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(1/499) Interaction of amylin with calcitonin gene-related peptide receptors in the microvasculature of the hamster cheek pouch in vivo.

1. This study used intravital microscopy to investigate the receptors stimulated by amylin which shares around 50% sequence homology with the vasodilator calcitonin gene-related peptide (CGRP) in the hamster cheek pouch microvasculature in vivo. 2. Receptor agonists dilated arterioles (diameters 20-40 microm). The -log of the concentrations (+/- s.e.mean; n = 8) causing 50% increase in arteriole diameter were: human betaCGRP (10.8 +/- 0.3), human alphaCGRP (10.8 +/- 0.4), rat alphaCGRP (10.4 +/- 0.3). Rat amylin and the CGRP2 receptor selective agonist [Cys(ACM2,7]-human alphaCGRP were 100 fold less potent (estimates were 8.5 +/- 0.4 and 8.2 +/- 0.3 respectively). 3. The GCRP1 receptor antagonist, CGRP8-37 (300 nmol kg(-1); i.v.) reversibly inhibited the increase in diameter evoked by human alphaCGRP (0.3 nM) from 178 +/- 22% to 59 +/- 12% (n = 8; P < 0.05) and by rat amylin (100 nM) from 138 +/- 23% to 68 +/- 24% (n = 6; P < 0.05). CGRP8-37 did not inhibit vasodilation evoked by substance P (10 nM; n = 4: P > 0.05). 4. The amylin receptor antagonist, amylin8-37 (300 nmol kg(-1); i.v.) did not significantly inhibit the increase in diameter evoked by human alphaCGRP (0.3 nM) which was 112 +/- 26% in the absence, and 90 +/- 29% in the presence of antagonist (n = 4; P < 0.05); nor that evoked by rat amylin (100 nM) which was 146 +/- 23% in the absence and 144 +/- 32% in the presence of antagonist (n = 4; P > 0.05). 5. The agonist profile for vasodilatation and the inhibition of this dilatation by CGRP8-37, although not the amylin8-37 indicates that amylin causes vasodilatation through interaction with CGRP1 receptors in the hamster cheek pouch.  (+info)

(2/499) In vitro analog of operant conditioning in aplysia. I. Contingent reinforcement modifies the functional dynamics of an identified neuron.

Previously, an analog of operant conditioning in Aplysia was developed using the rhythmic motor activity in the isolated buccal ganglia. This analog expressed a key feature of operant conditioning, namely a selective enhancement in the occurrence of a designated motor pattern by contingent reinforcement. Different motor patterns generated by the buccal central pattern generator were induced by monotonic stimulation of a peripheral nerve (i.e., n.2,3). Phasic stimulation of the esophageal nerve (E n.) was used as an analog of reinforcement. The present study investigated the neuronal mechanisms associated with the genesis of different motor patterns and their modifications by contingent reinforcement. The genesis of different motor patterns was related to changes in the functional states of the pre-motor neuron B51. During rhythmic activity, B51 dynamically switched between inactive and active states. Bursting activity in B51 was associated with, and predicted, characteristic features of a specific motor pattern (i.e., pattern I). Contingent reinforcement of pattern I modified the dynamical properties of B51 by decreasing its resting conductance and threshold for eliciting plateau potentials and thus increased the occurrences of pattern I-related activity in B51. These modifications were not observed in preparations that received either noncontingent reinforcement (i.e., yoke control) or no reinforcement (i.e., control). These results suggest that a contingent reinforcement paradigm can regulate the dynamics of neuronal activity that is centrally programmed by the intrinsic cellular properties of neurons.  (+info)

(3/499) In vitro analog of operant conditioning in aplysia. II. Modifications of the functional dynamics of an identified neuron contribute to motor pattern selection.

Previously, an analog of operant conditioning was developed using the buccal ganglia of Aplysia, the probabilistic occurrences of a specific motor pattern (i.e., pattern I), a contingent reinforcement (i.e., stimulation of the esophageal nerve), and monotonic stimulation of a peripheral nerve (i.e., n.2,3). This analog expressed a key feature of operant conditioning (i.e., selective enhancement of the probability of occurrence of a designated motor pattern by contingent reinforcement). In addition, the training induced changes in the dynamical properties of neuron B51, an element of the buccal central pattern generator. To gain insights into the neuronal mechanisms that mediate features of operant conditioning, the present study identified a neuronal element that was critically involved in the selective enhancement of pattern I. We found that bursting activity in cell B51 contributed significantly to the expression of pattern I and that changes in the dynamical properties of this cell were associated with the selective enhancement of pattern I. These changes could be induced by an explicit association of reinforcement with random depolarization of B51. No stimulation of n.2,3 was required. These results indicate that the selection of a designated motor pattern by contingent reinforcement and the underlying neuronal plasticity resulted from the association of reinforcement with a component of central neuronal activity that contributes to a specific motor pattern. The sensory stimulus that allows for occurrences of different motor acts may not be critical for induction of plasticity that mediates the selection of a motor output by contingent reinforcement in operant conditioning.  (+info)

(4/499) Spread of vasodilatation and vasoconstriction along feed arteries and arterioles of hamster skeletal muscle.

