No description available.

No description available.

Pui Lan Wong. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1993. / Includes bibliographical references (Leaves 109-122). / Abstract --- p.i / Acknowledgements --- p.iii / Chapter Chapter1 --- Introduction / Chapter 1.1 --- A general introduction on mast cells --- p.1 / Chapter 1.2 --- Activation of mast cells --- p.6 / Chapter 1.3 --- Mediators of mast cells --- p.18 / Chapter 1.4 --- Usage of β-adrenoceptor agonists in asthma therapy --- p.26 / Chapter 1.5 --- Aim of this study --- p.32 / Chapter Chapter2 --- Materials and methods / Chapter 2.1 --- Chemicals --- p.42 / Chapter 2.2 --- Buffers and stock solutions --- p.43 / Chapter 2.3 --- Source of mast cells --- p.45 / Chapter 2.4 --- Animal sensitization --- p.45 / Chapter 2.5 --- Isolation of mast cells --- p.46 / Chapter 2.6 --- Procedure for the investigation of the effects of adrenoceptor agonists on histamine release from mast cells --- p.48 / Chapter 2.7 --- Procedure for the investigation of propranolol antagonism --- p.49 / Chapter 2.8 --- Histamine assay --- p.50 / Chapter 2.9 --- Data analysis --- p.50 / Chapter Chapter3 --- Results / Chapter 3.1 --- Establishment of experimental conditions --- p.53 / Chapter 3.2 --- The effects of β-agonists on immunologically induced histamine release from guinea pig lung mast cells --- p.54 / Chapter 3.3 --- The effects of β-agonists and two anti-allergic drugs on immunologically induced histamine release from guinea pig lung mast cells --- p.56 / Chapter 3.4 --- The effects of β2-agonists on histamine release induced by non-immunological agents from guinea pig lung mast cells --- p.56 / Chapter 3.5 --- Antagonism by propranolol on the effects of β2-agonists on histamine release from guinea pig lung mast cells --- p.57 / Chapter 3.6 --- The effects of β2-agonists on immunologically induced histamine release from rat peritoneal mast cells --- p.58 / Chapter 3.7 --- The effects of β2-agonists on immunologically induced histamine release from human lung mast cells --- p.58 / Chapter 3.8 --- "Comparison of the effects of β2-agonists on immunologically induced histamine release from mast cells isolated from the rat peritoneum, the guinea pig lung and the human lung" --- p.59 / Chapter Chapter4 --- Discussion / Chapter 4.1 --- The effects of β-agonists on immunologically induced histamine release from guinea pig lung mast cells --- p.89 / Chapter 4.2 --- The effects of β2-agonists and two anti-allergic drugs on immunologically induced histamine release from guinea pig lung mast cells --- p.97 / Chapter 4.3 --- The effects of novel β2-agonists on histamine release induced by non-immunological agents from guinea pig lung mast cells --- p.99 / Chapter 4.4 --- The study of propranolol --- p.100 / Chapter 4.5 --- The heterogeneity of mast cells --- p.103 / Chapter Chapter5 --- General conclusion --- p.107 / References --- p.109

Ph.D.

No description available.

