Differential susceptibility to ageing of rat preganglionic neurones projecting to the major pelvic ganglion and of their afferent inputs

Dering, Monica A.; Ranson, Richard N.; Waboso, Henrietta N.; Watson, Alan Hugh David

doi:10.1016/s1566-0702(01)00366-6

Cited by 34 publications

(20 citation statements)

References 29 publications

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“…As such, ATP (and perhaps UTP) may serve as key extracellular regulators of neuronal development that protect developing neurons from proapoptotic stimuli. Moreover, because neurotrophin signaling and innervation of peripheral target tissues declines with age (Gavazzi and Cowen, 1996;Santer et al, 2002), based on the current findings, drugs that activate P2Y 2 receptors would appear to have potential to prevent this age-related decline, as well as apoptosis triggered by disease or injury.…”

Section: Discussionmentioning

confidence: 73%

Inhibition of Apoptosis by P2Y₂Receptor Activation: Novel Pathways for Neuronal Survival

Arthur

Georgi²,

Akassoglou³

et al. 2006

J. Neurosci.

102

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Cell survival is an essential function in the development and maintenance of the nervous system. We demonstrate here a previously unappreciated role for extracellular nucleotide signaling through the P2Y 2 receptor in the survival of neurons: PC12 (pheochromocytoma 12) cells and dorsal root ganglion neurons are protected from serum starvation-induced apoptosis by ATP, UTP, and ATP␥S, an effect mediated via P2Y 2 receptors, as demonstrated by small interfering RNA and genetic knock-out models. This protection occurs independently of neurophin signaling but requires Src activation of ERK (extracellular signal-regulated kinase) and Akt. Moreover, ATP␥S and NGF act synergistically to enhance neuronal survival through enhanced TrkA signaling. The results, which define a novel mechanism for inhibition of apoptosis, implicate parallel, interacting systems-extracellular nucleotides/P2Y 2 receptors and neurotrophin/TrkA-to sustain neuronal survival.

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Section: Discussionmentioning

confidence: 73%

Inhibition of Apoptosis by P2Y₂Receptor Activation: Novel Pathways for Neuronal Survival

Arthur

Georgi²,

Akassoglou³

et al. 2006

J. Neurosci.

102

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“…For example, immunohistochemical analyses in aged rats revealed significant age-associated declines in the serotonergic (5-HT) and noradrenergic innervation of various spinal cord regions including the intermediolateral cell nucleus, sacral parasympathetic nucleus, dorsal gray commissure and the ventral horn that contains Onuf’s nucleus, with the exception that 5-HT innervation of the sacral parasympathetic nucleus and noradrenergic innervation in the Onuf’s nucleus were maintained (517). Sympathetic preganglionic neurons in the L1-L2 spinal cord that project to the major pelvic ganglion also exhibit a number of age related degenerative changes such as reductions in the cell number, the length of their dendrites and the synaptic contacts made by glutamate-immunoreactive boutons onto the dendrites, although these changes are not seen in PGNs in the L6–S1 spinal cord (539). Frequent voiding produced by apomorphine-induced dopamine receptor activation is more pronounced in aged rats compared with young rats, suggesting that aged rats are more susceptible to altered central processing to induce bladder overactivity despite the decline in baseline bladder function with aging (93).…”

Section: Disease-induced Changes In Micturitionmentioning

confidence: 99%

Neural Control of the Lower Urinary Tract

Groat

Griffiths

Yoshimura

2014

Comprehensive Physiology

350

527

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This article summarizes anatomical, neurophysiological, pharmacological, and brain imaging studies in humans and animals that have provided insights into the neural circuitry and neurotransmitter mechanisms controlling the lower urinary tract. The functions of the lower urinary tract to store and periodically eliminate urine are regulated by a complex neural control system in the brain, spinal cord, and peripheral autonomic ganglia that coordinates the activity of smooth and striated muscles of the bladder and urethral outlet. The neural control of micturition is organized as a hierarchical system in which spinal storage mechanisms are in turn regulated by circuitry in the rostral brain stem that initiates reflex voiding. Input from the forebrain triggers voluntary voiding by modulating the brain stem circuitry. Many neural circuits controlling the lower urinary tract exhibit switch-like patterns of activity that turn on and off in an all-or-none manner. The major component of the micturition switching circuit is a spinobulbospinal parasympathetic reflex pathway that has essential connections in the periaqueductal gray and pontine micturition center. A computer model of this circuit that mimics the switching functions of the bladder and urethra at the onset of micturition is described. Micturition occurs involuntarily in infants and young children until the age of 3 to 5 years, after which it is regulated voluntarily. Diseases or injuries of the nervous system in adults can cause the re-emergence of involuntary micturition, leading to urinary incontinence. Neuroplasticity underlying these developmental and pathological changes in voiding function is discussed.

