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At least 217 records · Page 12Linked to original sources

TANNING IN THE ADULT FLY: A NEW FUNCTION OF NEUROSECRETION IN THE BRAIN.

Tanning in the newly emerged fly is induced by a hormone secreted by neurosecretory cells situated in the pars intercerebralis of the brain. The same hormone is contained in the compound ganglion of the thorax, in concentrations six times as high as in the brain. This hormone is believed to act directly on the eflector organ, and not through the secretion of ecdyson or a corpus allatum hormone; its release is effected through nervous impulses reaching the brain by way of the ventral nervous system a few minutes after the fly has emerged from the puparium. The hormone appears to be different from both the prothoraco-tropic and the gonadotropic hormones.

Animals↗

Neurosecretion of egg-laying hormone and other peptides from electrically active bag cell neurons of Aplysia.

1. Radiolabeled peptides released from an isolated cluster of bag cell neurons, during an after discharge, were compared with the polypeptide egg-laying hormone (ELH), 4,500 daltons, pI 9.0-9.3, as purified from homogenates of bag cell clusters. A peptide, labeled with methionine, leucine, and arginine, which is selectively released from after discharging bag cell clusters comigrates with marker ELH, purified from cluster homogenates, on P-6 gel filtration columns and subsequent isoelectric focusing gels. At least three other presumed peptides of unknown function are also released, including one of 5,000-6,000 mol wt, pI 4.5-5.0. 2. When bag cells afterdischarge in vitro, bioactive material is released that will induce egg laying when injected into an Aplysia. This released bioactive material also comigrates with bioactive material from cluster homogenates on P-6 columns. 3. These experiments demonstrate that ELH (4,500 mol wt, pI 9.0-9.3), as purified from bag cell cluster homogenates, is also the major form secreted from bag cells that induces egg laying. This purified ELH can now be used to study the physiological effects of a secreted neurohormone and their relationship to behavior.

Action Potentials↗

Ca2+ cooperativity in neurosecretion measured using photolabile Ca2+ chelators.

1. The photolabile Ca2+ chelator DM-nitrophen was injected into crayfish motor neuron terminals and photolyzed with light flashes of different intensity to determine the cooperativity of Ca2+ action in releasing neurotransmitter. 2. Each flash elicited a phasic postsynaptic response resembling an excitatory junctional potential, apparently due to a presynaptic "spike" in intracellular calcium concentration ([Ca2+]i). 3. When postsynaptic currents were measured under voltage clamp, a Ca2+ cooperativity of approximately 3-4 was inferred from a supralinear dependence of responses on changes in peak [Ca2+]i caused by flashes differing in intensity by 32-46%. 4. A similar Ca2+ cooperativity was inferred from postsynaptic potentials in response to flashes of varying intensity. 5. The time course of transmitter release indicated by flash responses had slightly slower rising and falling phases than excitatory postsynaptic potentials. There was also a slow tail of transmitter release lasting for approximately 200 ms after a flash. 6. This time course was explained quantitatively by simulations of DM-nitrophen photolysis and binding reactions and a model of Ca2+ activation of transmitter release.

Acetates↗

'Neurosecretion' by synaptic terminals and glandular discharge in the endocrine pancreas. Application of tannic acid to the teleost Xiphophorus helleri.

Nerve fibers within the large pancreatic islet of Xiphophorus helleri are apparently of a single type and form typical, well-differentiated synapses with the endocrine gland cells. A histochemical test for cholinesterases generates reaction product in association with the outer surfaces of the neuronal membranes. Two categories of presumptive secretory inclusions are present in the fiber terminals: secretory granules usually 80-120 nm in diameter have a wide distribution within the fibers, whereas electron-lucent synaptic vesicles 30-60 nm across often cluster adjacent to membrane thickenings and differentiated clefts. Infusion of tannic acid in high-K+ saline enabled sites of granule exocytosis to be visualized. These presumed sites of neuropeptide discharge were associated with morphologically undifferentiated regions of the terminal membranes. Tannic acid also facilitated the detection of exocytosis, involving granules of endocrine gland cells; discharged secretory material exposed to this agent retains immunoreactivity at a reduced level.

Animals↗

Regulation of cyclic adenosine 3',5'-monophosphate signaling and pulsatile neurosecretion by Gi-coupled plasma membrane estrogen receptors in immortalized gonadotropin-releasing hormone neurons.

