PubMed Health⌕ Search

Biomedical subjects

L G Bauce

Publications and source records attributed to L G Bauce.

11 recordsLinked to original sources
PubMed2006

Vasopressin autoreceptors and nitric oxide-dependent glutamate release are required for somatodendritic vasopressin release from rat magnocellular neuroendocrine cells responding to osmotic stimuli.

Magnocellular neuroendocrine cells of the supraoptic nucleus (SON) release vasopressin (VP) systemically and locally during osmotic challenge. Although both central VP and nitric oxide (NO) release appear to reduce osmotically stimulated systemic VP release, it is unknown whether they interact locally in the SON to enhance somatodendritic release of VP, a phenomenon believed to regulate systemic VP release. In this study, we examined the contribution of VP receptor subtypes and NO to local VP release from the rat SON elicited by systemic injection of 3.5 m saline. Treatment of SON punches with VP receptor antagonists decreased osmotically stimulated intranuclear VP release. Similarly, blockade of NO production, or addition of NO scavengers, reduced stimulated VP, glutamate, and aspartate release, suggesting that local NO production and activity are critical for osmotically induced intranuclear VP and excitatory amino acid release. An increase in endogenous NO release from SON punches in response to hyperosmolality was confirmed by enzymatic NO assay. Consistent with enhanced glutamate and VP release from stimulated rat SON punches, the ionotropic glutamate receptor blocker kynurenate decreased stimulated local VP release without affecting NO release. These data suggest that NO enhances local VP release in part by facilitating local release of glutamate/aspartate and that glutamate receptor activity is required for the stimulation of local VP release by osmotic challenge. Collectively, these results suggest that local VP receptors, NO, and glutamatergic signaling mediate the amplification of intranuclear VP release during hyperosmolality and may contribute to efficient, but not exhaustive, systemic release of VP during osmoregulatory challenge.

Amino Acids↗
PubMed2005

A novel role for endogenous pituitary adenylate cyclase activating polypeptide in the magnocellular neuroendocrine system.

Central release of vasopressin (VP) by the magnocellular neuroendocrine cells (MNCs) responsible for systemic VP release is believed to be important in modulating the activity of these neurons during dehydration. Central VP release from MNC somata and dendrites is stimulated by both dehydration and pituitary adenylate cyclase activating polypeptide (PACAP). Although PACAP is expressed in MNCs, its potential role in the magnocellular response to dehydration is unexplored. The current study demonstrates that prolonged dehydration increases immunoreactivity for PACAP-27, PACAP-38, and the type I PACAP receptor in the supraoptic nucleus (SON) of the rat. In addition, PACAP stimulates local VP release in the euhydrated rat SON in vitro, and this effect is reduced by the PACAP receptor antagonist PAC(6-27) (100 nm), suggesting the participation of PACAP receptors. Concomitant with its effects on local VP release, PACAP also reduces basal glutamate and aspartate release in the euhydrated rat SON. Furthermore, somatodendritic VP release elicited by acute dehydration is blocked by PAC(6-27), suggesting that endogenous PACAP participates in this response. Consistent with this, RIA revealed that local PACAP-38 release within the SON is significantly elevated during acute dehydration. These results suggest that prolonged activation of hypothalamic MNCs is accompanied by up-regulation of PACAP and the type I PACAP receptor in these cells and that somatodendritic VP release in response to acute dehydration is mediated by activation of PACAP receptors by endogenous PACAP released within the SON. A potential role for PACAP in promoting efficient, but not exhaustive, systemic release of VP from MNCs during physiological challenge is discussed.

Adaptation, Physiological↗
PubMed1997

Glutamate release in parabrachial nucleus and baroreflex alterations after vagal afferent activation.

The parabrachial nucleus (PBN) is a regulatory nucleus that relays visceral information from the brain stem to the cortex. Immunohistochemical studies have shown that the levels of various neuropeptides in the PBN were changed after visceral afferent activation. Because the major transmitter relaying visceral information through the PBN is glutamate, the present study asked if glutamate release into the PBN also was changed after vagal afferent activation in anesthetized male rats. The distally crushed vagus was stimulated (50 Hz, 1-2 mA, 1 s on, 2 s off) for 2 h. Dialysates of the PBN were collected every 30 min and assayed for glutamate using high-performance liquid chromatography. Extracellular glutamate concentrations were reduced during the vagal stimulation, increased fourfold compared with prestimulated levels after the stimulation was terminated, and returned to prestimulated levels over the next 2 h poststimulation. These changes were not due to alterations in blood pressure because sodium nitroprusside infusion for the same interval resulted in a similar hypotension, but increased glutamate release. Phenylephrine and sodium nitroprusside were infused intravenously to measure the cardiac baroreflex before, during, and after vagal stimulation. The pressor (but not the depressor) response was elevated during the period of enhanced glutamate release, and the baroreflex curve was shifted to the right (increased threshold) without a change in gain. These changes in the cardiac baroreflex were reduced, but still seen, when the PBNs were dialyzed bilaterally with the glutamate antagonists MK-801 and 6-cyano-7-nitroquinoxaline-2,3-dione. Thus visceral activation alters glutamate release in the PBN and has enduring effects on cardiac baroreflex function.