The activity of neurons in the prefrontal cortex (PFC) may underlie working memory processes in the brain. Both the performance of working memory tasks and the activity of PFC neurons are modulated by dopamine. The goal of the present thesis was to gain insight into the neural basis of working memory by studying the PFC, and the DA system in the PFC, from both a behavioral and cellular perspective. The functional contribution of the PFC to working memory processes in the rat was assessed in Chapter 2 of the present thesis using memory-based foraging tasks on an 8-arm radial maze. The results of these studies indicated that lidocaine-induced inactivations of the PFC selectively disrupted the ability to use mnemonic information to guide foraging, but not the ability to acquire or retain such information. The ability to use mnemonic information to guide foraging was also disrupted by microinjection of a D1 but not D2 receptor antagonist into the PFC. Chapters 3-5 investigated how PFC neurons process synaptic inputs to their dendrites to produce spike output. The intrinsic membrane properties and synaptic responses at the soma and dendrites of deep layer PFC pyramidal neurons were recorded using sharp intracellular or whole-cell patch-clamp techniques in a brain-slice preparation. Different passive and active membrane properties of the soma and dendrites of PFC neurons were observed. The distal dendrites of PFC neurons responded most effectively to strong, highly coincident synaptic inputs. Ca²⁺currents near the soma both amplified the effects of these inputs and modulated the spike output pattern. Spike output at the soma was also controlled by the interplay of slowly-inactivating Na⁺ and K⁺ currents. Chapter 6 investigated the modulation of PFC neurons by DA. DA or a D1 but not D2 receptor agonist increased the evoked firing of PFC neurons via a D1- mediated modulation of slowly-inactivating Na⁺ and K⁺ currents. Concurrently, D1 receptor activation reduced burst firing in PFC neurons, due to a attenuation of Ca²⁺ currents. D1 receptor activation also increased both GABA[sub A] IPSPs and NMDA EPSPs. The final chapter of this thesis integrated these data into a cellular model of PFC function and its modulation by DA. It is proposed that DA may tune PFC neurons such that they respond selectively to strong synchronized inputs from other cortical areas. In the presence of DA, working memory processes mediated by the PFC may be influenced selectively by stimuli of behavioral significance.

Thesis (Ph.D.)--University of Nebraska-Lincoln, 2007. / Title from title screen (site viewed July 9, 2007). PDF text: xv, 147 p. : ill. UMI publication number: AAT 3249674. Includes bibliographical references. Also available in microfilm and microfiche formats.

A procedure was developed to determine the effect of a dopamine (DA) antagonist (haloperidol) and a DA agonist (d-amphetamine) on rats' perceptions of the hedonic value of food. Eighteen rats were trained to discriminate between two quantities of sweet food pellets (1 and 4), in a forced-choice two-lever successive discrimination procedure. To control for non-specific perceptual effects of the treatments, the rats were also trained to discriminate between 1 and 4 tones. It was established that rats attended to the value of food, as well as the proportional differences in quantity, when discriminating food quantities. This was accomplished by altering the value of the food in two ways. Firstly, "hunger" was altered by changing the degree of food deprivation during testing. Secondly, unsweetened food pellets were introduced as probe cues. These two methods of altering the value of food pellets were utilized while quantity generalization gradients were determined, by presenting animals with 1,2, 3 and 4 numbers of stimuli as probe cues. Two measures were derived from these generalization gradients: the point of subjective equality (PSE), which is the calculated number of stimuli that would maintain responses equally distributed between the two levers, and the slope of the gradient. The PSE primarily reflects perceptual processes, while the slopes of the gradients provide an index of performance impairment. It was observed that decreasing the value of food by either decreasing food deprivation or reducing the sweetness of the food pellets resulted in the rats perceiving a given quantity of food as larger than before these treatments (decreased the food PSE). Neither altering food deprivation nor introducing novel tone probes had an effect on the numerical attributes of tones, as reflected by the tone PSE. Haloperidol (0.030, 0.50 and 0.083 mg/kg, i.p.) produced a statistically significant, but slight dose-dependent performance deficit, as reflected by the slope of the generalization gradients. It did not affect the perception of food pellet quantities at any dose, as reflected by the food PSE. Haloperidol decreased the number of tones a given quantity was perceived as by rats (increased the tone PSE). Amphetamine (0.25, 0.50 and 1.0 mg/kg, i.p.) decreased the perception of a given quantity of food (increased the food PSE) in a dose-dependent manner, without a significant effect on performance. Thus, amphetamine enhanced the hedonic value of food. Amphetamine also increased rats' perceptions of a given number of tones (decreased the tone PSE). It therefore appears that while d-amphetamine can enhance the perceived hedonic value of food, haloperidol has no effect on rats' perceptions of the hedonic value of food. Furthermore, evidence that DA systems are involved in the mechanism of an "internal clock" or "counter" was obtained. / Medicine, Faculty of / Graduate

