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T A Day

Publications and source records attributed to T A Day.

At least 73 records · Page 4Linked to original sources
PubMed1995

Hypovolaemic and osmotic stimuli induce distinct patterns of c-Fos expression in the rat subfornical organ.

Investigation of the effects of osmotic and hypovolaemic stimuli on the pattern of subfornical organ (SFO) c-fos expression yielded three distinct distributions of activated neurons. Hypertonic saline induced c-fos expression in peripheral SFO only. PEG/water induced c-fos in the central core of SFO and PEG/saline induced c-fos in both the central and peripheral regions. Isotonic saline failed to induce SFO c-fos expression. These results are consistent with the notion of functional segregation within the SFO.

Animals↗
PubMed1995

Immunohistochemical localization of a Shaker-related voltage-gated potassium channel protein in Schistosoma mansoni (Trematoda: Digenea).

We have recently isolated a cDNA (SKv1.1) encoding a Shaker-related K+ channel from the human parasitic trematode Schistosoma mansoni. In order to better understand the functions of SKv1.1 protein, the distribution of SKv1.1 protein in adult S. mansoni was analyzed by immunohistochemistry using a region-specific antibody. SKv1.1 proteins were widely expressed in the nervous and muscular systems. The strongest immunoreactivity (IR) was observed in the nervous system of both male and female. In the nervous system, IR for SKv1.1 proteins was localized in cell bodies and nerve fibers of the anterior ganglia, the central commissure, and the main nerve cords. IR was also observed in the dorsal and the ventral peripheral nerve nets, fine nerve fibers entering into a variety of structures such as the dorsal tubercles, longitudinal and ventral muscle fibers, and oral and ventral suckers. In the muscular system, SKv1.1 proteins were localized to the longitudinal, circular, and ventral muscle fibers of male as well as in isolated muscle fibers where native A-type K+ currents were measured. Moderate IR was also seen in a large number of cell bodies in the parenchyma. These results indicate that SKv1.1 protein may play an important role in the regulation of the excitability of neurons and muscle cells of S. mansoni.

Amino Acid Sequence↗
PubMed1995

Analysis of the kinetics and voltage-dependency of transient and delayed K+ currents in muscle fibers isolated from the flatworm Schistosoma mansoni.

There are two distinct voltage-dependent K+ currents in muscle fibers freshly isolated from the human flatworm parasite S. mansoni. Present is a delayed rectifier current with a tau act of 17 msec and tau inact > 3 sec. The delayed rectifier is very resistant to steady-state inactivation, with over 40% of the current non-inactivating, and over 15 sec required for the maximum inactivation of the other portion. The current is resistant to block by extracellular tetraethylammonium, is half-blocked by 10 mM 4-aminopyridine, and is insensitive to dendrotoxin. Also present is an "A" current with tau act < 1 msec and tau inact < 15 msec. The "A" current, like the delayed rectifier current, is resistant to block by external tetraethylammonium and is insensitive to dendrotoxin. Three micromoles of 4-aminopyridine produce a half-blockade of the "A" current. These two K+ currents are very similar to a delayed rectifier and "A" currents that have been described in a number of lower and more advanced animals.

4-Aminopyridine↗
PubMed1995

Cloning and functional expression of a Shaker-related voltage-gated potassium channel gene from Schistosoma mansoni (Trematoda: Digenea).

We have isolated a cDNA (SKv1.1) encoding a Shaker-related K+ channel from an adult cDNA library of the human parasitic trematode Schistosoma mansoni. The deduced amino acid sequence (512 aa, 56.5 kDa) contains 6 putative membrane-spanning domains (S1-S6) and a pore-forming domain (H5). SKv1.1 is grouped in the Shaker family, but forms a unique branch within this family, on the basis of dendrogram analysis. SKv1.1 shows significant sequence identity with most other Shaker channels, with 64-74% identity in the core region (S1-S6). It has the highest sequence identity with the K+ channel (Ak01a) from Aplysia. Northern blot analysis detected a single primary transcript of 2.8 kb. Southern blot analysis indicated that SKv1.1 is present as a single copy in the genomic DNA of S. mansoni. Expression of SKv1.1 in Xenopus oocytes produced a rapidly activating and inactivating outward K+ current which is highly sensitive to 4-aminopyridine, but is insensitive to tetraethylammonium, mast cell degranulating peptide, dendrotoxin and charybdotoxin. The presence of a Shaker homologue in Schistosoma suggests that Sh subfamilies may exist in other lower invertebrates as well as platyhelminths.

Amino Acid Sequence↗
PubMed1995

Head and neck squamous cell carcinoma metastatic to the orbital apex.

