Changes in Vagal Activity and Response to Muscarinic Receptor Agonists With Age

Kelliher, Gerald J.; Conahan, S T

doi:10.1093/geronj/35.6.842

Cited by 46 publications

(13 citation statements)

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“…Additional support for the notion of vagal motor deterioration comes from indirect observations. Vagal preganglionic control of the heart (probed physiologically and pharmacologically) is diminished in aged Fischer 344 rats (e.g., Kelliher and Conahan, 1980). In contrast to such suggestions of age-related dissolution of the DMNX, however, Soltanpour and Santer (1997) reported, after having found no change in the structure or activity of vagal motor neurons, that the DMNX was well preserved in 24-and 30-month-old rats.…”

Section: Vagal Extrinsic Innervation Of the Gi Tractmentioning

confidence: 95%

As the gut ages: Timetables for aging of innervation vary by organ in the Fischer 344 rat

Phillips

Powley

2001

J of Comparative Neurology

105

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To explore the effects of aging on the vagal innervation of the gastrointestinal (GI) tract, male Fischer 344 rats at 3 and 24 months of age were injected in the left nodose ganglion with 3 microl of either 4% wheat germ agglutinin-horseradish peroxidase (to label sensory endings) or 1% cholera toxin subunit B-horseradish peroxidase (to label motor endings). The stomach and duodenum were prepared as wholemounts and processed with tetramethyl benzidine. In addition, to study age-related changes in the myenteric plexus, the stomachs, small intestines, and large intestines from 3-, 12-, 21-, 24- and 27-month-old rats were prepared as wholemounts and processed with Cuprolinic Blue (to stain the neurons). Vagal afferent endings, motor terminal profiles, and myenteric neurons were counted and mapped with a sampling grid. In the stomach, both the vagal and myenteric innervation were stable between the ages of 3 and 24 months; however, a decrease in the number of myenteric neurons in the forestomach was noted at 27 months. In the small and large intestines, myenteric cell loss occurred by 12 months of age, progressed with age, and appeared to be governed by several general principles: (1) the rate of cell loss was organ-specific, with a gradient of increasing severity from proximal to distal in the gut; (2) within organs of the GI tract, the rate of cell loss differed between regions; and (3) for given regions, cell losses progressed linearly with increasing age. The findings suggest that a positive relationship exists between the density of vagal extrinsic innervation and myenteric neuron survival; however, whether this results from the vagal innervation and/or other factor(s) protecting or rescuing myenteric neurons from age-related attrition remains to be determined.

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Section: Vagal Extrinsic Innervation Of the Gi Tractmentioning

confidence: 95%

As the gut ages: Timetables for aging of innervation vary by organ in the Fischer 344 rat

Phillips

Powley

2001

J of Comparative Neurology

105

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“…Whilst the influence of age on muscarinic cholinoceptor function has been examined in several tissue types including the heart (Kelliher and Conahan 1980) and brain (Pedigo et al 1984) of the rat, few studies have examined the influence of age on the contractile responsiveness of airway smooth muscle to muscarinic agonists. In bovine (Wills and Douglas 1988) and guinea-pig (Wills-Karp 1991) tracheal smooth muscle, a decrease in the potency of some muscarinic agonists in old animals compared with younger animals has been reported.…”

Section: Introductionmentioning

confidence: 99%

Age-related changes in muscarinic cholinoceptor function in guinea-pig and rat airways

Preuss

Goldie

1999

Naunyn-Schmiedeberg's Arch Pharmacol

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The influence of age on muscarinic cholinoceptor-mediated contraction and inositol phosphate accumulation was examined in rat and guinea-pig isolated tracheal tissue. Significant age-related changes in the sensitivity of guinea-pig tracheal tissue to acetylcholine, but not carbachol, were observed in the early maturation phase of growth with a 3.3-fold increase in potency between birth and 2 weeks of age followed by a 3.2-fold fall in potency between 2 and 12 weeks of age. Further ageing did not significantly change the potency of acetylcholine or carbachol. Whilst acetylcholinesterase inhibition caused a significant increase in acetylcholine potency, this was independent of animal age. In rat isolated tracheal tissue, contractile responses to both acetylcholine and carbachol remained unchanged with respect to animal age. Significant age-related decreases in inositol phosphate accumulation were observed in response to carbachol in the guinea-pig and rat and to acetylcholine in guinea-pig but not rat isolated tracheal tissue. This study has demonstrated significant age-related changes in the responsiveness of isolated tracheal tissue to carbachol and acetylcholine which were also species-specific.

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“…Retrogradely transported The number of cardiac neurons may be decreased through several factors such as aging [1], diabetes [14,23] or infectious diseases such as the Chagas disease [24]. As cardiac neurons are part of the cholinergic system of the heart, a decrease in their number induce severe increase in chronotropic response to vagal stimulation [15,21,22,29].…”

Section: Discussionmentioning

confidence: 99%

Training alters cardiac neuron sizes in Wistar rats

Souza¹,

Gama²,

Santarém³

et al. 2009

Biol Sport

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Abstract. The action of the parasympathetic nerves on the heart is made through a group of neurons located on the surface of the atria. This study evaluated the effect of a chronic training protocol on the number and sizes of the cardiac neurons of Wistar rats. Whole mount preparations of the atria of 12-month old male sedentary and trained rats (40 weeks of running on a treadmill 3 times a week, 16 m/min) were assessed for number and size (maximal cellular profile area) of the cardiac neurons. The cardiac neurons were ascertained by using the NADH-diaphorase technique that stains the cell bodies of the neurons in dark blue. The number of cardiac neurons in the trained rats (P>0.05) did not change significantly. In the sedentary group there were small, medium sized and large neurons. However there was a notable increase in the percentage of small neurons in the rats submitted to the training compared to the sedentary group (P<0.05). Previous studies have shown that electrophysiologically, the small neurons are more easily excitable than the large neurons. It is possible that the results of the present work reflect an adaptation mechanism of the cardiac neurons presumably with the objective of increasing the excitability of the neurons for the vagal action and resulting facilitation of the sinusal bradycardia observed at rest and in the exercise. We concluded that the training affects significantly the size of the cardiac neurons in Wistar rats.

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Changes in Vagal Activity and Response to Muscarinic Receptor Agonists With Age

Cited by 46 publications

References 0 publications

As the gut ages: Timetables for aging of innervation vary by organ in the Fischer 344 rat

As the gut ages: Timetables for aging of innervation vary by organ in the Fischer 344 rat

Age-related changes in muscarinic cholinoceptor function in guinea-pig and rat airways

Training alters cardiac neuron sizes in Wistar rats

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