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PubMed1981

Early effect of glucose and oxygen deprivation on the spontaneous acetylcholine release from the myenteric plexus of the guinea pig ileum.

The early effects of glucose and oxygen deprivation on the spontaneous acetylcholine output from the myenteric plexus - longitudinal muscle preparation of the guinea pig ileum were studied using an incubation chamber that permitted rapid sample collection in 2-min intervals. Glucose deprivation or hypoxia resulted in a gradual decline in rate of spontaneous acetylcholine collection in 2-min intervals. Glucose deprivation or hypoxia resulted in a gradual decline in rate of spontaneous acetylcholine output. However, glucose deprivation plus hypoxia caused an acceleration in acetylcholine output within 10-15 min, which attained a rate seven times greater than observed under normal conditions. Recovery of low resting rates was obtained by reintroduction of oxygen and glucose into the bath medium. Neither morphine (2.7 x 10(-5) M) nor tetrodotoxin (1.6 x 10(-6) M) prevented the increase in acetylcholine output induced by energy deprivation. The substitution of Ca2+ by Mg2+, in the presence of EGTA, greatly reduced the acetylcholine output induced by energy deprivation. However, a small transitory output of acetylcholine was observed under these conditions which was resistant to tetrodotoxin and ot affected by depolarizing amounts of K+. The transitory output was repeatable by reintroduction of glucose and oxygen to the Ca2+-free medium with subsequent return to conditions of hypoxia and glucose deprivation. These results suggest that energy deprivation initially stimulates normal acetylcholine secretion by (a) increasing Ca2+ influx across the plasma membrane and (b) mobilizing an intracellular Ca2+ poll. This implies that processes involved in maintenance of normal low transmitter release are more sensitive to energy lack than the neurosecretion process itself.

Acetylcholine↗
PubMed1982

Positive feedback regulation of noradrenaline release from sympathetic nerves: a questionable hypothesis.

The effects of known agonists and of an antagonist on the stimulation-induced efflux of [3H]noradrenaline from left atria of guinea pigs was assessed. This was done to evaluate the hypothesis of presynaptic beta receptors mediating a positive feedback system. Isoproterenol (1.2 X 10(-8) M) enhanced the efflux of tritium with 50 pulses at all four test frequencies and did so to a similar extent at three of them. Exogenous noradrenaline (1.8 X 10(-6) M) inhibited efflux and isoproterenol was ineffective as an enhancer of efflux in its presence. Propranolol (1 X 10(-7) M) did not reliably increase the inhibitory effect of added noradrenaline on stimulation-induced efflux nor did the antagonist by itself under a variety of test conditions decrease the stimulation-induced efflux of tritium. It is concluded that the synaptic quantities of transmitter do not determine the magnitudes of the effects of exogenous agents on tritium efflux and that positive feedback, for both theoretical and empirical considerations, does not function during neurosecretion.

Animals↗
PubMed1997

Spontaneous acetylcholine release in mammalian neuromuscular junctions.

