Functional Properties of Cells in Rat Trigeminal Subnucleus Interpolaris Following Local Serotonergic Deafferentation

Misra, Bibhu R.; Klein, Bradley G.

doi:10.3109/08990229509063139

Cited by 5 publications

(4 citation statements)

References 86 publications

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“…It appeared unlikely that axotomy of ascending interpolaris axons might have caused such an effect, because a similar shrinkage of receptive fields was observed after midline lesions made rostrally to the crossing of SpVi axons, at the level of the oralis nucleus (our unpublished data). The severing of corticofugal axons, which travel medially in the brainstem, or lesion of serotonergic afferents to the SpVi neither appeared as plausible explanations because barrel cortex lesion or serotonine depletion do not reduce receptive field size in the SpVi (Jacquin et al, 1990b;Misra and Klein, 1995). Thus, in light of the present results, it seems most likely that the depressive effect of a midline lesion results from the severing of cholinergic axons or from a marked diminution of their activity.…”

Section: Synthesis Of Receptive Fields In the Spvimentioning

confidence: 52%

Cholinergic Modulation of Vibrissal Receptive Fields in Trigeminal Nuclei

Timofeeva¹,

Dufresne²,

Sı́k³

et al. 2005

J. Neurosci.

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In sensory systems, it is usually considered that mesopontine cholinergic neurons exert their modulatory action in the thalamus by enhancing the relay of sensory messages during states of neural network desynchronization. Here, we report a projection heretofore unknown of these cholinergic cells to the interpolar division of the brainstem trigeminal complex in rats. After FluoroGold injection in the interpolar nucleus, a number of retrogradely labeled cells were found bilaterally in the pedunculopontine tegmental nucleus, and immunostaining revealed that the vast majority of these cells were also positive for choline acetyltransferase. Immunostaining for the acetylcholine vesicular transporter confirmed the presence of cholinergic terminals in the interpolar nucleus, where electron microscopy showed that they make symmetric and asymmetric synaptic contacts with dendrites and axon terminals. In agreement with these anatomical data, recordings in slices showed that the cholinergic agonist carbachol depolarizes large-sized interpolaris cells and increases their excitability. Local application of carbachol in vivo enhances responses to adjacent whiskers, whereas systemic administration of the cholinergic antagonist scopolamine produces an opposite effect. Together, these results show that mesopontine cholinergic neurons exert a direct, effective control over receptive field size at the very first relay stations of the vibrissal system in rodents. As far as receptive field synthesis in the lemniscal pathway relies on intersubnuclear projections from the spinal complex, it follows that cholinergic modulation of sensory transmission in the interpolar nucleus will have a direct bearing on the type of messages that is forwarded to the thalamus and cerebral cortex.

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Section: Synthesis Of Receptive Fields In the Spvimentioning

confidence: 52%

Cholinergic Modulation of Vibrissal Receptive Fields in Trigeminal Nuclei

Timofeeva¹,

Dufresne²,

Sı́k³

et al. 2005

J. Neurosci.

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“…Immunohistochemistry was performed directly on the slides according to minor modification of methods previously outlined by this laboratory (Misra and Klein, 1995;Pittman, et al, 2003). Each antiserum used in this study has been widely used and was commercially available.…”

Section: Fixation Tissue Sectioning and Histochemistrymentioning

confidence: 99%

Pyrethroid and organophosphate insecticide exposure in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson’s disease: an immunohistochemical analysis of tyrosine hydroxylase and glial fibrillary acidic protein in dorsolateral striatum

