The vestibular system provides us with sensory information that is essential for maintaining balance and stability. When sensory input is lost due to unilateral vestibular damage (UVD), our ability to maintain stable gaze and posture becomes compromised. Over time, vestibular function is partially restored through a process known as vestibular compensation, which is associated with the rebalancing of activity in the vestibular nuclear complex (VNC) of the brainstem. However, the physiological mechanisms associated with vestibular compensation remain elusive. We addressed several different experimental objectives pertaining to plasticity and sensory adaptation associated with vestibular compensation. First, we demonstrated that systemic manipulation of γ-amino-butyric acid type B (GABAB) receptors altered the course of vestibular behavioural recovery within the first several hours after UVD. Second, we showed that immunohistochemical labeling of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit GluR4 was elevated in the VNC on the intact compared to lesioned side acutely following UVD. Third, we produced preliminary data suggesting that excitatory responses to vestibular nerve stimulation may be acutely potentiated by UVD on the intact side. Finally, we established that rapid sensory adaptation may increase the dynamic ranges of vestibular neurons and perhaps improve limited vestibular reflex function in the long term. Acutely following UVD, potentiation of vestibular nerve synapses appear to be associated with an increase in GluR4 subunit expression in the contralesional VNC. Also, such potentiation could be enhanced by acute modifications in pre-synaptic GABAB receptor activation. In the long term, and independent of these plastic changes, sensory adaptation may enable the vestibular system to overcome the persistent limitations imposed by UVD.

Aplysia Californica are marine mollusks with a relatively simple central nervous system that makes them ideal for investigating neurons. The bag-cell neuron is found in the Aplysia and is important due to its activity causing the onset of a series of behaviours which culminate in egg laying. The bag-cell neuron is generally not very active but can be stimulated into a long active period known as the afterdischarge in which the neuron releases a hormone that causes egg laying. The afterdischarge is due to a fundamental change in the electrophysiological properties of the bag-cell neuron. The purpose of this thesis is to determine a mathematical model for the electrical activity found in a single bag-cell neuron which can be used to investigate the afterdischarge behaviour.

The central nervous system shows sexual dimorphism in the structure and functions in vertebrates. Brain sexual differentiation is resulted from the neural development. The neural development of the brain is influenced by the genetic factors and the external environmental factors. Serotonin (5-HT) functions as a differentiation signal in the early developing period. There are seven 5-HT receptors (5-HT1¡B5-HT2¡B5-HT3¡B5-HT4¡B5-HT5¡B5-HT6¡B5-HT7 receptor) . The 5-HT cell is one of the earliest differentiated neurons in the brain. In the present study, the role of central 5-HT system for the temperature-related neural development was investigated. These results showed that the proliferation of neurons was enhanced by 5-HT. The elevated temperature-induced proliferation of 5-HT cell might be mediated by the 5-HT receptor 1A type. On the other hand, estrogen receptor £\ (ER£\) is involved in the estrogen-enhanced proliferation of 5-HT cell in the neural culture. The ER£\ antagonist suppressed the elevated temperature-induced proliferation of 5-HT cell. It is suggested that the ER£\ plays a role in the mechanism of high temperature-induced the proliferation of 5-HT cell.

Spontaneously hypertensive rats (SHR) are a well accepted model of primary hypertension. Among other features common to human hypertension, these rats exhibit sympathetic hyperactivity. The neurons of the superior mesenteric ganglion (SMG) from SHR display enhanced collateral sprouting, higher firing rates and hyperinnervation of the mesenteric arteries compared to the SMG neurons from age-matched, normotensive Wistar-Kyoto (WKY) rats. Furthermore, SMG neurons in SHR are exposed to different conditions than are SMG neurons from WKY rats, including enhanced oxidative stress, increased afferent stimulation, and an altered hormonal environment. In order to identify proteins with potential involvement in the establishment or maintenance of peripheral sympathetic hyperactivity in SHR, we used proteomic techniques to search for differences in protein expression between the SMG of SHR and the SMG of WKY rats at 16 and 22 weeks of age. We found an upregulation of predominantly fetally expressed T1 domain and haptoglobin and a downregulation of serine protease inhibitor 2.1 in SHR relative to WKY rats at 16 and 22 weeks; Apolipoprotein-A1 was also found to be upregulated in 22 week SHR SMGs compared to age-matched WKY SMGs. These identifications improve our understanding of the ganglionic microenvironment in SHR and represent targets for the development of novel therapies to treat primary hypertension. Hypertension is one of the defining components of the metabolic syndrome, together with insulin resistance, visceral adiposity and hyperlipidemia. Non-alcoholic fatty liver disease (NAFLD) is also a common feature of the metabolic disorder, and thus primary hypertension and NAFLD are common comorbidities. Despite these clinical connections, very little is known about the effects of primary hypertension on hepatic physiology. We used proteomic techniques to search for evidence of significant involvement of the liver in SHR phenotype at the molecular level. We detected changes in the expression of several proteins involved in the regulation of oxidative stress and lipid metabolism which together show that the liver is strongly involved in the pathologies associated with hypertension. Our results suggest several novel mechanisms for the initiation of oxidative stress in SHR which could contribute to new advances in the treatment of metabolic abnormalities associated with hypertension. / Thesis (Master, Anatomy & Cell Biology) -- Queen's University, 2009-10-27 10:11:05.052