Primary squamous cell carcinoma of the head and neck most commonly metastasizes to the lymph nodes, lung, bone, and liver. Many other rare sites of metastatic disease have been reported. To date, metastatic squamous cell carcinoma of the head and neck to the orbital apex has not been described. Presented are two cases, one tonsil and one parotid primary with metastatic disease to the orbital apex. Many tumors have been found to metastasize to the eye and orbit, but head and neck neoplasms are rarely reported. A review of the literature is presented in addition to the detailed case reports with their radiologic findings and clinical course. Surgical resection followed by postoperative radiotherapy appears the treatment of choice at this time.

Case Reports↗
PubMed1995

Rat vasopressin cell responses to simulated hemorrhage: stimulus-dependent role for A1 noradrenergic neurons.

c-fos expression mapping and electrophysiological recording experiments were done to clarify the role of the A1 noradrenergic cell group in the vasopressin response to hypotensive hemorrhage. In pentobarbital-anesthetized rats, moderate and severe hypotensive hemorrhages were simulated by brief occlusion of the inferior vena cava sufficient to reduce mean arterial pressure to approximately 50 or 30 mmHg, respectively. Both stimuli significantly increased the number of A1 region catecholamine cells displaying Fos-like immunoreactivity, this effect being most prominent at the level of the area postrema. Both stimuli also increased the number of supraoptic nucleus vasopressin cells displaying Fos-like immunoreactivity. Accordingly, electrophysiological studies involving separate animals confirmed that both moderate and severe caval occlusion significantly increased the firing of functionally identified vasopressin cells recorded in the supraoptic nucleus. However, although interruption of A1 region neuronal function by injection of gamma-aminobutyric acid at the level of the area postrema eliminated the increase in vasopressin cell firing elicited by moderate caval occlusion, it did not block the response to severe caval occlusion. These findings suggest that, in the rat, the vasopressin response to an acute reduction in central blood volume, such as that produced by hemorrhage, depends on the A1 projection only if the stimulus is of moderate intensity. Severe stimuli appear to involve activation of both the A1 projection and an additional vasopressin-stimulatory pathway that bypasses the A1 region.

Animals↗
PubMed1995

The use of tissue expanders in the correction of ectropion in an animal model.

The use of tissue expanders in eyelid reconstruction has seen limited application. To determine the efficacy of tissue expanders in the correction of cicatricial ectropion, an animal model was developed. Lower-eyelid blepharoplasty with overcorrection was performed on 18 New Zealand white rabbits. After 1 month, if significant ectropion was present, tissue expanders (1.8-cm3 Cylindrical/Microdome [CUI Corporation, Carpinteria, Calif.]) were inserted on one side, the other eye being the control. These were inflated in the following weeks to a total volume of 2 cm3. The tissue expanders were then removed, and the animals were followed for 1 month. Although the early results were encouraging, the ectropion progressed toward its preoperative severity. It appears that lower-eyelid ectropion remains a therapeutic problem that is only partially corrected with tissue expansion alone.

Animals↗
PubMed1995

Role of ventrolateral medulla catecholamine cells in hypothalamic neuroendocrine cell responses to systemic hypoxia.

Systemic hypoxia stimulates the release of vasopressin (VP) and adrenocorticotropin hormone (ACTH). To examine the involvement of catecholamine cell groups of the ventrolateral medulla (VLM) in the neuroendocrine responses, we have used the c-fos activity mapping technique to compare the effects of hypoxia on VLM catecholamine cells to those on neurosecretory VP and putative corticotropin releasing factor (CRF) containing cells. A limited degree of catecholamine cell activation was evident at predominantly mid-VLM levels at 12% oxygen in the inspired air. Further reduction in inpsirate oxygen levels enhanced recruitment of caudally located VLM catecholamine cells considered to form part of the A1 noradrenergic cell group. Threshold for activation of VP and putative CRF cells occurred at the 10% oxygen level. Unexpectedly, this stimulus also activated neurosecretory oxytocin (OT) cells. With increasing hypoxic severity the number of activated supraoptic VP and OT cells was not significantly different to that observed at the 10% level. However, paraventricular neuroendocrine responses continued to increase with putative CRF containing cells of the medial parvocellular zone having nearly double the level of activity (as measured by the number of cells within this region displaying Fos-like immunoreactivity; FLI) at 6% compared to that apparent to the 10% level of hypoxia. Paraventricular VP cells displaying FLI were also increased at the most severe levels of hypoxia but this effect was much less marked than the medial parvocellular response. Consistent with a role for VLM catecholamine cells in generation of neuroendocrine cell responses to hypoxia, unilateral VLM lesions, restricted to the caudal two thirds of the catecholamine cell column, resulted in significant reductions in the responses of all three cell types. These results, in addition to establishing a role for VLM catecholamine cells in neuroendocrine cell responses to systemic hypoxia, have important general implications for catecholamine cell group involvement in neuroendocrine regulation.

Animals↗
PubMed1994

c-fos expression in hypothalamic neurosecretory and brainstem catecholamine cells following noxious somatic stimuli.

