Search

Abstract: The goal of this study was to create a heat map indicating the probabilistic location of major ganglia of the cervical sympathetic trunk (CST). Detailed dissections of human cadaveric specimens, followed by spatial registration and analysis of the cervical sympathetic ganglia in the neck and upper thorax regions (C1–T1) were performed in 104 neck specimens (both sides from 52 cadavers). Unbiased parametric mapping, visualized with a heat map, revealed a general pattern of two major ganglia located on both sides of the neck: The superior cervical ganglion (SCG) was located 80–90mm superior to the point at which the vertebral artery entered the transverse foramen (VA–TF); the stellate ganglion (SG) was located approximately 10mm inferior to the VA–TF in 80% of our sample, or surrounding the VA–TF in the remaining 20% of our sample. In between these ganglia, a highly variable number of smaller and less prevalent ganglia were present on either side of the neck. The middle ganglia on the right side of the neck were located closer to the SCG, possibly indicative of the middle cervical ganglion. On the left side the middle ganglia were located closer to the SG, perhaps indicative of the vertebral ganglion or the inferior cervical ganglion. Individual specimens could be classified into one of seven different patterns of cervical trunks. The results may help surgeons and anesthesiologists more accurately target and preserve these structures during medical procedures. [Copyright &y& Elsevier]

Abstract: The principal aim of this study was to determine whether prolonged chronic footshock stress can evoke sustained changes in blood pressure in rats and to elucidate possible underlying neurochemical mechanisms as mediated by the sympathoadrenal system. Adult male Wistar rats instrumented for telemetric recording of arterial pressure, heart rate and locomotor activity were subjected to six weeks of inescapable unpredictable electrical footshocks (FS+) or were exposed to shock chambers but were not shocked (FS−). Compared to FS− animals, FS+ animals had significantly reduced body weight gain (by 30%), locomotor activity (by 25%) and social interaction time (by 30%) — symptoms commonly induced by chronic stress and depression in humans. These changes were associated with small, but significant increases in systolic blood pressure (by 7%) and pulse pressure (by 11%) in FS+ rats relative to FS− rats. We have also found neurochemical alterations in sympathoadrenal pathways (that lasted for at least one week post-stress) including about 2–3 fold increases in the levels of tyrosine hydroxylase phosphorylation in the sympathetic ganglia and adrenal gland and a 1.8-fold increase in the expression of the Angiotensin II receptor type 1 protein in the adrenal gland of FS+ rats relative to FS− rats. We conclude that uncontrollable and unpredictable footshock stress can lead to elevation in systolic blood pressure when applied for an extended period of time (six weeks) in Wistar rats, and that these changes could be mediated by stress-induced modifications in sympathoadrenal pathways. [Copyright &y& Elsevier]

Abstract: Expression of CB in the sympathetic ganglia was investigated by immunohistochemistry. The distribution of CB immunoreactivity was studied in the superior cervical ganglion (SCG), stellate ganglion (SG) and celiac ganglion (CG) from rats and cats of different ages (newborn, 10-day-old, 20-day-old, 30-day-old, two-month-old, six-month-old). We observed that the percentage of CB-immunoreactive (IR) neurons decreased during early postnatal development in rats and cats. In all studied ganglia of both species, the percentage of CB-IR neurons was high in newborn and 10-day-old animals and significantly decreased up to 30days of life. In rats of all ages, the largest percentage of CB-IR neurons was observed in the SG compared to the SCG and CG. In the cat sympathetic ganglia, the number of CB-IR neurons decreased more rapidly during the first two months of life, and only scattered CB-IR neurons were found in the sympathetic ganglia of two-month-old and six-month-old cats. In cats, the highest percentage of CB-IR neurons was observed in the SG, while the lowest percentage was found in the CG. The difference in size between CB+ and CB− neurons equally changed during development. Finally, the changes in the size and percentages of CB-IR neurons were complete in rats at the first month of life, and in cats at the end of the second month. [Copyright &y& Elsevier]

Abstract: We compared the excitability of secretomotor B and vasomotor C neurons using virtual nicotinic synapses implemented with the dynamic clamp technique. In response to fast synaptic conductance (g syn) waveforms modeled after B cell synaptic currents, it took 17.1±1.2nS to elicit spikes in 104 B cells and 3.3±0.3nS in 35 C cells. After normalizing for whole-cell capacitance, C cells were still more excitable than B cells (76±5pS/pF vs. 169±8pS/pF). Stimulating C cells with slower g syn waveforms, identical to synaptic currents in C cells, further accentuated the difference between cell types. The phenotypic excitability difference did not correlate with time in culture (1–12days) and could not be explained by resting potential (B cells: −65.6±0.9mV, C cells: −63.1±1.6mV) or input conductance density, which was greater in C cells (24.4±4.3pS/pF) than B cells (14.5±1.5pS/pF). Action potentials elicited by virtual EPSPs had a threshold voltage for firing that was −28.4±0.7mV in C cells and −19.7±0.4mV B cells, and an upstroke velocity and peak spike potential that were greater in B cells. The repetitive firing properties of B and C cells were similar; 69–78% phasic, 11–16% adapting and 11–15% tonic. We propose that B and C neurons express different types of Na+ channels that shape how they integrate nicotinic synaptic potentials. [Copyright &y& Elsevier]