The activity of neurons in the prefrontal cortex (PFC) may underlie working memory processes in the brain. Both the performance of working memory tasks and the activity of PFC neurons are modulated by dopamine. The goal of the present thesis was to gain insight into the neural basis of working memory by studying the PFC, and the DA system in the PFC, from both a behavioral and cellular perspective. The functional contribution of the PFC to working memory processes in the rat was assessed in Chapter 2 of the present thesis using memory-based foraging tasks on an 8-arm radial maze. The results of these studies indicated that lidocaine-induced inactivations of the PFC selectively disrupted the ability to use mnemonic information to guide foraging, but not the ability to acquire or retain such information. The ability to use mnemonic information to guide foraging was also disrupted by microinjection of a D1 but not D2 receptor antagonist into the PFC. Chapters 3-5 investigated how PFC neurons process synaptic inputs to their dendrites to produce spike output. The intrinsic membrane properties and synaptic responses at the soma and dendrites of deep layer PFC pyramidal neurons were recorded using sharp intracellular or whole-cell patch-clamp techniques in a brain-slice preparation. Different passive and active membrane properties of the soma and dendrites of PFC neurons were observed. The distal dendrites of PFC neurons responded most effectively to strong, highly coincident synaptic inputs. Ca²⁺currents near the soma both amplified the effects of these inputs and modulated the spike output pattern. Spike output at the soma was also controlled by the interplay of slowly-inactivating Na⁺ and K⁺ currents. Chapter 6 investigated the modulation of PFC neurons by DA. DA or a D1 but not D2 receptor agonist increased the evoked firing of PFC neurons via a D1- mediated modulation of slowly-inactivating Na⁺ and K⁺ currents. Concurrently, D1 receptor activation reduced burst firing in PFC neurons, due to a attenuation of Ca²⁺ currents. D1 receptor activation also increased both GABA[sub A] IPSPs and NMDA EPSPs. The final chapter of this thesis integrated these data into a cellular model of PFC function and its modulation by DA. It is proposed that DA may tune PFC neurons such that they respond selectively to strong synchronized inputs from other cortical areas. In the presence of DA, working memory processes mediated by the PFC may be influenced selectively by stimuli of behavioral significance. / Arts, Faculty of / Psychology, Department of / Graduate

Estrogen is the natural agonist of the estrogen receptor (ER). However, certain plant-derived compounds or phytoestrogens have been identified that mimic estrogens and act as agonists and/or antagonists of ERs, depending on subtype and target tissue. Understanding how phytoestrogens interact with ERs, and therefore effect the estrogenic response, may prove beneficial in hormone replacement therapy and in the prevention and treatment of hormone-related diseases. Using Thin Layer Chromatography, gas chromatography/mass spectrometry (GC/MS), and proton nuclear nagnetic resonance (HNMR), I identified 4-ethoxymethylphenol (4EM) found in Maclura pomifera. While most phytoestrogens are heterocyclic compounds, 4EM is a simple phenol that acts as an agonist of ER-alpha and -beta in HeLa and MCF-7 cells. To study the effect of 4EM on ER-alpha and -beta activity, I performed transient transfection assays and showed that 4EM activates ER dependent gene transcription in a dose dependent manner in both ER subtypes. Further, 4EM- mediated transcription in ER-alpha, like estrogen, was enhance in the presense of co-activators, SRC-1 (steroid receptor coactivator-1), CBP (CREB binding proteins), and E6-AP (E6-associated protein) and inhibited by trans-4- hydroxytamoxifen (4HT). I found that 4EM was specific for ER and did not activate transcription of the progesterone receptor in HeLa cells.