Noxious somatic stimuli elicit vasopressin secretion, an effect thought to result from activation of a facilitatory input from A1 catecholamine cells of the medulla oblongata. To better characterize the A1 cell response and effects on other neuroendocrine A1 projection targets, particularly within the paraventricular nucleus, we have now mapped c-fos expression in neurochemically identified catecholamine and neurosecretory cells following a noxious somatic stimulus. Unilateral hind paw pinch significantly increased c-fos expression in contralateral A1 cells whereas other brainstem catecholamine cell groups were unaffected. Expression of c-fos was also increased in the supraoptic nucleus, this effect being more pronounced for vasopressin than oxytocin neurosecretory cells and, as with A1 cells, primarily on the side contralateral to the stimulated paw. In contrast, the increase in the paraventricular nucleus was greater in oxytocin rather than in vasopressin cells. Additionally there was a significant rise in c-fos expression in medial parvocellular paraventricular nucleus cells of noxiously stimulated animals. Notably, the majority of tuberoinfundibular corticotropin-releasing factor cells are located in this medial parvocellular zone. These results are consistent with and expand on those previously reported from electrophysiological and anatomical studies. The finding of differing neurosecretory cell responses between supraoptic and paraventricular nuclei has interesting implications with regard to the afferent control of neurosecretory cell activity. For example, the substantially greater activation of supraoptic versus paraventricular nucleus vasopressin cells, despite being innervated by the same medullary noradrenergic cell group, raises the possibility of a differential input or differences in responsiveness. Furthermore, the activation of paraventricular nucleus parvocellular cells is consistent with suggestions that the A1 cell group provides an excitatory input to this population.

Animals↗
PubMed1994

Serotonin and its requirement for maintenance of contractility in muscle fibres isolated from Schistosoma mansoni.

Muscle fibres isolated from adult Schistosoma mansoni contracted in a dose-dependent manner when exposed to elevated K+ with a maximum response obtained with 25 mM K+. These contractions were dependent on extracellular Ca2+ since Co2+ (5 mM) or nicardipine (1 microM) blocked the high K+ contractions. Serotonin (300 nM or higher) was required for maintenance of high K+ contractions. With concentrations of serotonin less than 300 nM the response was dose dependent. 5-Methoxytryptamine or alpha-methylserotonin at 1 microM as well as 10 microM tryptamine were able to substitute for serotonin, but 1 microM 5-carboxyamidotryptamine was ineffective. The order of potency for antagonists (10 microM) was: methiothepin > metergoline > Ly-278,584 = ketanserin. This pattern of responsiveness does not fit well with any known mammalian serotonin receptor subtype. Since forskolin, an adenylate cyclase activator, is able to mimic the action of serotonin and H89, a protein kinase inhibitor, is able to block the effect of serotonin, the effect of serotonin on contractility of the muscle may be via a cAMP-dependent pathway.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1994

Platyhelminth FMRFamide-related peptides (FaRPs) contract Schistosoma mansoni (Trematoda: Digenea) muscle fibres in vitro.

Molluscan FMRFamide and two recently discovered platyhelminth FMRFamide-related peptides (FaRPs), GNFFRFamide from the cestode Moniezia expansa and RYIRFamide from the terrestrial turbellarian Artioposthia triangulata, cause dose-dependent contractions of individual muscle fibres from Schistosoma mansoni in vitro. The most potent FaRP tested was the turbellarian peptide RYIRFamide, which produced a concentration-dependent effect between 10(-9) and 10(-7) M. FMRFamide and GNFFRFamide were less potent, inducing contractions between 10(-8)-10(-6) M and 10(-7)-10(-5) M respectively. The contractile effect of each of these peptides was blocked by the presence of 1 microM FMR-D-Famide. FMRF free acid did not elicit contraction of the muscle fibres. The FaRP-induced contractions did not occur if the Ca2+ was omitted and 0.5 microM EGTA was added to the extracellular medium. The FaRP-induced contractions were not blocked by the Ca2+ channel blockers nicardipine, verapamil or diltiazem, although high K+-induced contractions of these fibres were blocked by nicardipine. These data indicate the presence of FaRP receptors on schistosome muscle fibres and demonstrate their ability to mediate muscle contraction. The action of these endogenous flatworm peptides on schistosome muscle is the first demonstration of a direct excitatory effect of any putative neurotransmitter on the muscle of a flatworm, and establishes a role for FaRPs in neuromuscular transmission in trematodes. In addition, it provides the first evidence that the peptidergic nervous system is a rational target for chemotherapeutic attack in parasitic platyhelmiths.

Amino Acid Sequence↗
PubMed1994

Initiation of rat vasopressin cell responses to simulated hypotensive hemorrhage.