1. In arterioles of the hamster cheek pouch, vasodilatation and vasoconstriction can spread via the conduction of electrical signals through gap junctions between cells that comprise the vessel wall. However, conduction in resistance networks supplying other tissues has received relatively little attention. In anaesthetized hamsters, we have investigated the spread of dilatation and constriction along feed arteries and arterioles of the retractor muscle, which is contiguous with the cheek pouch. 2. When released from a micropipette, acetylcholine (ACh) triggered vasodilatation that spread rapidly along feed arteries external to the muscle and arterioles within the muscle. Responses were independent of changes in wall shear rate, perivascular nerve activity, or release of nitric oxide, indicating cell-to-cell conduction. 3. Vasodilatation conducted without decrement along unbranched feed arteries, yet decayed markedly in arteriolar networks. Thus, branching of the conduction pathway dissipated the vasodilatation. 4. Noradrenaline (NA) or a depolarizing KCl stimulus evoked constriction of arterioles and feed arteries of the retractor muscle that was constrained to the vicinity of the micropipette. This behaviour contrasts sharply with the conduction of vasodilatation in these microvessels and with the conduction of vasoconstriction elicited by NA and KCl in cheek pouch arterioles. 5. Focal electrical stimulation produced constriction that spread rapidly along feed arteries and arterioles. These responses were inhibited by tetrodotoxin or prazosin, confirming the release of NA along perivascular sympathetic nerves, which are absent from arterioles studied in the cheek pouch. Thus, sympathetic nerve activity co-ordinated the contraction of smooth muscle cells as effectively as the conduction of vasodilatation co-ordinated their relaxation. 6. In the light of previous findings in the cheek pouch, the properties of vasoconstriction and vasodilatation in feed arteries and arterioles of the retractor muscle indicate that substantive differences can exist in the nature of signal transmission along microvessels of tissues that differ in structure and function.  (+info)

(5/499) Upregulation of connexin 26 is a feature of keratinocyte differentiation in hyperproliferative epidermis, vaginal epithelium, and buccal epithelium.

In epidermis, it has been suggested, intercellular communication through gap junctions is important in coordinating cell behavior. The connexins, may facilitate selective assembly or permeability of gap junctions, influencing the distribution of metabolites between cells. Using immunohistochemistry, we have compared the distribution of connexins 26 and 43 with that of proliferating cells (Ki67 labeling) in normal epidermis, hyperplastic epidermis (tape-stripped epidermis, psoriatic lesions, and viral warts), and vaginal and buccal epithelia. Connexin 43 was abundant in spinous layers of all epidermal specimens and in vaginal and buccal epithelia. Connexin 26 was absent from the interfollicular and interductal epidermis of normal hair-bearing skin, and nonlesional psoriatic epidermis but present at very low levels in plantar epidermis. Connexin 26 was prominent in lesional psoriatic epidermis and viral warts and in vaginal and buccal epithelia. In three independent experiments connexin 26 appeared in a patchy intercellular distribution in the basal epidermis within 24 h of tape stripping, proceeding to more extensive distribution in basal and suprabasal layers by 48 h. The increase in connexin 26 preceded that in cell proliferation. In vaginal epithelium, buccal epithelium, and viral warts connexin 26 was restricted mainly to suprabasal, nonproliferating cells. In psoriatic lesional epidermis connexin 26 was also located mainly in suprabasal, nonproliferating cells. Connexin 26 was present in a patchy distribution in the basal layer of psoriatic lesional epidermis, but double labeling for connexin 26 and Ki67 showed that many connexin 26 positive basal cells were nonproliferative, suggesting that connexin 26 may be related to differentiation rather than to proliferation. These observations would be consistent with a role for connexin 26 containing gap junctions during both early and later stages of keratinocyte differentiation in hyperplastic epidermis and in vaginal and buccal epithelia.  (+info)

(6/499) Chronic exposure to nicotine alters endothelium-dependent arteriolar dilatation: effect of superoxide dismutase.

