PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “GANGLIA”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMed1995

Varicella-zoster virus (VZV) transcription during latency in human ganglia: prevalence of VZV gene 21 transcripts in latently infected human ganglia.

Reverse transcriptase-linked PCR was used to determine the prevalence of varicella-zoster virus (VZV) gene 21 transcription in latently infected human ganglia. Under conditions wherein reverse transcriptase-linked PCR detected > or = 1,000 transcripts, VZV gene 21 RNA, but not VZV gene 40 RNA, was found in ganglia but not other tissues from five of seven humans.

Base Sequence↗
PubMed2006

Neurobiology of basal ganglia and Tourette syndrome: basal ganglia circuits and thalamocortical outputs.

In summary, the scheme of basal ganglia function presented here, in conjunction with known features of anatomical organization and dopamine neurotransmission provides a hypothesis for the pathophysiology of tics. According to the hypothesis, clusters of striatal neurons (matrisomes) become abnormally active in inappropriate contexts leading to inhibition of GPi or SNpr neurons that would normally be active to supress unwanted movements. The inhibition of htese GPi or SNpr neurons would then disinhibit thalamocortical circuits. Leading to the production of tics. Activity-dependent dopamine effects would inappropriately reinforce these activity patterns leading to stereotyped repetion. Over time, exactly which striatal neuronal clusters are overactive may change under various influences so that the produced movement change over time. This hypothesis is testable directly but requires a valid animal model of tics or higher resolution functional imaging techniques. Continuing work on basic basal ganglia physiology, pathophysiology, and functional imaging in TS is advancing our knowledge of neural circuit abnormalities in TS, but much more work is still needed.

Animals↗
PubMed1994

Oral-oesophageal inoculation of mice with herpes simplex virus type 1 causes latent infection of the vagal sensory ganglia (nodose ganglia).

Herpes simplex virus type 1 (HSV-1) gingivostomatitis during childhood is known to result in a latent infection of the trigeminal ganglion neurons, which innervate the oral mucosa. During latency the viral genome is maintained in a non-infectious state. However, stimuli such as stress, fever or localized trauma can cause HSV-1 to reactivate in neurons and produce recrudescent disease in the peripheral tissues. Recently, HSV-1 proteins and nucleic acids have been detected in biopsies from human duodenal and gastric ulcers, raising the possibility that HSV-1 latency within the enteric nervous system is involved in this chronic recurrent gastrointestinal disorder. The studies in mice described here were done to determine whether HSV-1 latency could be established in neurons that innervate the murine gut. We found that after either intraperitoneal or oral-oesophageal inoculation of mice, HSV-1 establishes a latent infection in nodose ganglia of the vagus nerve, whose sensory neurons project to the gastrointestinal tract. This animal model of HSV-1 latency in the vagal sensory ganglia will be useful to examine the possible relationship between HSV-1 and recurrent gastrointestinal disease.

Animals↗
PubMed1982

Ionic behaviors and nerve growth factor dependence in developing embryonic chick ganglia. I. Studies with intact dorsal root ganglia.

We have recently shown that intact and dissociated 8-day embryonic (E8) chick dorsal root ganglia (DRG) lose the ability to regulate their intracellular Na+, K+ levels when deprived of nerve growth factor (NGF) for 6 h; recovery occurs within minutes of NGF presentation. These ganglionic neurons are believed to depend on NGF for survival and neurite production over a defined period of embryonic life--between about E6 and E15 in the chick. Using intact DRG from E6-E16 chick embryos we determined developmental changes in: (i) 22Na+ accumulation in the presence and absence of NGF, or in the presence of ouabain; and (ii) intra- and extracellular fluid spaces. Sodium accumulation, in the presence of NGF, increases from E6 to E10. It parallels the total fluid space under ouabain but then decreases conspicuously between E10 and E16, despite little change in the latter. NGF thus prevents Na+ accumulation during the early period, and becomes increasingly irrelevant for this behavior in later (after E10) development. These data are interpreted as indicating that: (i) NGF is required for ionic control by DRG neurons up to E10; and (ii) indigenous behaviors for the control of ion pump mechanism(s) are progressively acquired by these cells from E10 to E16, in parallel with the decreasing ionic relevance of NGF. These findings are consistent with the view that the ionic responses to NGF correlate closely with the survival and neurite-promoting effects of this factor.

Age Factors↗
PubMed1985

Pharmacological characteristics of three silent giant neurons, v-LPSN, v-1-VOrN and v-VLN, identified on the ventral surface in the left parietal and the visceral ganglia of the suboesophageal ganglia of an African giant snail (Achatina fulica Férussac).

