Generation patterns of immunocytochemically identified cholinergic neurons in rat brainstem

Phelps, Patricia E.; Brennan, Lynn A.; Vaughn, James E.

doi:10.1016/0165-3806(90)90165-u

Cited by 39 publications

(22 citation statements)

References 28 publications

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“…Embryonic day 17 is well after the peak times at which the cholinergic populations in these regions are generated (Brady et al, 1989;Phelps et al, 1990). Isolated colonies were expanded and screened for ChAT activity.…”

Section: Establishment Of Cholinergic Cell Linesmentioning

confidence: 99%

Establishment of Cholinergic Neuron-like Cell Lines with Differential Vulnerability to Nitrosative Stress

Personett

Williams²,

Baskerville³

et al. 2007

CNR

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Cholinergic cell lines were established by fusion of embryonic day 17 wild-type neurons from rat basal forebrain (BF) and upper brainstem (BS) with N18tg neuroblastoma cells. Isolated clones expressed choline acetyltransferase (ChAT) and neuronal nitric oxide synthase (nNOS) activities that were increased upon differentiation with retinoic acid. Clones from the BF expressed high levels of the tyrosine kinase type A (TrkA) receptor expression and activation of the mitogen-activated kinase ERK2 upon treatment with nerve growth factor. Like wild-type cholinergic populations, the six clones studied were variably resistant to nitric oxide (NO) excess from addition of S-nitroso-N-acetyl-D, L-penicillamine (SNAP). Of these, the BS2 clone exhibited resistance like in vivo BS cholinergic neurons, while the MS10 clone mimicked in vivo BF vulnerability. Apoptosis in response to NO excess was preceded by increases in mitochondrial responses bax/bcl-2 ratios, but cytochrome C was not released. Mitochondrial levels of apoptosis initiating factor (AIF) were either unchanged or increased, and only in MS clones was endonuclease G (EndoG) released. Microarray data indicated the existence of endoplasmic reticular (ER) stress and caspase-4 and caspase-12 were involved in the pathway to DNA fragmentation. The array data also indicated a survival role for mdm2, and its blockade rendered vulnerable the brainstem survivor clone BS2. Akt and ERK1/2 pathways were activated in response to NO and their blockade increased DNA fragmentation. Blockade of GSK-3 alpha/beta, a downstream target of Akt, reduced SNAP toxicity and this was more prominent in basal forebrain clones. We have identified two cholinergic cell lines useful for molecular studies of cholinergic vulnerability. We hypothesize that, in cholinergic neurons, control of ER stress signaling may be a major factor in differential vulnerability.

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Section: Establishment Of Cholinergic Cell Linesmentioning

confidence: 99%

Establishment of Cholinergic Neuron-like Cell Lines with Differential Vulnerability to Nitrosative Stress

Personett

Williams²,

Baskerville³

et al. 2007

CNR

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“…GDNF, however, is not exclusively dopaminergicspecific since it increases the activity of choline acetyltransferase (ChAT) in neuronal cultures from the rat embryonic ventral mesencephalon and promotes the survival of purified rat spinal motoneurons in vitro Henderson et al, 1994). Ventral mesencephalic cultures, in addition to dopaminergic neurons from the substantia nigra and ventral tegmental area, contain cholinergic neurons from cranial motor nuclei and from the pedunculopontine nucleus (Altman and Bayer, 1981;Phelps et al, 1990;Zurn and Werren, 1994). GDNF increases ChAT activity in the cranial motoneurons present in these cultures as well as in cultured spinal motoneurons, but not in septal, striatal, or pedunculopontine cholinergic neurons .…”

Section: Introductionmentioning

confidence: 99%

Combined effects of GDNF, BDNF, and CNTF on motoneuron differentiation in vitro

et al. 1996

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“…ChAT, the biosynthesizing enzyme for acetylcholine, is presently the most specific indicator for monitoring the functional state of cholinergic neurons and is contained in vagal preganglionic motor neurons of the DMV (27,34). Changes in ChAT mRNA levels have been used to evaluate enzyme response to stimuli (28,30).…”

mentioning

confidence: 99%

Hypothyroidism increases Fos immunoreactivity in cholinergic neurons of brain medullary dorsal vagal complex in rats