Spontaneous secretion of the neurotransmitter acetylcholine in mammalian neuromuscular synapsis depends on the Ca2+ content of nerve terminals. The Ca2+ electrochemical gradient favors the entry of this cation. We investigated the possible involvement of three voltage-dependent Ca2+ channels (VDCC) (L-, N-, and P/Q-types) on spontaneous transmitter, release at the rat neuromuscular junction. Miniature end-plate potential (MEPP) frequency was clearly reduced by 5 microM nifedipine, a blocker of the L-type VDCC, and to a lesser extent by the N-type VDCC blocker, omega-conotoxin GVIA (omega-CgTx, 5 microM). On the other hand, nifedipine and omega-CgTx had no effect on K(+)-induced transmitter secretion. omega-Agatoxin IVA (100 nM), a P/Q-type VDCC blocker, prevents acetylcholine release induced by K+ depolarization but failed to affect MEPP frequency in basal conditions. These results suggest that in the mammalian neuromuscular junction Ca2+ enters nerve terminals through at least three different channels, two of them (L- and N-types) mainly related to spontaneous acetylcholine release and the other (P/Q-type) mostly involved in depolarization-induced neurotransmitter release. Ca(2+)-binding molecule-related spontaneous release apparently binds Ca2+ very rapidly and would probably be located very close to Ca2+ channels, since the fast Ca2+ chelator (BAPTA-AM) significantly reduced MEPP frequency, whereas EGTA-AM, exhibiting slower kinetics, had a lower effect. The increase in MEPP frequency induced by exposing the preparation to hypertonic solutions was affected by neither external Ca2+ concentration nor L-, N-, and P/Q-type VDCC blockers, indicating that extracellular Ca2+ is not necessary to produce hyperosmotic neurosecretion. On the other hand, MEPP frequency was diminished by BAPTA-AM and EGTA-AM to the same extent, supporting the view that hypertonic response is promoted by "bulk" intracellular Ca2+ concentration increases.

Acetylcholine↗
PubMed1999

Syntaxin 1A inhibits regulated CFTR trafficking in xenopus oocytes.

The cystic fibrosis transmembrane conductance regulator (CFTR) is an epithelial cell Cl channel, whose gating activity and membrane trafficking are controlled by cAMP/protein kinase A (PKA)-mediated phosphorylation. CFTR Cl currents are regulated also by syntaxin 1A (A. P. Naren, D. J. Nelson, W. W. Xie, B. Jovov, J. Pevsner, M. K. Bennett, D. J. Benos, M. W. Quick, and K. L. Kirk. Nature 390: 302-305, 1997), a protein best known for its role in membrane trafficking and neurosecretion. To examine the mechanism of syntaxin 1A inhibition, we expressed these proteins in Xenopus oocytes and monitored agonist-induced changes in plasma membrane capacitance and cell surface fluorescence of CFTR that contains an external epitope tag. cAMP stimulation elicited large increases in membrane capacitance and in cell surface labeling of flag-tagged CFTR. Coexpression of CFTR with syntaxin 1A, but not syntaxin 3, inhibited cAMP-induced increases in membrane capacitance and plasma membrane CFTR content. Injection of botulinum toxin/C1 rapidly reversed syntaxin's effects on current and capacitance, indicating that they cannot be explained by an effect on CFTR synthesis. Functional expression of other integral membrane proteins, including Na-coupled glucose transporter hSGLT1, inwardly rectified K channel hIK1, P2Y2 nucleotide receptor, and viral hemagglutinin protein, was not affected by syntaxin 1A coexpression. These findings indicate that acute regulation of the number of CFTR Cl channels in plasma membrane is one mechanism by which cAMP/PKA regulates Cl currents. Inhibition of plasma membrane CFTR content by syntaxin 1A is consistent with the concept that syntaxin and other components of the SNARE machinery are involved in regulated trafficking of CFTR.

Animals↗
PubMed1999

CFTR is functionally active in GnRH-expressing GT1-7 hypothalamic neurons.