Three giant neurons, named v-LPSN, v-1-VOrN and v-VLN, were identified on the ventral surface of the left parietal ganglion and the visceral ganglion in the suboesophageal ganglia of an African giant snail (Achatina fulica Férussac). They lacked the spontaneous spike discharges in the normal state. The pharmacological features of the three neurons, in relation to the principal common neurotransmitter substances and their derivatives were examined. The v-LPSN (ventral-left parietal silent neuron) (diameter: about 130 microns) is situated in the left parietal ganglion close to the visceral ganglion. The neuron was excited by histamine (the minimum effective concentration [MEC]: 3 X 10(-4) M) and inhibited slightly by acetylcholine (Ach) and its related substances. The v-1-VOrN (ventral-left-visceral oral neuron) (diameter: about 130 microns) is situated in the left and oral part of the visceral ganglion. The neuron was inhibited markedly by dopamine (DA) (MEC: 3 X 10(-4) M) and slightly by Ach and its related substances. No substance producing a marked excitation of the neuron has been found yet. The v-VLN (ventral-visceral large neuron) (diameter: about 300 microns) is found in the centre of the visceral ganglion. The neuron was excited by L-norepinephrine (MEC: 10(-4) M), DL-octopamine (MEC: 2 X 10(-4) M), 5-hydroxytryptamine (MEC: 10(-4) M) and beta-hydroxy-L-glutamic acid (MEC: 10(-4) M) and inhibited by DA (MEC: 10(-4) M), GABA (MEC: 3 X 10(-5) M) and Ach (MEC: 10(-4) M). L-Epinephrine showed varied effects (MEC: 10(-4) M), which were either excitatory or inhibitory.

Action Potentials↗
PubMed2006

Immunohistochemical localization of histamine H3 receptors in rodent skin, dorsal root ganglia, superior cervical ganglia, and spinal cord: potential antinociceptive targets.

Activation of histamine H3 receptors (H3Rs) reduces inflammation and nociception, but the existence of H3Rs on peripheral innervation has never been demonstrated. Here we use antibodies to locate H3Rs in whisker pads, hairy and glabrous hind paw skin, dorsal root ganglia (DRGs), and spinal cords of rats, wild type mice, and H3R knockout (H3KO) mice. Although H3Rs have been hypothesized to be on C and sympathetic fibers, H3R-like immunoreactivity (H3R-LI) was only detected on presumptive periarterial A delta fibers and on A beta fibers that terminated in Meissner's corpuscles and as lanceolate endings around hair follicles. The H3R-positive periarterial fibers were thin-caliber and coexpressed immunoreactivity for calcitonin gene-related peptide (CGRP), substance P, acid sensing ion channel 3, and 200 kDa neurofilament protein (NF). H3R-LI was also detected on epidermal keratinocytes and Merkel cells, but not on Merkel endings, C fibers, any other A delta fibers, or sympathetic fibers. In DRGs, H3R-LI was preponderantly on medium to large neurons coexpressing NF-LI and mostly CGRP-LI. In dorsal horn, CGRP-positive fibers with and without H3R-LI ramified extensively in lamina II; many of the former formed a plexus in lamina V. Low levels of H3R-LI were also present on A beta fibers penetrating superficial and into deeper laminae. The distribution of H3R-LI was similar in rats and wild type mice, but was eliminated or strongly reduced in A delta fibers and A beta fibers, respectively, in H3KO mice. Taken with recently published behavioral results, the present findings suggest that periarterial, peptidergic, H3R-containing A delta fibers may be sources of high threshold mechanical nociception.

Animals↗
PubMed1997

Central regulation of sympathetic ganglia development: heterogeneous response of paravertebral, prevertebral, and terminal ganglia.

These studies expand previous observations regarding the central control of neuronal maturation and indicate that paravertebral, prevertebral, and terminal ganglia are all under central influences, but in varying degrees. These variations are probably related to the relative contributions that central pathways exert on specific peripheral neuronal populations during growth and development as well as the various roles of more peripheral developmental modulators such as target organs and hormones, especially in the case of the HG. It is apparent, therefore, that during development central injury may result in heterogeneous deficits depending on the unique intrinsic and extrinsic environment that each ganglion population shares.

Adrenal Medulla↗
PubMed1977

Isolation of Herpes simplex virus from human trigeminal ganglia, including ganglia from one patient with multiple sclerosis.

Herpes-simplex virus (H.S.V.) was isolated from 18 of 39 trigeminal ganglia (T.G.) obtained within 12 h of death. The virus was isolated from ten persons who had died of trauma, from one case of lymphoma, and from one case of multiple sclerosis. In the cadaver with histologically confirmed multiple sclerosis, large bilateral areas of demyelination were present near the points of entry of the nerve root, and the possibility that H.S.V. migration to the root entry zone caused demyelination cannot be excluded.

Adolescent↗
PubMed2003

Estrogen receptors in the spinal cord, sensory ganglia, and pelvic autonomic ganglia.

Until relatively recently, most studies of the effects of estradiol in the nervous system focused on hypothalamic, limbic, and other brain centers involved in reproductive hormone output, feedback, and behaviors. Almost no studies addressed estradiol effects at the spinal cord or peripheral nervous system level. Prior to the mid-1960s-1970s, few studies examined neural components of reproductive endocrine organs (e.g., ovary or testis) or the genital organs (e.g., uterus or penis) because available data supported endocrine regulation of these structures. Over the last two decades interest in and studies on the innervation of the genital organs have burgeoned. Because of the responsiveness of genital organs to sex steroid hormones, these neural studies seeded interest in whether or not autonomic and sensory neurons that innervate these organs, along with their attendant spinal cord circuits, also are responsive to sex hormones. From the mid-1980s there has been a steady growth of interest in, and studies of the neuroanatomy, neurochemistry, neural connectivity, and neural functional aspects in reproductive organs and the response of these parameters to sex steroids. Thus, with the growth of probes and techniques, has come studies of anatomy, neurochemistry, and circuitry of sex hormone-responsive neurons and circuits in the spinal cord and peripheral nervous system. This review focuses on estrogen receptors in sensory, autonomic, and spinal cord neurons in locales that are associated with innervation of female reproductive organs.

Animals↗