Afferent Pathways↗
PubMed1995

Dopaminergic transmission between identified neurons from the mollusk, Lymnaea stagnalis.

1. Dopaminergic transmission was investigated in the central nervous system (CNS) of the freshwater snail, Lymnaea stagnalis. 2. The giant pedal neuron, designated as right pedal dorsal one (RPeD1), makes chemical, monosynaptic connections with a number of identified follower cells in the CNS. Previous work has shown that RPeD1 is an interneuron and a important component of the Lymnaea respiratory central pattern generator. In this study, the hypothesis that RPeD1 uses dopamine as its neurotransmitter was tested by chromatographic, pharmacological, and electrophysiological methods. Characterization of RPeD1's transmitter pharmacology is essential to clearly understand its role in Lymnaea. 3. Earlier studies demonstrated that the soma of RPeD1 contains dopamine. This was quantitated in the present study by high-performance liquid chromatography (with electrochemical detection) of isolated RPeD1 somata and growth cones, which yielded 0.8 +/- 0.3 and 0.10 +/- 0.08 pmol of dopamine per soma and growth cone, respectively. 4. Bath or pressure application of dopamine to follower cells of RPeD1, in situ, mimicked the effects of RPeD1 stimulation. Dose-response curves were constructed for the excitatory effect of dopamine on follower cells, visceral dorsal two and three (VD2/3) (ED50 = 39 microM; Hill coefficient = 1.03), and the inhibitory effect of dopamine on follower cell, visceral dorsal four (ED50 = 33 microM; Hill coefficient = 0.92). 5. The following dopamine agonists (100 microM) were tested by bath application: 2-amino-6,7-dihydroxy-1,2,3,4-tetrahydronaphthalene (ADTN), apopmorphine, 2-bromo-alpha-ergocryptine, deoxyepinephrine (DE), mesulergine, (-) quinpirole, SKF 38393, and tyramine. Only the general dopamine agonists, ADTN and DE, mimicked RPeD1's effects on its follower cells. 6. When VD2/3 was isolated and plated in vitro, it maintained a depolarizing response to dopamine. This response was reduced by intracellular injection of the G-protein blocker, GDP-beta-S (2 mM in electrode). Similarly, incubation of VD2/3, in vitro for approximately 18 h, with pertussis toxin (PTX; 5 micrograms/ml), the G-protein inactivating exotoxin, also reduced the dopamine response. Injecting GDP or incubating in heat-inactivated PTX did not effect the response. 7. Several dopamine antagonists were used in an attempt to block RPeD1's synapses: chlorpromazine, ergonovine, fluphenazine, haloperidol, 6-hydroxydopamine, SCH 23390, (+/-) sulpiride, and tubocurarine. Only the D-2 dopamine receptor antagonist, (+/-) sulpiride, reversibly blocked synaptic transmission from RPeD1 to its follower cells. Both the (+) and the (-) enantiomer of sulpiride also antagonized synaptic transmission. A dose-inhibition curve for (+/-) sulpiride was constructed (IC50 = 47 microM).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

A method for continuous blood sampling during cold water immersion.

A technique, consisting of a pre-calibrated, catheter-peristaltic pump combination, for continuous blood sampling was tested using six volunteers during a 20 min immersion in cold water at 14.7 +/- 0.9 degrees C. The device offered the advantage of continued collection of blood samples from an antecubital vein during the experiment with little discomfort for the subjects and in sufficient volume for assay of plasma constituents eg. catecholamines.

Blood Specimen Collection↗
PubMed1993

Identification, characterisation and in vitro reconstruction of an interneuronal network of the snail Helisoma trivolvis.