We have demonstrated the expression of the cystic fibrosis transmembrane conductance regulator (CFTR) gene, mRNA, and protein within the rat and human brains, in areas regulating sexual differentiation and function. We have found that GT1-7, a gonadotropin-releasing hormone (GnRH)-secreting hypothalamic neuronal cell line, expresses the CFTR gene, mRNA, and protein and cAMP-dependent (36)Cl efflux. A linear 7-pS Cl- conductance, which is stimulated by ATP and cAMP analogs and inhibited by glibenclamide, consistent with CFTR activity, has been identified in GT1-7 cells. Antisense oligo(dN) generated against exon 10 of the CFTR gene transcript (mRNA) inhibit GnRH secretion into media [312 +/- 73, 850 +/- 150, 963 +/- 304, and 912 +/- 74 pg GnRH/4 x 10(6) cells for antisense, sense, missense, and no oligo(dN), respectively; P < 0. 029 for antisense oligo(dN)-treated vs. normal cells]. No changes in intracellular synthesis of GnRH were noted [1,400 +/- 371 and 1,395 +/- 384 pg GnRH/4 x 10(6) cells for antisense and sense oligo(dN), respectively]. Antisense oligo(dN), but not sense or missense oligo(dN), inhibited cAMP-dependent 36Cl efflux. The expression of CFTR protein, detected by Western blotting, was also inhibited 68% by preincubation of cells with antisense oligo(dN). GT1-7 hypothalamic neurons express the CFTR gene, mRNA, and protein, which modulate neurosecretion. Abnormal neuropeptide vesicle trafficking by mutant CFTR may help to explain some of the diverse manifestations of cystic fibrosis.

3T3 Cells↗
PubMed1987

Pressure and length adaptations in isolated cat stomach.

Correlations were made between the adaptation of gastric pressure and longitudinal muscle tension. Isolated cat stomachs were filled with physiological solution and longitudinal strips marked in five segments over the lesser and the greater curvature (LC and GC). Strip length changed the most in the proximal segments of GC. Volume changes led to triphasic changes in gastric pressure. On filling, there was a pressure peak and pressure accommodation to a new base-line pressure. On emptying there was an initial pressure nadir that was followed by a pressure recovery. When isolated longitudinal strips were stretched and released to their lengths at specific gastric volumes, they generated triphasic tension adaption and recovery. Strips from the proximal greater curvature generated the highest base-line tension, highest peak tension, and largest amplitude of tension adaptations. Addition of KCl, carbachol, or physostigmine increased base-line tension and tension adaptations in parallel, whereas atropine reduced them. Tetrodotoxin had no effect. The base-line tension of the isolated cat stomach is maintained by a tonic cholinergic neurosecretion but its tension adaptations do not require neural control.

Animals↗
PubMed1988

Peripheral chemoreceptor control of neurohypophysial blood flow.

Neurohypophysial blood flow responses to hypoxic hypoxia were studied under conditions of vagotomy, carotid sinus denervation, and combined vagotomy and carotid sinus denervation. Arterial O2 tension was lowered from 128 +/- 3 to 31 +/- 1 Torr, whereas pH and arterial CO2 tension remained constant. Denervation of either carotid sinus or aortic arch chemoreceptors alone does not attenuate the dilation of neurohypophysial vessels that accompanies hypoxic hypoxia. Combined denervation, however, completely blocks this response for the neurohypophysis but not for any other brain region studied. Hypoxic hypoxia resulted in an increase in plasma vasopressin (AVP) from approximately 8 to approximately 40 pg/ml. This increase occurred in the intact, vagotomy, and carotid sinus-denervation conditions. This neurosecretory response was also completely inhibited by combined denervation. For most brain regions peripheral chemoreceptors are not involved in the blood flow response; however, the response of the neurohypophysis appears to be mediated via these chemoreceptors, presumably by altering the neuroeffector activity to this region. In addition our data suggest a temporal relationship between neurohypophysial vasodilation and neurosecretion of AVP.

Animals↗
PubMed1986

Chronic push-pull brain perfusion in unrestrained rhesus macaques.

A system was developed to permit perfusion of local brain regions and simultaneous peripheral blood sampling in free-moving caged monkeys. The system comprises a calvarial headpiece that contains multiple push-pull cannulas (PPC), a flexible stainless steel tether, a four-channel fluid swivel, and a surgical procedure for simultaneous multisite brain cannulation. Rhesus macaques were fitted surgically with an indwelling jugular catheter and PPC directed into the third ventricle, median eminence, and preoptic area. These animals were tethered for periods of 14-70 h during which brain perfusates and peripheral blood samples were collected at 10- to 30-min intervals through the tether-swivel assembly. Levels and pulsatile patterns of gonadotropin-releasing hormone in 10-min perfusate samples and luteinizing hormone and cortisol in sequential plasma samples were quantified by specific radioimmunoassays. The normal endocrine profiles in these animals suggest that this system provides a valuable method to study patterns of neurosecretions in an unrestrained simian.

