Effects of age on sympathetic innervation of the myenteric plexus and gastrointestinal smooth muscle of Fischer 344 rats

Phillips, Robert; Rhodes, Brie S.; Powley, Terry L.

doi:10.1007/s00429-006-0123-z

Cited by 40 publications

(58 citation statements)

References 45 publications

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“…Rodents appear to experience a dramatic age-related degeneration of sympathetic motor neurons innervating the myenteric plexus with advancing age, which could explain agerelated decline in colonic transit [13]. Furthermore, the same study demonstrated a significant level of cholinergic vagal afferent age-related degenerative changes.…”

Section: Extrinsic Innervationmentioning

confidence: 70%

The Aging Colon: The Role of Enteric Neurodegeneration in Constipation

Wiskur

Meerveld

2010

Curr Gastroenterol Rep

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Constipation is a common problem in the elderly, and abnormalities in the neural innervation of the colon play a significant role in abnormalities in colonic motility leading to delayed colonic transit. The scope of this review encompasses the latest advances to enhance our understanding of the aging colon with emphasis on enteric neurodegeneration, considered a likely cause for the development of constipation in the aging gut in animal models. Neural innervation of the colon and the effects of aging on intrinsic and extrinsic nerves innervating the colonic smooth muscle is discussed. Evidence supporting the concept that neurologic disorders, such as Parkinson's disease, not only affect the brain but also cause neurodegeneration within the enteric nervous system leading to colonic dysmotility is presented. Further research is needed to investigate the influence of aging on the gastrointestinal tract and to develop novel approaches to therapy directed at protecting the enteric nervous system from neurodegeneration.

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Section: Extrinsic Innervationmentioning

confidence: 70%

The Aging Colon: The Role of Enteric Neurodegeneration in Constipation

Wiskur

Meerveld

2010

Curr Gastroenterol Rep

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“…The presence or absence of aging effects on the innervation and function of the stomach could be critical for the satiation process in older people. At a structural level, the aging stomach is more notable for decreasing levels of sympathetic innervation than for loss of afferent fibers (23,24). Motor responses in the stomach are likely to influence the passage of water through the gut, and consequently age associated sympathetic fiber loss could effect the accurate coding of water volume in the stomach.…”

Section: Discussionmentioning

confidence: 99%

“…The contrast between maximum thirst and baseline revealed two loci of activation in the cingulate cortex in both groups: the aMCC [Y, (12,24,26); O, (12, 18, 48); Talairach coordinates] and the pACC (BA32) [Y, (8,38,2); O, (14,36,14)] (Fig. 2).…”

Section: Figmentioning

confidence: 99%

Effect of aging on regional cerebral blood flow responses associated with osmotic thirst and its satiation by water drinking: A PET study

Farrell

Zamarripa

Shade

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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Levels of thirst and ad libitum drinking decrease with advancing age, making older people vulnerable to dehydration. This study investigated age-related changes in brain responses to thirst and drinking in healthy men. Thirst was induced with hypertonic infusions (3.1 ml/kg 0.51M NaCl) in young (Y) and older (O) subjects. Regional cerebral blood flow (rCBF) was measured with positron emission tomography (PET). Thirst activations were identified by correlating rCBF with thirst ratings. Average rCBF was measured from regions of interest (ROI) corresponding to activation clusters in each group. The effects of drinking were examined by correlating volume of water drunk with changes in ROI rCBF from maximum thirst to postdrinking. There were increases in blood osmolality (Y, 2.8 ؎ 1.8%; O, 2.2 ؎ 1.4%) and thirst ratings (Y, 3.1 ؎ 2.1; O, 3.7 ؎ 2.8) from baseline to the end of the hypertonic infusion. Older subjects drank less water (1.9 ؎ 1.6 ml/kg) than younger subjects (3.9 ؎ 1.9 ml/kg). Thirst-related activation was evident in S1/M1, prefrontal cortex, anterior midcingulate cortex (aMCC), premotor cortex, and superior temporal gyrus in both groups. Postdrinking changes of rCBF in the aMCC correlated with drinking volumes in both groups. There was a greater reduction in aMCC rCBF relative to water drunk in the older group. Aging is associated with changes in satiation that militate against adequate hydration in response to hyperosmolarity, although it is unclear whether these alterations are due to changes in primary afferent inflow or higher cortical functioning.cingulate cortex ͉ positron emission tomography U nder usual ambient conditions, volumes of water sufficient to maintain fluid balance are consumed in the routine of regular meals (1, 2). Heat or vigorous activity may cause dehydration, resulting in thirst and the desire to drink. Aging alters thirst and drinking responses, making older people vulnerable to body fluid imbalance (3). This study compared the pattern of brain responses in younger and older men during the development and the satiation of thirst. The aim of the study was to assess the role of cortical and subcortical processes in agerelated changes of thirst and drinking.There are two major physiological changes that cause the onset of thirst; increased blood/CSF osmolality and decreased volume of extracellular fluid. Studies differ on the effects of aging on the relations among blood tonicity, blood volume, and thirst. Increase of blood osmolality through the systemic infusion of hypertonic solutions has been reported to demonstrate either no age-related change in thirst ratings (4, 5) or decreased thirst responses in older men (6). Head-out water immersion drives water into the intrathoracic cavity, leads to increased blood volume and cardiac filling pressure in both young and older subjects, and has been used to assess the effects of blood volume changes on thirst ratings. Head-out immersion leads to a decrease in thirst in young subjects, but does not change thirst ratings in older subjects...