Hypotensive hemorrhage is a major stimulus for vasopressin (VP) release, but in rats it is uncertain which receptors initiate this response. We have investigated this issue using transient occlusion of the inferior vena cava to simulate hypotensive hemorrhage. Single-unit recording experiments done in the supraoptic nucleus of pentobarbital-anesthetized rats demonstrated that severe caval occlusion, sufficient to drop mean arterial pressure (MAP) below 30 mmHg, excited 88% of putative VP neurosecretory cells and a similar proportion of putative oxytocin (OT) cells. Responsive VP cells increased their firing by 8.5 +/- 0.6 spikes/s within 11.2 +/- 0.8 s of the fall in MAP. This response was unrelated to the size of the fall in MAP and was unchanged by combined sinoaortic denervation (SAD) and vagal denervation, by T1 spinal section, or by administration of the angiotensin-converting enzyme inhibitor captopril, except that spinal section decreased the response latency. Moderate caval occlusion, sufficient to drop MAP to approximately 50 mmHg, did not excite any of the OT cells tested but did excite 65% of VP cells, causing a 3.8 +/- 0.3 spikes/s increase in firing after a delay of 9.0 +/- 1.3 s. This response was proportional to the size of the preceding fall in MAP, and after combined SAD and vagal denervation only 20% of VP cells still responded. Elimination of sinoaortic or vagal afferents alone had no effect on VP cell responses to moderate caval occlusion, except that SAD significantly increased the response latency. These data suggest that in rat the mechanisms that initiate the VP response to hypotensive hemorrhage depend on stimulus intensity.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1993

Neuropeptide Y modulation of A1 noradrenergic neuron input to supraoptic vasopressin cells.

A1 noradrenaline (NA) neurons provide a direct excitatory input to supraoptic nucleus (SON) vasopressin (VP) cells. Many A1 cells contain neuropeptide Y (NPY) and past studies have established that NPY exerts excitatory postsynaptic effects on VP cell activity. We have now investigated whether NPY might also modulate A1 input to VP cells via presynaptic mechanisms. Experiments done in pentobarbitone-anesthetized rats demonstrated that SON application of NPY (10 microM) excited VP cells but also depressed their response to activation of the A1 input. These two effects were not correlated, suggesting independent mechanisms. The putative Y1 agonist [Leu31,Pro34]NPY (10 microM) also excited VP cells but did not alter their response to activation of the A1 input. In contrast, the putative Y2 receptor agonist Ac-[Leu28,Leu31]NPY24-36 mimicked the synaptic depression produced by NPY but did not significantly alter spontaneous activity. These data are consistent with the proposal that NPY acts on Y1-like receptors to excite VP cells but can also act on a presynaptic Y2-like receptor to depress A1-VP cell synaptic transmission.

Animals↗
PubMed1993

Alpha 2-adrenoceptor modulation of A1 noradrenergic neuron input to supraoptic vasopressin cells.

The A1 noradrenaline (NA) cell group of the caudal medulla provides a direct excitatory input to supraoptic nucleus (SON) vasopressin (VP) cells. We have now investigated the possibility that NA released from A1 terminals acts presynaptically to modulate A1 input to VP cells. Initial experiments done in pentobarbitone anaesthetized rats established that SON application of NA excited VP cells but also depressed their response to activation of the A1 input. Moreover, the latter effect was mimicked by the alpha 2-adrenoceptor agonist clonidine and antagonised by intravenous administration of the alpha 2-adrenoceptor antagonist yohimbine. Further studies showed that yohimbine also prevented the relative decline in synaptic excitation of VP cells normally observed as A1 activation frequency increases. These data are consistent with the proposal that NA, released from the SON terminals of A1 NA cells, acts via alpha 2-adrenoceptors to depress A1 transmitter release and thus A1 influence on VP cells.

Animals↗
PubMed1993

ATP mediates an excitatory noradrenergic neuron input to supraoptic vasopressin cells.

Although A1 noradrenaline (NA) neurons of the caudal medulla provide a direct, excitatory input to supraoptic vasopressin cells, they do not use NA as their primary transmitter. We have now tested the possibility that adenosine 5'-triphosphate (ATP) may fulfill this role. Extracellular recordings from rat supraoptic nucleus demonstrated that locally applied ATP excites neurosecretory vasopressin cells and that this effect is mimicked by the ATP receptor-agonist alpha,beta-methylene ATP and blocked by the ATP receptor-blocker suramin. Suramin did not block the excitatory effect of locally applied NA on vasopressin cells but did block excitations produced by vagus nerve stimulation, such excitations having previously been shown to involve a pathway in which the final relay is an input from the A1 cell group. These results indicate that certain central NA neurons use ATP as a transmitter and also provide the first demonstration of a specific physiological role for central purinergic neurons, i.e. regulation of secretion of the neurohormone vasopressin.

Adenosine Triphosphate↗