Animals↗
PubMed1998

Dopamine, sensory discharge, and stimulus interaction with CO2 and O2 in cat carotid body.

It is hypothesized that carotid body chemosensory activity is coupled to neurosecretion. The purpose of this study was to examine whether there was a correspondence between carotid body tissue dopamine (DA) levels and neuronal discharge (ND) measured from the carotid sinus nerve of perfused cat carotid bodies and to characterize interaction between CO2 and O2 in these responses. ND and tissue DA were measured after changing from normoxic, normocapnic control bicarbonate buffer (PO2 >120 Torr, PCO2 25-30 Torr, pH approximately 7.4) to normoxic hypercapnia (PCO2 55-57 Torr, pH 7.1-7.2) or to hypoxic solutions (PO2 30-35 Torr) with normocapnia (PCO2 25-30 Torr, pH approximately 7.4) or hypocapnia (PCO2 10-15 Torr, pH 7.6-7.8). Similar temporal changes for ND and tissue DA were found for all of the stimuli, although there was a much different proportional relationship for normoxic hypercapnia. Both ND and DA increased above baseline values during flow interruption and normocapnic hypoxia, and both decreased below baseline values during hypoxic hypocapnia. In contrast, normoxic hypercapnia caused an initial increase in ND, from a baseline of 175 +/- 12 (SE) to a peak of 593 +/- 20 impulses/s within 4.6 +/- 0.9 s, followed by adaptation, whereas ND declined to 423 +/- 20 impulses/s after 1 min. Tissue DA initially increased from a baseline of 17.9 +/- 1.2 microM to a peak of 23.2 +/- 1.2 microM within 3.0 +/- 0.7 s, then declined to 2.6 +/- 1.0 microM. The substantial decrease in tissue DA during normoxic hypercapnia was not consistent with the parallel changes in DA with ND that were observed for hypoxic stimuli.

Animals↗
PubMed1993

Passive current flow and morphology in the terminal arborizations of the posterior pituitary.

1. Patch-clamp techniques were used to study the morphology and electrotonic properties of the terminal arborizations of the posterior pituitary. 2. Neurobiotin-labeling experiments revealed axons and swellings connected to the structure that was patch clamped. The large swellings were en passant and situated along axons in a topological arrangement identical to that of the small varicosities. Axons had many varicosities and few branches, reflecting a predominant architectural motif of beads on a string rather than berries on a bush. 3. Cable theory was used to analyze passive current transients produced by voltage steps under whole-cell clamp. Most charging transients were not consistent with an equivalent cylinder representation as posited by the Rall model for a motoneuron. A few charging transients were consistent with the Rall model and provided estimates for basic membrane and cable properties. 4. Some of the charging transients that violated predictions of the Rall model were consistent with an alternative model, in which the patch-clamped swelling was assumed to be coupled to another swelling by a segment of axon. This model was called the Dumbbell model, and it, together with the neurobiotin-labeling experiments, indicated that a significant number of large swellings were less than one length constant away from another large swelling. 5. Large swellings can have diameters approximately 30 times larger than the diameters of the connecting axons. These swellings lie along the axon such that action potentials must propagate through them to spread excitation through the entire terminal arborization. These large swellings could be sites where action-potential propagation is more likely to fail. 6. The information presented here about neurohypophysial nerve terminals should be useful in further investigations of how terminal arborization geometry and membrane properties influence neurosecretion and synaptic transmission.

Animals↗
PubMed1996

Hyperosmotic regulation of voltage-gated calcium currents in rat anterior pituitary cells.