Immortalized GnRH neurons (GT1-7) express receptors for estrogen [estrogen receptor-alpha and -beta(ERalpha and ERbeta)] and progesterone (progesterone receptor A) and exhibit positive immunostaining for both intracellular and plasma membrane ERs. Exposure of GT1-7 cells to picomolar estradiol concentrations for 5-60 min caused rapid, sustained, and dose-dependent inhibition of cAMP production. In contrast, treatment with nanomolar estradiol concentrations for 60 min increased cAMP production. The inhibitory and stimulatory actions of estradiol on cAMP formation were abolished by the ER antagonist, ICI 182,780. The estradiol-induced inhibition of cAMP production was prevented by treatment with pertussis toxin, consistent with coupling of the plasma membrane ER to an inhibitory G protein. Coimmunoprecipitation studies demonstrated an estradiol-regulated stimulatory interaction between ERalpha and Galphai3 that was prevented by the ER antagonist, ICI 182,780. Exposure of perifused GT1-7 cells and hypothalamic neurons to picomolar estradiol levels increased the GnRH peak interval, shortened peak duration, and increased peak amplitude. These findings indicate that occupancy of the plasma membrane-associated ERs expressed in GT1-7 neurons by physiological estradiol levels causes activation of a Gi protein and modulates cAMP signaling and neuropeptide secretion.

Animals↗

Gonadotropin-releasing hormone (GnRH) receptor expression and membrane signaling in early embryonic GnRH neurons: role in pulsatile neurosecretion.

The characteristic pulsatile secretion of GnRH from hypothalamic neurons is dependent on an autocrine interaction between GnRH and its receptors expressed in GnRH-producing neurons. The ontogeny and function of this autoregulatory process were investigated in studies on the properties of GnRH neurons derived from the olfactory placode of the fetal rat. An analysis of immunocytochemically identified, laser-captured fetal rat hypothalamic GnRH neurons, and olfactory placode-derived GnRH neurons identified by differential interference contrast microscopy, demonstrated coexpression of mRNAs encoding GnRH and its type I receptor. Both placode-derived and immortalized GnRH neurons (GT1-7 cells) exhibited spontaneous electrical activity that was stimulated by GnRH agonist treatment. This evoked response, as well as basal neuronal firing, was abolished by treatment with a GnRH antagonist. GnRH stimulation elicited biphasic intracellular calcium ([Ca2+]i) responses, and both basal and GnRH-stimulated [Ca2+]i levels were reduced by antagonist treatment. Perifused cultures released GnRH in a pulsatile manner that was highly dependent on extracellular Ca2+. The amplitude of GnRH pulses was increased by GnRH agonist stimulation and was diminished during GnRH antagonist treatment. These findings demonstrate that expression of GnRH receptor, GnRH-dependent activation of Ca2+ signaling, and autocrine regulation of GnRH release are characteristics of early fetal GnRH neurons and could provide a mechanism for gene expression and regulated GnRH secretion during embryonic migration.

Action Potentials↗

Serotonin (5-HT) receptor subtypes mediate specific modes of 5-HT-induced signaling and regulation of neurosecretion in gonadotropin-releasing hormone neurons.

Serotonin (5-HT), the endogenous nonselective 5-HT receptor agonist, activates the inositol 1,4,5-triphosphate/calcium (InsP3/Ca2+) signaling pathway and exerts both stimulatory and inhibitory actions on cAMP production and GnRH release in immortalized GnRH neurons. The high degree of similarity between the signaling and secretory responses elicited by GnRH and 5-HT prompted us to target specific 5-HT receptor subtypes to deconvolute the complex actions of these agonists on signal transduction and GnRH release. Specific mRNA transcripts for 5-HT1A, 5-HT2C, 5-HT4, and 5-HT7 were identified in immortalized GnRH neurons (GT1-7). The rate of firing of spontaneous action potentials (APs) by hypothalamic GnRH neurons and cAMP production and pulsatile GnRH release in GT17 cells were profoundly inhibited during activation of the Gi-coupled 5-HT1A receptor. Treatment with a selective agonist to activate the Gq-coupled 5-HT2C receptor increased the rate of firing of spontaneous APs, stimulated InsP3 production and caused a delayed increase in GnRH release. Selective activation of the Gs-coupled 5-HT4 receptor also increased the rate of firing of APs, stimulated cAMP production, and caused a sustained and robust increase in GnRH release. The ability of 5-HT receptor subtypes expressed in GnRH neurons to activate single or multiple G proteins in a time- and dose-dependent manner differentially regulates the phospholipase C/InsP3/Ca2+, and adenylyl cyclase/cAMP signaling pathways, and thereby regulates the frequency and amplitude of pulsatile GnRH release. This process, in conjunction with the modulation of spontaneous electrical activity of the GnRH neuron, contributes to the control of the pulsatile mode of neuropeptide secretion that is characteristic of GnRH neuronal function in vivo and in vitro.

Action Potentials↗