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“…This innervation arises from intraspinal as well as supraspinal sources, because some of the glutamate-immunoreactive input to SPN persists after a complete spinal cord transection (Llewellyn-Smith et al, 1997a;Llewellyn-Smith and Weaver, 2001). Sacral PPN that project to the MPG also receive synapses from glutamate-immunoreactive boutons (Santer et al, 2002), but whether this glutamatergic input comes from supraspinal and/or intraspinal sources is not yet known.…”

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confidence: 99%

VGLUT1 and VGLUT2 innervation in autonomic regions of intact and transected rat spinal cord

Llewellyn‐Smith

Martin

Fenwick

et al. 2007

J of Comparative Neurology

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Fast excitatory neurotransmission to sympathetic and parasympathetic preganglionic neurons (SPN and PPN) is glutamatergic. To characterize this innervation in spinal autonomic regions, we localized immunoreactivity for vesicular glutamate transporters (VGLUTs) 1 and 2 in intact cords and after upper thoracic complete transections. Preganglionic neurons were retrogradely labeled by intraperitoneal Fluoro-Gold or with cholera toxin B (CTB) from superior cervical, celiac, or major pelvic ganglia or adrenal medulla. Glutamatergic somata were localized with in situ hybridization for VGLUT mRNA. In intact cords, all autonomic areas contained abundant VGLUT2-immunoreactive axons and synapses. CTB-immunoreactive SPN and PPN received many close appositions from VGLUT2-immunoreactive axons. VGLUT2-immunoreactive synapses occurred on Fluoro-Gold-labeled SPN. Somata with VGLUT2 mRNA occurred throughout the spinal gray matter. VGLUT2 immunoreactivity was not noticeably affected caudal to a transection. In contrast, in intact cords, VGLUT1-immunoreactive axons were sparse in the intermediolateral cell column (IML) and lumbosacral parasympathetic nucleus but moderately dense above the central canal. VGLUT1-immunoreactive close appositions were rare on SPN in the IML and the central autonomic area and on PPN. Transection reduced the density of VGLUT1-immunoreactive axons in sympathetic subnuclei but increased their density in the parasympathetic nucleus. Neuronal cell bodies with VGLUT1 mRNA occurred only in Clarke's column. These data indicate that SPN and PPN are densely innervated by VGLUT2-immunoreactive axons, some of which arise from spinal neurons. In contrast, the VGLUT1-immunoreactive innervation of spinal preganglionic neurons is sparse, and some may arise from supraspinal sources. Increased VGLUT1 immunoreactivity after transection may correlate with increased glutamatergic transmission to PPN.

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Differential susceptibility to ageing of rat preganglionic neurones projecting to the major pelvic ganglion and of their afferent inputs

Cited by 34 publications

References 29 publications

Inhibition of Apoptosis by P2Y₂Receptor Activation: Novel Pathways for Neuronal Survival

Inhibition of Apoptosis by P2Y₂Receptor Activation: Novel Pathways for Neuronal Survival

Neural Control of the Lower Urinary Tract

VGLUT1 and VGLUT2 innervation in autonomic regions of intact and transected rat spinal cord

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Differential susceptibility to ageing of rat preganglionic neurones projecting to the major pelvic ganglion and of their afferent inputs

Cited by 34 publications

References 29 publications

Inhibition of Apoptosis by P2Y2Receptor Activation: Novel Pathways for Neuronal Survival

Inhibition of Apoptosis by P2Y2Receptor Activation: Novel Pathways for Neuronal Survival

Neural Control of the Lower Urinary Tract

VGLUT1 and VGLUT2 innervation in autonomic regions of intact and transected rat spinal cord

Contact Info

Product

Resources

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Inhibition of Apoptosis by P2Y₂Receptor Activation: Novel Pathways for Neuronal Survival

Inhibition of Apoptosis by P2Y₂Receptor Activation: Novel Pathways for Neuronal Survival