Interaction of vasomotor and exocrine neurons in bullfrog paravertebral sympathetic ganglia

Ford, Christopher P.; Ivanoff, Alexander Y.; Smith, Peter A.

doi:10.1139/y00-033

Cited by 3 publications

(1 citation statement)

References 25 publications

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“…This mechanism may enable presynaptic neuron (in this case, sympathetic ganglion cells) to release neurotransmitter during bursts of high frequency activity [102]. The GnRH-induced modulations of ionic currents in the sympathetic ganglion cells described thus far are suggested to coordinate an interaction between vasomotor and exocrine outflow in the sympathetic nervous system [103, 104]. Such neuromodulatory actions of GnRH may occur in the central nervous system as well [105].…”

Section: Gnrh Neurons In the Peripheral Nervous Systemmentioning

confidence: 99%

Multiple functions of non-hypophysiotropic gonadotropin releasing hormone neurons in vertebrates

Umatani

Oka

2019

Zoological Lett

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Gonadotropin releasing hormone (GnRH) is a hypophysiotropic hormone that is generally thought to be important for reproduction. This hormone is produced by hypothalamic GnRH neurons and stimulates the secretion of gonadotropins. On the other hand, vertebrates also have non-hypophysiotropic GnRH peptides, which are produced by extrahypothalamic GnRH neurons. They are mainly located in the terminal nerve, midbrain tegmentum, trigeminal nerve, and spinal cord (sympathetic preganglionic nerves). In vertebrates, there are typically three gnrh paralogues ( gnrh1 , gnrh2 , gnrh3 ). GnRH-expression in the non-hypophysiotropic neurons ( gnrh1 or gnrh3 in the terminal nerve and the trigeminal nerve , gnrh2 in the midbrain tegmentum) occurs from the early developmental stages. Recent studies have suggested that non-hypophysiotropic GnRH neurons play various functional roles. Here, we summarize their anatomical/physiological properties and discuss their possible functions, focusing on studies in vertebrates. GnRH neurons in the terminal nerve show different spontaneous firing properties during the developmental stages. These neurons in adulthood show regular pacemaker firing, and it has been suggested that these neurons show neuromodulatory function related to the regulation of behavioral motivation, etc. In addition to their recognized role in neuromodulation in adult, in juvenile fish, these neurons, which show more frequent burst firing than in adults, are suggested to have novel functions. GnRH neurons in the midbrain tegmentum show regular pacemaker firing similar to that of the adult terminal nerve and are suggested to be involved in modulations of feeding (teleosts) or nutrition-related sexual behaviors (musk shrew). GnRH neurons in the trigeminal nerve are suggested to be involved in nociception and chemosensory avoidance, although the literature on their electrophysiological properties is limited. Sympathetic preganglionic cells in the spinal cord were first reported as peptidergic modulatory neurons releasing GnRH with a putative function in coordinating interaction between vasomotor and exocrine outflow in the sympathetic nervous system. The functional role of non-hypophysiotropic GnRH neurons may thus be in the global modulation of neural circuits in a manner dependent on internal conditions or the external environment.

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Section: Gnrh Neurons In the Peripheral Nervous Systemmentioning

confidence: 99%

Multiple functions of non-hypophysiotropic gonadotropin releasing hormone neurons in vertebrates

Umatani

Oka

2019

Zoological Lett

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Possible role of phosphatidylinositol 4,5, bisphosphate in luteinizing hormone releasing hormone‐mediated M‐current inhibition in bullfrog sympathetic neurons

Ford

Stemkowski

Smith

2004

Eur J of Neuroscience

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Luteinizing hormone releasing hormone (LHRH) is a physiological modulator of neuronal excitability in bullfrog sympathetic ganglia (BFSG). Actions of LHRH involve suppression of the noninactivating, voltage-dependent M-type K+ channel conductance (gM). We found, using whole-cell recordings from these neurons, that LHRH-induced suppression of gM was attenuated by the phospholipase C (PLC) inhibitor U73122 (10 microM) but not by the inactive isomer U73343 (10 microM). Buffering internal Ca2+ to 117 nM with intracellular 20 mM BAPTA + 8 mM Ca2+ or to < 10 nM with intracellular 20 mM BAPTA + 0.4 mM Ca2+ did not attenuate LHRH-induced gM suppression. Suppression of gM by LHRH was not antagonized by the inositol 1,4,5 trisphosphate (InsP3) receptor antagonist heparin (approximately 300 microM). Preventing phosphatidylinositol-4,5-bisphosphate (PIP2) synthesis by blocking phosphatidylinositol-4-kinase with wortmannin (10 microM) or with the nonhydrolysable ATP analogue AMP-PNP (3 mM) prolonged recovery of LHRH-induced gM suppression. This effect was not produced by blocking phosphatidyl inositol-3-kinase with LY294002 (10 microM). Rundown of gM was attenuated when cells were dialysed with 240 microM di-octanoyl PIP2 or 240 microM di-octanoyl phosphatidylinositol-3,4,5-trisphosphate (PIP3) but not with 240 microM di-octanoyl phosphatidylcholine. LHRH-induced gM suppression was competitively antagonized by dialysis with 240 microM di-octanoyl PIP2, but not with di-octanoyl phosphatidylcholine. These results would be expected if LHRH-induced gM suppression reflects a PLC-mediated decrease in plasma membrane PIP2 levels.

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Neurotrophic Regulation of Calcium Channels by the Peptide Neurotransmitter Luteinizing Hormone Releasing Hormone

2003

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We exploited the simple organization of bullfrog paravertebral sympathetic ganglia (BFSG) to test whether the neurotransmitter peptide luteinizing hormone releasing hormone (LHRH), which generates the late slow EPSP, could also exert long-term neurotrophic control of ion channel expression. Whole-cell recordings from B-cells in BFSG showed that removal of all of the sources of ganglionic LHRH for 10 d by cutting preganglionic C-fibers in vivo caused a 28% reduction in Ca2+ current density. When BFSG B-neurons were dissociated from adult bullfrogs and maintained in a defined-medium, neuron-enriched, low-density, serum-free culture, the ICa density was increased by 49% after 6-7 d in the presence of 0.45 microm LHRH. This increase was not associated with alterations in the voltage dependence of Ca2+ current activation or inactivation and reflected a selective increase in N-type Ca2+ channel current. The increase in ICa density induced by LHRH was blocked by the transcription inhibitor actinomycin D. These results suggest that chronic exposure to a neurotransmitter that acts through G-protein-coupled receptors exerts long-term control of ion channel expression in a fully differentiated, adult sympathetic neuron in vitro or in vivo.

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Interaction of vasomotor and exocrine neurons in bullfrog paravertebral sympathetic ganglia

Cited by 3 publications

References 25 publications

Multiple functions of non-hypophysiotropic gonadotropin releasing hormone neurons in vertebrates

Multiple functions of non-hypophysiotropic gonadotropin releasing hormone neurons in vertebrates

Possible role of phosphatidylinositol 4,5, bisphosphate in luteinizing hormone releasing hormone‐mediated M‐current inhibition in bullfrog sympathetic neurons

Neurotrophic Regulation of Calcium Channels by the Peptide Neurotransmitter Luteinizing Hormone Releasing Hormone

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