Yuan¹,

Yang²

2005

American Journal of Physiology-Endocrinology and Metabolism

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Hypo-or hyperthyroidism is associated with autonomic disorders. We studied Fos expression in the medullary dorsal motor nucleus of the vagus (DMV), nucleus tractus solitarii (NTS), and area postrema (AP) in four groups of rats with different thyroid states induced by a combination of drinking water and daily intraperitoneal injection for 1-4 wk: 1) tap water and vehicle; 2) 0.1% propylthiouracil (PTU) and vehicle; 3) PTU and thyroxine (T 4; 2 g/100 g); and 4) tap water and T 4 (10 g/100 g). The numbers of Fos immunoreactive (IR) positive neurons in the DMV, NTS, and AP were low in euthyroid rats but significantly higher in the 4-wk duration in hypothyroid rats, which were prevented by simultaneous T4 replacement. Hyperthyroidism had no effect on Fos expression in these areas. There were significant negative correlations between T4 levels and the numbers of Fos-IRpositive neurons in the DMV (r ϭ Ϫ0.6388, P Ͻ 0.008), NTS (r ϭ Ϫ0.6741, P Ͻ 0.003), and AP (r ϭ Ϫ0.5622, P Ͻ 0.004). Double staining showed that Fos immunoreactivity in the DMV of hypothyroid rats was mostly localized in choline acetyltransferase-containing neurons. Thyroid hormone receptors ␣1 and ␤2 were localized in the observed nuclei. These results indicate that thyroid hormone influences the DMV/NTS/AP neuronal activity, which may contribute to the vagal-related visceral disorders observed in hypothyroidism. thyroid hormone; dorsal motor nucleus of the vagus; nucleus tractus solitarii; vagus nerve; area postrema HYPOTHYROIDISM IS A PREVALENT DISEASE worldwide and has a high incidence in elderly patients with nonthyroidal disease (3, 39). Extensive cardiovascular, gastrointestinal (GI), and metabolic disorders, such as sinus bradycardia, altered GI secretion and motility, and hyperlipidemia are the main clinical symptoms of hypothyroidism. These symptoms indicate autonomic dysfunction with a relative vagal dominance (43, 44) and correlate to increased mortality from cardiovascular and cerebrovascular diseases in those with a history of overt or subclinical thyroid disorders (29, 39). How thyroid hormone regulates vagal activities, particularly the central mechanism, is still poorly understood.On the basis of solidly established physiological role of medullary thyrotropin-releasing hormone (TRH)-containing vagal regulatory pathways in the central regulation of GI functions (47), we recently revealed that feedback regulation of TRH gene expression by thyroid hormone in the medullary raphe pallidus (Rpa), raphe obscurus (Rob), and parapyramidal region (PPR) may contribute to hypothyroidism-induced autonomic disorders (49 -52). TRH-containing projections arising from these nuclei innervate the dorsal vagal complex (DVC) (20) and the sympathetic motor neurons in the intermediolateral cell column of the spinal cord (40). Our previous studies showed that hypothyroidism increases TRH mRNA levels in the Rpa, Rob, and PPR and induces Fos expression, a widely accepted parameter indicating brain neuronal activation, in the TRH-synthesizing neurons in these nucl...

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Generation patterns of immunocytochemically identified cholinergic neurons in rat brainstem

Cited by 39 publications

References 28 publications

Establishment of Cholinergic Neuron-like Cell Lines with Differential Vulnerability to Nitrosative Stress

Establishment of Cholinergic Neuron-like Cell Lines with Differential Vulnerability to Nitrosative Stress

Combined effects of GDNF, BDNF, and CNTF on motoneuron differentiation in vitro

Hypothyroidism increases Fos immunoreactivity in cholinergic neurons of brain medullary dorsal vagal complex in rats

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