1. We describe three interneurones and their follower cells in the central ganglionic ring of Helisoma trivolvis. 2. The largest neurone on the dorsal surface of the left pedal ganglion is shown to be an interneurone that contains dopamine and makes monosynaptic connections with a large number of follower cells in the visceral and left parietal ganglia. This neurone is designated as left pedal dorsal 1 (LPeD1). 3. Another giant neurone is located on the dorsal surface of the right pedal ganglion. Although the position and morphology of this cell, designated right pedal dorsal 1 (RPeD1), are similar to those of LPeD1, it contains serotonin rather than dopamine. This neurone was found to synapse only on LPeD1, no other follower cells have so far been discovered. The connections between LPeD1 and RPeD1 are mutually inhibitory. 4. A small FMRFamide-immunoreactive neurone, identified here as visceral dorsal 4 (VD4), is located on the dorsal surface of the visceral ganglion. This neurone has a large number of follower cells throughout the central ganglionic ring. Among these follower cells are LPeD1 and RPeD1. The transmitter utilized by VD4 at these synapses is probably FMRFamide. In addition, VD4 receives excitatory inputs from LPeD1 that appear to be chemical and monosynaptic. 5. To test further the monosynaptic and specific nature of the connections within the network, the three interneurones were isolated and cultured in vitro. In these circumstances, the three neurones extended neurites and formed synapses which, with one exception (occasional electrical coupling between LPeD1 and RPeD1), were of similar type to those observed in vivo. 6. The identification and characterization of these three interneurones and their follower cells should greatly facilitate future studies of the Helisoma trivolvis nervous system. Furthermore, the possibility that this three-cell network can be reconstructed in vitro should aid our understanding of the mechanisms underlying synapse formation and neuronal plasticity.

Animals↗
PubMed1988

Plasma catecholamines in conscious rabbits after central administration of vasopressin.

Arterial levels of epinephrine (E) were significantly raised for all times sampled, after intracerebroventricular (i.c.v.) injection of arginine vasopressin (AVP) (1 nmol) into conscious rabbits. Venous levels of norepinephrine (NE) were significantly raised within the first 4 min after a similar i.c.v. injection of AVP. The significant increases in arterial E and venous NE correspond in time and therefore could account for changes in heart rate and blood pressure elicited by centrally injected AVP. Therefore, AVP could influence cardiovascular function by increasing the activity of the sympatho-adrenomedullary system.

Animals↗
PubMed1986

Transient depletion of serotonin in the nervous system of Helisoma.

The present study shows that the drug 5,7-dihydroxytryptamine (5,7-diHT) can be used reliably to deplete the neurotransmitter serotonin (5-HT) from the nervous system of the snail Helisoma. The depletion is more effective in axonal and synaptic regions (85-90%) than in the somata (55%), is reasonably specific for serotonin (dopamine is affected to a much lesser extent), and is transient, with normal levels of neurotransmitter being restored by 2 months. A physiological correlate of 5-HT depletion has been shown in that an EPSP elicited by a cerebral serotonergic neuron (C1) onto a buccal motoneuron (B19) is much smaller during depletion and also recovers with time as 5-HT regains normal concentration. Despite the severe 5-HT depletion and physiological impairment, the gross morphology of neuron C1 remains indistinguishable from controls. Serotonergic depletion is not accompanied by development of receptor supersensitivity nor by the production of serotonin in extraneuronal sources.

5,7-Dihydroxytryptamine↗
PubMed1981

Synthesis and assay for activity of a proposed anorexogenic agent, L-pyroglutamyl-L-histidyl-glycine.

L-Pyroglutamyl-L-histidyl-glycine has been reported to be an anorexogenic agent in female mice. In this report the synthesis of this tripeptide is described. The synthetic material was injected into female and male mice and into male rats. In no instance did the animals decrease their food intake. Further, the weights of peptide-treated animals were the same as those of control (saline-treated) animals. The results suggest that L-pyroglutamyl-L-histidyl-glycine is not an anorexogenic agent.

Animals↗
PubMed1979

Synthesis of a series of residue 1 (pyroglutamic acid) analogs of thyrotrophin releasing hormone.

This report describes the synthesis of 23 analogs of thyrotrophin releasing hormone, L-pyroglutamic acid-L-histidyl-L-prolineamide, where only the pyroglutamic acid moiety is modified. Twelve of the analogs contain different heterocyclic rings or are derivatized pyrrolidone rings. The syntheses of these pyroglutamic acid analogs are also described. Peptide bond formation was generally achieved by catalyzing carbodiimide coupling with 1-hydroxybenzotriazole. The histidine side chain was protected with the 2,4-dinitrophenyl group during di- and tripeptide synthesis and was removed with benzenethiol Final purification of tripeptides involved passage of synthetic material over a Dowex 1--X4 (bicarbonate) column. The route for synthesis of thyrotrophin releasing hormone and its analogs is highly efficient, since the native hormone may be obtained with 90% efficiency.

Amino Acids↗