Dodd

Klein

2009

Toxicol Ind Health

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The pyrethroid insecticide permethrin and the organophosphate insecticide chlorpyrifos can experimentally produce Parkinson's disease (PD)-associated changes in the dopaminergic nigrostriatal pathway, short of frank degeneration, although at doses considerably higher than from a likely environmental exposure. The ability of permethrin (200 mg/kg), chlorpyrifos (50 mg/kg), or combined permethrin + chlorpyrifos to facilitate nigrostriatal damage in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (30 mg/kg) C57BL/6 mouse model of PD was investigated in three separate experiments. Tyrosine hydroxylase (TH) and glial fibrillary acidic protein (GFAP) immunohistochemistry assessed nigrostriatal degeneration or nigrostriatal damage more subtle than frank degeneration. Four fields in the dorsolateral caudate-putamen were examined at two rostrocaudal locations. The dopaminergic neurotoxin MPTP decreased striatal TH immunopositive neuropil and increased GFAP immunopositive neuropil. Neither permethrin nor chlorpyrifos, alone or in combination, altered the effects of MPTP upon TH or GFAP immunostaining. Permethrin alone increased striatal GFAP immunopositive neuropil but not when combined with chlorpyrifos treatment. Therefore, combined administration of the two insecticides appeared to protect against an increase in a neuropathological indicator of striatal damage seen with permethrin treatment alone. Differences compared with analysis of entire striatum emphasize the value of varying the topographic focus used to assess nigrostriatal degeneration in studies of insecticides in PD.

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“…Immunohistochemistry was performed directly on the slides according to a modification of methods previously outlined by this laboratory (Klein and Blaker 1990;Klein et al 1992;Misra and Klein 1995). Each antiserum used in this study was commercially available and has been used in a multitude of studies on the nervous system, many of which involve analysis of striatal tissue (e.g., Lew et al 1992;Pu et al 1994;Freed et al 1995;Kordower et al 1996;Vaughan et al 1996;Wirth, Rufer, and Unsicker 1996;Betarbet et al 1997;Zimmer, Ennis, and Shipley 1997;Sortwell, Collier, and Sladek 1998;Sugama et al 2003).…”

Section: Fixation Tissue Sectioning and Histochemistrymentioning

confidence: 99%

Immunohistochemical Changes in the Mouse Striatum Induced by the Pyrethroid Insecticide Permethrin

2003

Self Cite

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Epidemiological studies have linked insecticide exposure and Parkinson's disease. In addition, some insecticides produce damage or physiological disruption within the dopaminergic nigrostriatal pathway of non-humans. This study employed immunohistochemical analysis in striatum of the C57BL/6 mouse to clarify tissue changes suggested by previous pharmacological studies of the pyrethroid insecticide permethrin. Dopamine transporter, tyrosine hydroxylase, and glial fibrillary acidic protein immunoreactivities were examined in caudate-putamen to distinguish changes in amount of dopamine transporter immunoreactive protein from degeneration or other damage to dopaminergic neuropil. Weight-matched pairs of pesticide-treated and vehicle-control mice were dosed and sacrificed on the same days. Permethrin at 0.8, 1.5 and 3.0 mg/kg were the low doses and at 200 mg/kg the high dose. Brains from matched pairs of mice were processed on the same slides using the avidin-biotin technique. Four fields were morphometrically located in each of the serial sections of caudate-putamen, digitally photographed, and immunopositive image pixels were counted and compared between members of matched pairs of permethrin-treated and vehicle-control mice. For low doses, only 3.0 mg/kg produced a significant decrease in dopamine transporter immunostaining. The high dose of permethrin did not produce a significant change in dopamine transporter or tyrosine hydroxylase immunostaining, but resulted in a significant increase in glial fibrillary acidic protein immunostaining. These data suggest that a low dose of permethrin can reduce the amount of dopamine transporter immunoreactive protein in the caudate-putamen. They also suggest that previously reported reductions in dopamine uptake of striatal synaptosomes of high-dose mice may be due to nondegenerative tissue damage within this region as opposed to reductions of dopamine transporter protein or death of nigrostriatal terminals. These data provide further evidence that insecticides can affect the primary neurodegenerative substrate of Parkinson's disease.

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Functional Properties of Cells in Rat Trigeminal Subnucleus Interpolaris Following Local Serotonergic Deafferentation

Cited by 5 publications

References 86 publications

Cholinergic Modulation of Vibrissal Receptive Fields in Trigeminal Nuclei

Cholinergic Modulation of Vibrissal Receptive Fields in Trigeminal Nuclei

Pyrethroid and organophosphate insecticide exposure in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson’s disease: an immunohistochemical analysis of tyrosine hydroxylase and glial fibrillary acidic protein in dorsolateral striatum

Immunohistochemical Changes in the Mouse Striatum Induced by the Pyrethroid Insecticide Permethrin

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