Intraocular projections from the pterygopalatine ganglion in the cat

Kuchiiwa, Satoshi

doi:10.1002/cne.903000303

Cited by 22 publications

(8 citation statements)

References 23 publications

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“…We have also demonstrated that large nNOS Ϫ neurons underwent apoptosis in diabetic animals, although not to the same extent as the nitrergic neurons. It is known that besides the palatine salivary glands, the sphenopalatine ganglion also innervates lacrimal glands and vasculature in the orbit (32,33). Our results therefore might suggest a pathophysiological mechanism by which autonomic neuropathy could be involved in xerostomia (34), glaucoma (35), and decreased lacrimation (36) observed in diabetic patients.…”

Section: Discussionmentioning

confidence: 99%

Nitrergic Neurodegeneration in Cerebral Arteries of Streptozotocin-Induced Diabetic Rats

2005

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Although autonomic neuropathy is recognized as an independent risk factor for stroke in diabetes, the mechanism by which autonomic nerves are involved in this pathology is unknown. Parasympathetic (cholinergic) nerves of the autonomic nervous system are known to innervate and to cause relaxation of cerebral arteries by releasing nitric oxide (NO); hence, they are called nitrergic nerves. However, the effect of diabetes on nitrergic nerves is unknown. Here, we show that perivascular nitrergic nerves around the cerebral arteries degenerate in two phases in streptozotocin-induced diabetic rats. In the first phase, perivascular nitrergic nerve fibers remain intact while they lose their neuronal NO synthase content. This phase is reversible with insulin treatment. In the second phase, nitrergic cell bodies in the ganglia are lost via apoptosis in an irreversible manner. Throughout the two phases, irreversible thickening of the smooth muscle layer of cerebral arteries is observed. This is the first demonstration of nitrergic degeneration in diabetic cerebral arteries, which could elucidate the link between diabetic autonomic neuropathy and stroke. Diabetes 54:212-219, 2005 D iabetes is associated with an increased risk of cardiovascular disease-in particular, coronary heart disease and stroke (1-4). Mortality from stroke has been demonstrated to be increased significantly by diabetes (2). Hypertension, smoking, and dyslipidemia are major risk factors for the occurrence of strokes in diabetic patients (4). Recently, autonomic neuropathy has been described as a significant independent risk factor for diabetes-related stroke (5). However, the mechanism by which autonomic neuropathy might be involved in the pathogenesis of stroke has not been elucidated.Autonomic nerves are known to innervate cerebral arteries (6). Parasympathetic (cholinergic) nerves, which contain neuronal nitric oxide synthase (nNOS), have been shown in the walls of cerebral blood vessels in many species, including humans (7). These nerves are now called "nitrergic nerves" (8) and have been shown to originate mainly from the sphenopalatine ganglia (9 -12). Stimulation of perivascular nitrergic nerves has been demonstrated to relax the cerebral arteries by the action of nitric oxide (NO) and to increase the cortical blood flow (6,13-15). It is not known whether the nitrergic nerves in the cerebral vasculature are affected during diabetes. We therefore investigated the effect of diabetes on the morphology and nNOS content of these nerves in the cerebral arteries of streptozotocin (STZ)-induced diabetic rats. RESEARCH DESIGN AND METHODS Induction of diabetes.Male Wistar rats (225-250 g) were treated with STZ (75 mg/kg i.p.) or vehicle (saline) as described previously (16,17). Hyperglycemia was defined as a nonfasting blood glucose concentration Ͼ20 mmol/l. Insulin was administered 8 and 12 weeks after STZ injection using sustainedrelease insulin rods (7 mm, ϳ2 units/day; LinBit, LinShin Canada, Toronto, ON, Canada). Rats were killed 4, 8, 12, 16, and 20 w...

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Section: Discussionmentioning

confidence: 99%

Nitrergic Neurodegeneration in Cerebral Arteries of Streptozotocin-Induced Diabetic Rats

2005

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“…The skull of the animal was firmlv fixed in a stereotaxic frame. Cranial nerves and the infraorbital nerve were prepared for stimulation as follows: the infra-orbital nerve was identified either at its exit through the infra-orbital foramen or within the nasal cavity as described by Kuchiiwa (1990). The roots of the facial and glossopharyngeal cranial nerves were cut from their origins at the brain stem after an extensive craniectomy.…”

Section: Sites and Modes Of Stimulationmentioning

confidence: 99%

Somatosensory stimulation causes autonomic vasodilatation in cat lip.

Izumi¹,

Karita²

1992

The Journal of Physiology

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SUMMARY1. Electrical stimulation of the infra-orbital nerve and the maxillary buccal gingiva caused an increase in ipsilateral lip blood flow in a stimulus intensitydependent manner in anaesthetized cats.2. The reflex vasodilator response was resistant to blockade by antimuscarinic (atropine), antiadrenergic (phentolamine and propranolol) and antihistaminergic (tripelennamine) but sensitive to ganglionic blocking agent (hexamethonium).3. The reflex vasodilator response was unaffected by section of the ipsilateral cervical sympathetic trunk and facial nerve root, but was completely abolished by ipsilateral section of the glossopharyngeal nerve root.4. The vasodilator response elicited by stimulation of the facial and glossopharyngeal nerves was never affected by lesion of the ipsilateral pterygopalatine ganglion.5. Local anaesthesia or section of the inferior alveolar nerve abolished the vasodilator effects of stimulation of the facial and the glossopharyngeal nerves.6. These results suggest that there is a somato-autonomic reflex vasodilator system mediated via final neurons that are not cholinergic, and that the parasympathetic vasodilator fibres emerge from the brain stem with the glossopharyngeal nerve and reach the blood vessels via the otic ganglion and the inferior alveolar nerve in the cat mandibular lip.

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“…Noncholinergic nerves primarily release VIP and control intraocular pressure and blood flow [89, 95]. VIP has also been shown to stimulate mucus production and VIP receptors are located on mucus-producing goblet cells [87].…”

Section: Parasympathetic Control Of the Eyementioning

confidence: 99%

Role of Parasympathetic Nerves and Muscarinic Receptors in Allergy and Asthma

Scott

Fryer

2012

Chemical Immunology and Allergy

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Parasympathetic nerves control the symptoms and inflammation of allergic diseases primarily by signaling through peripheral muscarinic receptors. Parasympathetic signaling targets classic effector tissues such as airway smooth muscle and secretory glands and mediates acute symptoms of allergic disease such as airway narrowing and increased mucus secretion. In addition, parasympathetic signaling modulates inflammatory cells and non-neuronal resident cell types such as fibroblasts and smooth muscle contributing to chronic allergic inflammation and tissue remodeling. Importantly, muscarinic antagonists are experiencing a rebirth for the treatment of asthma and may be useful for treating other allergic diseases.

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Intraocular projections from the pterygopalatine ganglion in the cat

Cited by 22 publications

References 23 publications

Nitrergic Neurodegeneration in Cerebral Arteries of Streptozotocin-Induced Diabetic Rats

Nitrergic Neurodegeneration in Cerebral Arteries of Streptozotocin-Induced Diabetic Rats

Somatosensory stimulation causes autonomic vasodilatation in cat lip.

Role of Parasympathetic Nerves and Muscarinic Receptors in Allergy and Asthma

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