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“…In earlier reports, we have characterized neuropathies as well as neuronal and glial losses in the standard rat model of aging, the Fischer 344 rat (Phillips et al, 2004b(Phillips et al, , 2006. The neuropathies commonly consist of dystrophic or markedly swollen neurites.…”

Section: Dystrophic Swellings In Alpha-synuclein-positive Processes Imentioning

confidence: 99%

Alpha-synuclein-immunopositive myenteric neurons and vagal preganglionic terminals: Autonomic pathway implicated in Parkinson's disease?

et al. 2008

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The protein alpha-synuclein is implicated in the development of Parkinson's disease. The molecule forms Lewy body aggregates that are hallmarks of the disease, has been associated with the spread of neuropathology from the peripheral to the central nervous system, and appears to be involved with the autonomic disorders responsible for the gastrointestinal (GI) symptoms of individuals afflicted with Parkinson's. To characterize the normative expression of alpha-synuclein in the innervation of the GI tract, we examined both the postganglionic neurons and the preganglionic projections by which the disease is postulated to retrogradely invade the CNS. Specifically, in Fischer 344 and Sprague Dawley rats, immunohistochemistry in conjunction with injections of the tracer DextranTexas Red was used to determine, respectively, the expression of alpha-synuclein in the myenteric plexus and in the vagal terminals. Alpha-synuclein is expressed in a subpopulation of myenteric neurons, with the proportion of positive somata increasing from the stomach (~3%) through duodenum (proximal, ~6%; distal, ~13%) to jejunum (~22%). Alpha-synuclein is co-expressed with the nitrergic enzyme NOS or the cholinergic markers calbindin and calretinin in regionally specific patterns: ~90% of forestomach neurons positive for alpha-synuclein express NOS, whereas ~92% of corpus-antrum neurons positive for alpha-synuclein express cholinergic markers. Vagal afferent endings in the myenteric plexus and the GI smooth muscle do not express alpha-synuclein, whereas, virtually all vagal preganglionic projections to the gut express alpha-synuclein, both in axons and in terminal varicosites in apposition with myenteric neurons. Vagotomy eliminates most, but not all, alpha-synuclein-positive neurites in the plexus. Some vagal preganglionic efferents expressing alphasynuclein form varicose terminal rings around myenteric plexus neurons that are also positive for the protein, thus providing a candidate alpha-synuclein-expressing pathway for the retrograde transport of putative Parkinson's pathogens or toxins from the ENS to the CNS.

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Effects of age on sympathetic innervation of the myenteric plexus and gastrointestinal smooth muscle of Fischer 344 rats

Cited by 40 publications

References 45 publications

The Aging Colon: The Role of Enteric Neurodegeneration in Constipation

The Aging Colon: The Role of Enteric Neurodegeneration in Constipation

Effect of aging on regional cerebral blood flow responses associated with osmotic thirst and its satiation by water drinking: A PET study

Alpha-synuclein-immunopositive myenteric neurons and vagal preganglionic terminals: Autonomic pathway implicated in Parkinson's disease?

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