, activated microglia and macrophages, providing a useful tool with which to quantitate the neuroprotective effects of centrally acting anti-inflammatory compounds.

  • non angiotensin ii 125i cgp42112 binding is a sensitive marker of neuronal injury in brainstem following unilateral nodose Ganglionectomy comparison with markers for activated microglia
    Neuroscience, 2004
    Co-Authors: Carli L. Roulston, Andrew J. Lawrence, Bevyn Jarrott, Robert E Widdop
    Abstract:

    Abstract Previously we reported that a non-angiotensin II [ 125 I] CGP42112 binding site is up-regulated in rat brainstem nuclei as a result of unilateral nodose Ganglionectomy. In the present study, we compared non-angiotensin II [ 125 I] CGP42112 binding with microglia/macrophage activation following nodose Ganglionectomy, using both in vitro autoradiography and immunohistochemistry. Specific [ 125 I] CGP42112 binding was observed in the nucleus of the solitary tract (NTS) and revealed an AT 2 receptor component as well as a non-angiotensin II receptor component. Subsequent to unilateral nodose Ganglionectomy, [ 125 I] CGP42112 binding in the ipsilateral NTS was increased approximately two-fold and was also induced in the ipsilateral dorsal motor nucleus (DMX) and the nucleus ambiguus (n.amb). This non-angiotensin II [ 125 I] CGP42112 binding site was displaced by CGP42112 but not other ligands. Increased [ 3 H] PK11195 binding (a known marker of reactive gliosis) was also observed in the same brainstem nuclei as non-angiotensin II [ 125 I] CGP42112 binding after nodose Ganglionectomy. The similarity in binding patterns between [ 125 I] CGP42112 and [ 3 H] PK11195 was shown to be primarily due to retrograde degeneration in the ipsilateral NTS, DMX and n.amb, as both radioligands were localized to similar cellular targets within the interstial space and over cellular debris. Immunohistochemical data confirmed reactive gliosis within the ipsilateral NTS, DMX and n.amb, following nodose Ganglionectomy, which was predominantly characterized by an increase in OX-42 immunoreactivity (a marker for activated microglia/macrophages), with only a small increase in glial fibrillary acidic protein immunoreactivity (a marker of astrogliosis) detected. These data demonstrate for the first time that non-angiotensin II [ 125 I] CGP42112 binding is associated with activated microglia, as well as macrophages, following unilateral nodose Ganglionectomy. Furthermore, these studies also demonstrate the potential use of non-angiotensin II [ 125 I] CGP42112 binding as a marker for quantitating inflammatory events which occur as a result of damage to the CNS.

  • localization of at2 receptors in the nucleus of the solitary tract of spontaneously hypertensive and wistar kyoto rats using 125i cgp42112 upregulation of a non angiotensin ii binding site following unilateral nodose Ganglionectomy
    Brain Research, 2003
    Co-Authors: Carli L. Roulston, Andrew J. Lawrence, Bevyn Jarrott, Robert E Widdop
    Abstract:

    Abstract We have examined the binding distribution of a selective AT 2 receptor ligand [ 125 I] CGP42112 in the brain of adult Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). AT 2 receptor localization was also examined in the rat brainstem following unilateral nodose Ganglionectomy. Specific [ 125 I] CGP42112 binding was observed in discrete brain regions from both rat strains, including the nucleus of the solitary tract (NTS), and did not differ between WKY and SHR. [ 125 I] CGP42112 binding in the NTS revealed an AT 2 receptor component that was displaceable by PD 123319 and Ang II (50–58%), as well as a non-angiotensin II receptor component (42–49%). Following unilateral nodose Ganglionectomy, [ 125 I] CGP42112 binding density on the denervated side of the NTS was increased approximately two-fold in both WKY and SHR. This increased [ 125 I] CGP42112 binding density in the ipsilateral NTS was comprised of a greater non-angiotensin II component than that observed in the sham groups, since only ∼30% was displaced by PD123319 and angiotensin II. Furthermore, [ 125 I] CGP42112 also revealed high binding density on the denervated side in the dorsal motor nucleus and the nucleus ambiguus in both WKY and SHR. AT 2 receptor immunoreactivity was also visualised in the NTS of sham operated rats, but was not observed in the dorsal motor nucleus or the nucleus ambiguus, nor was it up-regulated following nodose Ganglionectomy. These results demonstrate, for the first time, an AT 2 receptor binding site in the NTS, as well as a non-angiotensin II [ 125 I] CGP42112 binding site. These studies also demonstrate that nodose Ganglionectomy represents a useful model in which to study a non-angiotensin II [ 125 I] CGP42112 binding site that is up-regulated following degeneration of afferent vagal nerves.

  • the distribution of nitric oxide synthase adenosine deaminase and neuropeptide y immunoreactivity through the entire rat nucleus tractus solitarius effect of unilateral nodose Ganglionectomy
    Journal of Chemical Neuroanatomy, 1998
    Co-Authors: Andrew J. Lawrence, Margie Castillomelendez, Karen J Mclean, Bevyn Jarrott
    Abstract:

    Abstract The present study has employed immunocytochemistry on free-floating sections of adult rat medulla oblongata to characterise the distribution of nitric oxide synthase- (NOS), adenosine deaminase- (ADA) and neuropeptide Y- (NPY) immunoreactivity (IR) throughout the entire rostro–caudal axis of the nucleus tractus solitarius (NTS). In addition, unilateral nodose Ganglionectomy was performed in a group of rats to determine whether any observed immunoreactivity was associated with central vagal afferent terminals. NOS-IR was found throughout the entire NTS, in cells, and both varicose and non-varicose fibres. Furthermore, unilateral nodose Ganglionectomy resulted in a clear reduction in NOS-IR (visualised with diaminobenzidine) in a highly restricted portion of the ipsilateral medial NTS. Similarly, ADA- and NPY-containing cells, fibres and terminals were also found throughout the adult rat NTS. However, following unilateral nodose Ganglionectomy, there was no apparent reduction in either ADA-IR or NPY-IR on the denervated side of the NTS. These data indicate a role for nitric oxide, purines and neuropeptide Y as neuromodulators within the rat NTS, although only nitric oxide appears to be primarily associated with vagal afferent input. Adenosine deaminase and neuropeptide Y-containing neurons appear to be predominantly postsynaptic to vagal input, although their possible association with vagal afferents cannot be completely excluded.

Swati Dey - One of the best experts on this subject based on the ideXlab platform.

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