The first goal of this study was to determine whether chronic injection of nicotine alters endothelium-dependent arteriolar dilatation. We measured the diameter of cheek pouch resistance arterioles (approximately 50 microm in diameter) in response to endothelium-dependent (acetylcholine and ADP) and -independent (nitroglycerin) agonists in control hamsters and hamsters treated with nicotine (2 microg. kg-1. day-1 for 2-3 wk). In control hamsters, acetylcholine (0.1 and 1.0 microM) dilated arterioles by 13 +/- 2 and 31 +/- 3%, respectively, and ADP (1.0 and 10 microM) dilated arterioles by 18 +/- 1 and 30 +/- 1%, respectively. In contrast, acetylcholine (0.1 and 1.0 microM) dilated arterioles by only 5 +/- 2 and 12 +/- 3%, respectively, and ADP (1.0 and 10 microM) dilated arterioles by only 7 +/- 2 and 13 +/- 3%, respectively, in animals treated with nicotine (P < 0.05 vs. response in control hamsters). Nitroglycerin produced similar dose-related dilatation of cheek pouch arterioles in control and nicotine-treated hamsters. Our second goal was to examine a possible mechanism for impaired endothelium-dependent arteriolar dilatation during chronic treatment with nicotine. We found that superfusion of the cheek pouch microcirculation with superoxide dismutase (150 U/ml) restored impaired endothelium-dependent, but did not alter endothelium-independent, arteriolar dilatation in hamsters treated with nicotine. Superfusion with superoxide dismutase did not alter endothelium-dependent or -independent arteriolar dilatation in control hamsters. We suggest that chronic exposure to nicotine produces selective impairment of endothelium-dependent arteriolar dilatation via a mechanism related to the synthesis/release of oxygen-derived free radicals.  (+info)

(7/499) Collection of genomic DNA by buccal swabs for polymerase chain reaction-based biomarker assays.

Studies in molecular and genetic epidemiology require a high-throughput, low cost, and reliable means of genomic DNA collection. Buccal (cheek) swabs have been proposed as a means of achieving these goals, but there is little information about the practical application of this approach. From January 1995 to December 1997, we processed 995 buccal swabs for use in polymerase chain reaction (PCR)-based genotype assays in the context of ongoing molecular epidemiologic studies. Six hundred forty-seven of these swabs were processed immediately after collection and 348 were received by mail. We were able to obtain at least one genotype from 99.7% (645 of 647) of fresh-processed and 97.4% (330 of 339) of mailed biosamples. A PCR success rate of 90.3% (2,546 genotypes from 2,819 assays) was achieved. Genotypes were obtained from 96.1% (1, 865 genotypes from 1,941 assays) of fresh-processed biosamples and 77.6% (681 genotypes from 878 assays) of mailed biosamples. PCR success rates at any single locus ranged from 92.6 to 98.8% (fresh-processed) and 75.5 to 79.6% (mailed). The PCR success rate among fresh-processed biosamples was significantly higher than among mailed biosamples (Fisher's exact test p < 0.0001), and more attempts were required to obtain a successful PCR result for mailed biosamples as compared to fresh-processed biosamples. For one locus (CYP3A4), a subset of mailed biosamples was purified if two or more PCR failures occurred. Additional genotypes were obtained in 58.3% of these previously failed biosamples. Time from biosample receipt to DNA extraction had no effect on PCR success. After storage of processed biosamples for as long as 3 years, there was no appreciable decrease in the rate of PCR success. These results suggest that adequate DNA for PCR-based applications can be obtained from buccal swabs, but sampling or processing considerations may be important in obtaining optimal results.  (+info)

(8/499) Cheek and tongue pressures in the molar areas and the atmospheric pressure in the palatal vault in young adults.

The pressures acting on the maxillary and mandibular posterior teeth from the tongue and cheeks were measured in 24 adults aged 22-29 years. In addition, the pressure in the palatal vault was recorded. The pressure at two maxillary (buccal and lingual) and two mandibular (buccal and lingual) measuring points, and in the palatal vault was recorded simultaneously. Repeated recordings of the pressures at rest, and during chewing and swallowing were made. The pressures at rest were of similar magnitude (about 2 g/cm2) at the buccal and lingual sides of the mandibular posterior teeth. The median resting pressure at the maxillary posterior teeth was 2.7 g/cm2 on the buccal side and 1.0 g/cm2 on the lingual side. The difference in the maxilla was significant, but not in the mandible. It was concluded that the equilibrium of tooth position is maintained by the pressure from the cheeks and the tongue. During chewing and swallowing the pressures on the lingual side of the teeth were greater than those on the buccal side. At rest about half of the subjects had a negative pressure at the palatal vault, but no correlations between the resting pressure at the palatal vault and the resting pressures on the teeth were found.  (+info)