Abstract: Superoxide anion (O2 −•) production was previously reported to be increased in celiac ganglia (CG) during DOCA–salt hypertension, possibly via activation of the reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase. This suggested a role for neuronal NADPH oxidase in autonomic neurovascular control. However, the expression and localization of NADPH oxidase in the peripheral neurons are not fully known. The purpose of this study was to examine the subcellular localization of NADPH oxidase in sympathetic and sensory ganglion neurons and perivascular nerve fibers. In rat CG, p22phox and neuropeptide Y (NPY) were colocalized in all neurons. P22phox was also localized to dorsal root ganglia (DRG) neurons that contain calcitonin gene related peptide (CGRP). In mesenteric arteries, p22phox and p47phox were colocalized with NPY or CGRP in perivascular nerve terminals. A similar pattern of nerve terminal staining of p22phox and p47phox was also found in cultured CG neurons and nerve growth factor (NGF)-differentiated PC12 cells. These data demonstrate a previously uncharacterized localization of NADPH oxidase in perivascular nerve fibers. The presence of a O2 −•-generating enzyme in close vicinity to the sites of neurotransmitter handling in the nerve fibers suggests the possibility of novel redox-mediated mechanisms in peripheral neurovascular control. [Copyright &y& Elsevier]

Abstract: The neural crest is an excellent model system to study cell fate and cell guidance signaling. Neural crest cells emerge from a common multipotent subpopulation and follow stereotypical migratory pathways to contribute to many diverse peripheral structures throughout the vertebrate embryo. The neural tube and diverse embryonic microenvironments from which the neural crest originate and migrate through are important sources of signals, yet it is still unclear how a common pool of neural crest stem and progenitor cells diversify and become distributed along specific stereotypical migratory paths. In the post-otic hindbrain and trunk, the neural crest emerge and contribute to the autonomic nervous system, and failure of proper cell navigation and differentiation often leads to congenital disorders that include dysautonomias, Hirschprung''s disease, and neuroblastoma cancer. Recent exciting studies of neural crest cell behaviors have revealed the interplay of several molecular signaling pathways that guide and shape autonomic precursor cells to and into proper target structures, suggesting further work may help to better understand autonomic nervous system assembly, derived from a convergence of time-lapse imaging and molecular analyses. In this mini-review, we summarize recent fluorescent cell labeling strategies and cell behavior analyses that elucidate the role of molecular signals on the migration of autonomic precursor cells. We highlight advances in our understanding of the autonomic precursor cell behaviors and fate determination studied within the embryonic microenvironment. [Copyright &y& Elsevier]

Abstract: Information about the conditions of all tissues in the body is conveyed to the central nervous system through afferent neurons. Uniquely amongst peripheral organs, the intestine has numerous additional afferent neurons, intrinsic primary afferent neurons that have their cell bodies and processes in the enteric plexuses and do not project to the central nervous system. They detect conditions within the gut and convey that information to intrinsic reflex pathways that are also entirely contained inside the gut wall. Intrinsic primary afferent neurons respond both to the presence of material in the gut lumen and to distension of the gut wall and initiate reflex changes in contractile activity, fluid transport across the mucosa and local blood flow. They also function as nociceptors that initiate tissue-protective propulsive and secretory reflexes to rid the gut of pathogens. The regulation of excitability of intrinsic primary afferent neurons is through multiple ion channels and ion channel regulators, and their excitability is critical to setting the strength of enteric reflexes. The intestine also provides afferent signals to sympathetic pre-vertebral ganglia. The signals are conveyed from the gut by intestinofugal neurons that have their cell bodies within enteric ganglia and form synapses in the sympathetic ganglia. Intestinofugal neurons form parts of the afferent limbs of entero-enteric inhibitory reflexes. Because the unusual afferent neurons of the small intestine and colon make their synaptic connections outside the central nervous system, the neurons and the reflex centres that they affect are potential targets for non-central penetrant therapeutic compounds. [Copyright &y& Elsevier]

Changes in the distribution of NADPH-diaphorase (NADPH-d) and acetylcholinesterase (AChE) were studied in neurons of the stellate ganglion in newborn, 10-, 20-day-old, 1-, 2-, 4- and 6-month-old kittens. AChE-positive neurons were revealed in the stellate ganglion (SG) from birth onwards. The number of these neurons increased until 20 days of postnatal life and then declined in 1- and 2-month-old kittens. A small number of weakly stained, NADPH-d-positive cells were found in newborn kittens, while intensely stained neurons first appeared in 10-day-old animals and increased in number up to the second month of life. The size of AChE-positive neurons was larger in comparison with NADPH-d-positive cells in the stellate ganglion of all animals under study. We suggest that putative vasodilator neurons or cells innervating sweat glands exhibit different development patterns from the moment of birth. [Copyright &y& Elsevier]