The superior mesenteric ganglion (SMG) provides sympathetic input to areas of the small intestine, colon, spleen, and mesenteric lymph nodes. Interactions between the nervous and immune systems in the SMG influence sympathetic regulation of gastrointestinal (GI) and immune function. Previous work in our laboratory has demonstrated changes in SMG neuron activity resulting from exposure to inflammatory mediators such as tumour necrosis factor α (TNFα). The current project focused on interactions between mast cells and sympathetic neurons. Mast cells within the SMG release mediators, including histamine, that can act on neurons and alter their activity. We tested the hypothesis that histamine influences signaling in SMG neurons by inhibiting calcium ion influx during cell depolarization using immunohistochemistry and calcium imaging. Immunohistochemistry revealed H3R on the majority of tyrosine hydroxylase-positive sympathetic neurons in the ganglia. Dissociated neurons were incubated in the ratiometric fluorescent calcium indicator dye Fura-2 acetoxymethyl ester, then superfused with extracellular solution containing histamine receptor agonists (histamine, HTMT, imetit) and antagonists (thioperamide) before being depolarized with a KCL solution (70 mM). Application of both histamine (10 μM) and the H3 receptor agonist imetit (100 nM) caused a decrease in depolarization-induced calcium ion influx. However, the inhibition of calcium ion influx became smaller as the concentration of histamine was increased (100 μM, 1 mM) until the inhibition was no longer statistically significant. Application of H3R antagonist thioperamine (300nM) reversed the inhibition of calcium ion influx caused by histamine (10 μM). Application of H1R & H2R agonist histamine trifluoromethyl toluidide (HTMT) (10 μM) caused an increase in calcium ion influx during depolarization. We conclude that activation of H3R decreases calcium ion influx through voltage-gated calcium ion channels, while activation of H1R / H2R increases calcium ion influx. H3R has a higher affinity for histamine, and therefore is preferentially activated at lower concentrations. Increases in histamine receptor activation may alter SMG input to the spleen, mesenteric lymph nodes, small intestine, and colon, resulting in changes in immune and gut function, such as those described in irritable bowel syndrome. / Thesis (Master, Neuroscience Studies) -- Queen's University, 2011-08-29 11:15:09.484

Aplysia Californica are marine mollusks with a relatively simple central nervous system that makes them ideal for investigating neurons. The bag-cell neuron is found in the Aplysia and is important due to its activity causing the onset of a series of behaviours which culminate in egg laying. The bag-cell neuron is generally not very active but can be stimulated into a long active period known as the afterdischarge in which the neuron releases a hormone that causes egg laying. The afterdischarge is due to a fundamental change in the electrophysiological properties of the bag-cell neuron. The purpose of this thesis is to determine a mathematical model for the electrical activity found in a single bag-cell neuron which can be used to investigate the afterdischarge behaviour.

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 5 uppsatser.

A method for the determination of low concentrations (<10PPM) of rare earths in minerals and rocks by neutron activation analysis is presented. A 10 min irradiation of sample and standard required no chemical purification owhile a 20hr, irradiation required an ion exchange purification before actual counting. A Li-drifted germanium detector an 1600 channel gamma spectrometer provided sufficient resolution to allow determination of La, Pr, Sm, Eu, Dy, Ho, Yb and Lu in two apatite samples. The results are generally higher than those obtained by other neutron activation analyses. The specific causes are uncertain and can be resolved best by further study and modification of this neutron activation analysis. / Thesis / Bachelor of Science (BSc)

The discovery of mirror neurons and the mirror neuron system is one of the most interesting breakthroughs in the field of neuroscience in recent years. The topic stretches over a wide spectrum of research fields but one of the more prominent areas is concerned with the role of mirror neurons in autism spectrum disorder. It is hypothesized that an impaired mirror neuron system may be one of the main causes underlying the deficits seen in autistic individuals. Parallel to the broken mirror theory of autism there are critical voices claiming there is not enough empirical evidence to support such a theory. Research carried out in the area seems to offer support for both contradictory approaches making it hard to conclude the definite role of mirror neurons in this developmental disorder. Future research may offer conclusive answers concerning the role of the mirror neuron system in autism spectrum disorder as well as other important questions regarding the functional properties of the brain areas under question.

<p>The discovery of mirror neurons and the mirror neuron system is one of the most interesting breakthroughs in the field of neuroscience in recent years. The topic stretches over a wide spectrum of research fields but one of the more prominent areas is concerned with the role of mirror neurons in autism spectrum disorder. It is hypothesized that an impaired mirror neuron system may be one of the main causes underlying the deficits seen in autistic individuals. Parallel to the broken mirror theory of autism there are critical voices claiming there is not enough empirical evidence to support such a theory. Research carried out in the area seems to offer support for both contradictory approaches making it hard to conclude the definite role of mirror neurons in this developmental disorder. Future research may offer conclusive answers concerning the role of the mirror neuron system in autism spectrum disorder as well as other important questions regarding the functional properties of the brain areas under question.</p>