Effects of substance P (SP) and selective tachykinin agonists on neurotransmission at guinea-pig intracardiac ganglia were studied in vitro. Voltage responses of neurons to superfused tachykinins and nerve stimulation were measured using intracellular microelectrodes. Predominant effects of SP (1 μM) were to cause slow depolarization and enable synaptic transmission at low intensities of nerve stimulation. Augmented response to nerve stimulation occurred with 29 of 40 intracardiac neurons (approx. 73%). SP inhibited synaptic transmission at 23% of intracardiac neurons but also caused slow depolarization. Activation of NK3 receptors with 100 nM [MePhe 7]neurokinin B caused slow depolarization, enhanced the response of many intracardiac neurons to low intensity nerve stimulation or local application of acetylcholine, and triggered action potentials independent of other stimuli in 6 of 42 neurons. The NK1 agonist [Sar 9,Met(O2)11]SP had similar actions but was less effective and did not trigger action potentials independently. Neither selective agonist inhibited cholinergic neurotransmission. We conclude that SP can function as a positive or negative neuromodulator at intracardiac ganglion cells, which could be either efferent neurons or interneurons. Potentiation occurs primarily through NK3 receptors and may enable neuronal responses with less preganglionic nerve activity. Inhibition of neurotransmission by SP is most likely explained by the known blocking action of this peptide at ganglionic nicotine receptors.

Yukako Hattori, Tadao Usui, Daisuke Satoh, Sanefumi Moriyama, Kohei Shimono, Takehiko Itoh, Katsuhiko Shirahige, Tadashi Uemura, Sensory-Neuron Subtype-Specific Transcriptional Programs Controlling Dendrite Morphogenesis: Genome-wide Analysis of Abrupt and Knot/Collier, Developmental Cell, Volume 27, Issue 5, 9 December 2013, Pages 530-544, ISSN 1534-5807 / 京都大学 / 0048 / 新制・課程博士 / 博士(生命科学) / 甲第18418号 / 生博第298号 / 新制||生||39(附属図書館) / 31276 / 京都大学大学院生命科学研究科統合生命科学専攻 / (主査)教授 上村 匡, 教授 西田 栄介, 教授 荒木 崇 / 学位規則第4条第1項該当 / Doctor of Philosophy in Life Sciences / Kyoto University / DFAM

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Stress plays a significant role in neural development and brain function. To better understand the mechanisms underlying the impact of stress on brain development and neuroendocrine function, this study focuses on the phenylethanolamine-N-methyltransferase (Pnmt) enzyme as a key mediator of stress hormone signaling. Pnmt is activated as part of a positive feedback mechanism during stress to convert norepinephrine to epinephrine and amplify the sympathetic response. Most of our knowledge about Pnmt is derived from its role in the systemic production of epinephrine from adrenal chromaffin cells, but it is also known to be expressed in the central nervous system, including the brainstem, retina, hypothalamus, and cerebellum. Given the importance of the central nervous system in modulating stress responses, this project sought to investigate cellular Pnmt expression in the central nervous system using a genetic-marking strategy with a Pnmt-Cre-recombinase knock-in driver strain (Pnmt+/Cre) and a β-galactosidase (βGal) reporter strain (R26R+/βGal) in parallel with Pnmt-specific immunofluorescent histochemical staining to identify Pnmt+ cells in the adult mouse cerebellum, hypothalamus, and cerebral cortex. The results show extensive patterns of active and historical Pnmt protein expression throughout the cerebellum and hypothalamus, with significant neuropeptide Y co-expression in the hypothalamus and considerable historical Pnmt expression throughout the cerebral cortex. To quantify baseline Pnmt mRNA levels across embryonic and postnatal neural development and elucidate differential Pnmt isoform expression through tissue-specific regulation in the developing brain, quantitative polymerase chain reaction (qPCR) was performed in the brainstem, cerebellum, and cerebral cortex with isoform-specific primers. Initial results show a developmental, tissue-specific Pnmt isoform shift between embryonic and postnatal neural development by an intron-retention alternative splicing mechanism. Ultimately, these findings provide an anatomical "blueprint" for investigating the role of central nervous system Pnmt expression in health and disease, and emphasize the role of Pnmt in early neural development, illustrating how stress impacts the formation of neural connections during formative periods of brain maturation.

This study demonstrates the direct delivery of plasmid gene constructs into spinal motor neurons utilizing retrograde axoplasmic transport. The plasmid vectors contained the Lac Z gene under the control of both the Rous sarcoma virus (RSV) and Simian virus (SV)40 promoters. β-Galactosidase expression was observed in α and γ motor neurons by histochemical staining following direct injection into the sciatic nerve or gastrocnemius muscle. The presence of LacZ gene constructs was confirmed by the polymerase chain reaction (PCR). The ability to introduce gene constructs into motor neurons allows for the study of gene regulation and permits the development of gene therapy strategies for motor neuron diseases including the spinal muscular atrophies (SMA) and amyotrophic lateral sclerosis (ALS).

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The effects of hypothermia on cultured mammalian (mouse) spinal cord neurons which had been subjected to a defined physical trauma (amputation of a primary dendrite 100μM from the perikaryon) were investigated.

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