No description available.

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

No description available.

Noncholinergic neurotransmission was studied in vitro in the guinea pig inferior mesenteric ganglion (IMG) using the technique of intracellular recording. First, the role of substance P (SP) in noncholinergic transmission was examined. Forty-four percent of IMG neurons depolarized upon superfusion of SP (1-10 x 10⁻⁷M); however, some neurons that were insensitive to SP still exhibited slow excitatory potentials (EPSPs) in response to nerve stimulation. During exposure to SP, slow EPSPs were depressed by 52% compared to paired control EPSPs. In animals treated with systemic doses of capsaicin (50-350 mg/kg), mean slow EPSP amplitude was 3.5 mV compared to 6.8 mV in untreated animals. Arginine-vasopressin (AVP) was tested for its electrophysiological effects on IMG neurons and synaptic transmission. AVP (0.5-10 x 10⁻⁷M) produced a depolarization in 67% of neurons, accompanied by an increase in membrane resistance of 44%. The depolarizations and increase in resistance were blocked by a specific V₁ receptor antagonist. During AVP-induced depolarizations, slow EPSPs were reversibly depressed in the majority of neurons by a mean of 71% relative to paired control EPSPs. The V₁ antagonist blocked slow EPSPs in only 10% of neurons tested. A group of neurons exhibiting slow EPSPs was exposed separately to both AVP and SP. Some neurons were exclusively sensitive to either SP or AVP, others were sensitive to both peptides, and still others were sensitive to neither peptide. The physiologic role of noncholinergic transmission was examined using a preparation consisting of a segment of distal colon attached to the IMG. Distension of the colon segment produced a slow depolarization resistant to cholinergic antagonists in 44% of IMG neurons. Distension-induced noncholinergic depolarizations increased in amplitude with colonic intraluminal pressure and with membrane hyperpolarization, and were accompanied by an increase in membrane input resistance of 21%. Capsaicin in vivo reduced the number of neurons exhibiting the noncholinergic mechanosensory depolarization, and in vitro capsaicin and SP desensitization reduced the amplitude of the depolarization. These results suggest that (1) both SP and AVP may be transmitters of noncholinergic potentials in the IMG, (2) some IMG neurons receive heterogeneous peptidergic innervation, and (3) noncholinergic transmission in the IMG is involved in sensory regulation of visceral autonomic function.

The development, maintenance, and survival of neurons depend on the function of neurotrophins such as nerve growth factor (NGF). One population of neurons that rely heavily on NGF for axonal growth and survival is the postganglionic sympathetic neurons. Trauma or disease resulting in injury to the peripheral nervous system causes an increase in the levels of this neurotrophin. This augmentation promotes the collateral sprouting of postganglionic sympathetic axons into those tissues having elevated levels of NGF. Often, NGF-induced sympathetic sprouting occurs in tissues that are normally innervated by these fibers however, high levels of NGF can also promote sprouting of axons into tissues that are normally devoid of sympathetic fibers, such as the sensory ganglia. When postganglionic sympathetic axons grow into the environment of sensory ganglia, they can converge and wrap around a subset of somata (i.e., cell bodies) belonging to primary sensory neurons. This phenomenon, referred to as sympathosensory plexuses is observed in adult mice and rats following peripheral nerve injury, and is also seen in adult transgenic mice that ectopically over express NGF. The overall aim for this project is to examine the morphological and neurochemical features, as well as the overall consequence of sympathosensory plexuses in nerve-injured adult mice and in adult transgenic mice that over express NGF. We hope that this novel information will add to our understanding of the underlying mechanisms associated with the formation of sympathosensory plexuses that occur following injury. / Thesis (Ph.D, Neuroscience Studies) -- Queen's University, 2013-07-23 18:51:47.902

The development, maintenance, and survival of neurons depend on the function of neurotrophins such as nerve growth factor (NGF). One population of neurons that rely heavily on NGF for axonal growth and survival is the postganglionic sympathetic neurons. Trauma or disease resulting in injury to the peripheral nervous system causes an increase in the levels of this neurotrophin. This augmentation promotes the collateral sprouting of postganglionic sympathetic axons into those tissues having elevated levels of NGF. Often, NGF-induced sympathetic sprouting occurs in tissues that are normally innervated by these fibers however, high levels of NGF can also promote sprouting of axons into tissues that are normally devoid of sympathetic fibers, such as the sensory ganglia. When postganglionic sympathetic axons grow into the environment of sensory ganglia, they can converge and wrap around a subset of somata (i.e., cell bodies) belonging to primary sensory neurons. This phenomenon, referred to as sympathosensory plexuses is observed in adult mice and rats following peripheral nerve injury, and is also seen in adult transgenic mice that ectopically over express NGF. The overall aim for this project is to examine the morphological and neurochemical features, as well as the overall consequence of sympathosensory plexuses in nerve-injured adult mice and in adult transgenic mice that over express NGF. We hope that this novel information will add to our understanding of the underlying mechanisms associated with the formation of sympathosensory plexuses that occur following injury. / Thesis (Ph.D, Neuroscience Studies) -- Queen's University, 2013-07-23 18:51:47.902

141 leaves : / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (M.D.)--University of Adelaide, Dept. of Human Physiology and Pharmacology, 1970

No description available.

Thesis (M.D.) -- University of Adelaide, Dept. of Human Physiology and Pharmacology, 1970.

Dissertation (Ph.D.).--University of Texas Graduate School of Biomedical Sciences at San Antonio, 2007. / Vita. Includes bibliographical references.