1. The sensitivity of voltage-gated calcium currents to hyperosmotic media containing mannitol or sucrose (373-723 mOsm) and to the dihydropyridine (DHP) calcium channel agonist Bay K 8644 was examined in enriched populations of rat anterior pituitary somatotrophs by using the whole cell mode of the patch-clamp technique. 2. Hyperosmotic media reduced the amplitude of voltage-gated calcium currents. With a 61.9% increase in extracellular medium osmolarity (523 mOsm), low voltage-activated (LVA) calcium currents were reduced to 67.9 +/- 17.8% of control size and high voltage-activated (HVA) calcium currents were reduced to 57.0 +/- 5.7% (mean +/- SD) of control size. The hyperosmotic suppression of HVA calcium currents was usually accompanied with a negative shift of 6.0 +/- 2.9 mV (mean +/- SD) in the activation curve of HVA currents. 3. The DHP calcium-channel agonist Bay K 8644 (10 microM), which stimulates hormone secretion from somatotrophs, increased the amplitude of HVA calcium currents to 212.6 +/- 67.2% of their control size, prolonged their tail currents, and negatively shifted the activation curve of HVA calcium currents by 6.2 +/- 2.8 mV. 4. Hyperosmotic media reduced the amplitude of DHP-sensitive HVA calcium currents and their associated prolonged tail currents, thus providing direct evidence for hyperosmotic suppression of DHP-sensitive currents. 5. Hence, exposure of pituitary cells to hyperosmotic media reduced voltage-sensitive calcium influx through LVA and DHP-sensitive HVA calcium channels. The inhibition of calcium influx through DHP-sensitive channels, which are implicated in regulation of hormone secretion in these cells, suggests that inhibitory hyperosmotic effects on hormone secretion from pituitary cells may stem from inhibition of calcium influx, before the exocytotic process. These results may also be relevant to effects of hypertonicity on neurosecretion in the nervous system.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1997

Facilitation at the lobster neuromuscular junction: a stimulus-dependent mobilization model.

Frequency facilitation is a process whereby neurosecretion increases as a function of stimulation frequency during repetitive synaptic activity. To examine the physiological basis underlying facilitation, we have estimated the frequency dependence of the synaptic parameters n (number of units capable of responding to a nerve impulse) and P (average probability of responding) at the lobster neuromuscular junction. Both n and P increase as a function of frequency, suggesting that the efficiency of quantal docking and quantal fusion is regulated by repetitive synaptic activity. In experiments in which facilitation is strong and quantal content does not saturate over the frequency range tested, the value of P saturates at low frequencies of stimulation, and increases in quantal content at higher frequencies of stimulation are due to an increase in n. Therefore the value of P does not limit facilitation. We propose that transmitter release is limited by the rates of quantal mobilization and demobilization, and that each excitatory stimulus causes additional mobilization of quanta to dock at the presynaptic release sites. In such a model the binomial parameter n will correspond to the number of quanta docked at the release sites and available for release. We have developed and solved kinetic equations that describe how the number of docked quanta changes as a function of time and of stimulation frequency. The stimulus-dependent mobilization model of facilitation predicts that the reciprocal value of the quantal content depends linearly on the reciprocal product of the stimulation frequency and the probability of release. Fits of the experimental data confirm the accuracy of this prediction, showing that the model proposed here quantitatively describes frequency facilitation. The model predicts that high rates of quantal demobilization will produce strong frequency facilitation.

Algorithms↗
PubMed2001

Biophysical properties, pharmacology, and modulation of human, neuronal L-type (alpha(1D), Ca(V)1.3) voltage-dependent calcium currents.

Voltage-dependent calcium channels (VDCCs) are multimeric complexes composed of a pore-forming alpha(1) subunit together with several accessory subunits, including alpha(2)delta, beta, and, in some cases, gamma subunits. A family of VDCCs known as the L-type channels are formed specifically from alpha(1S) (skeletal muscle), alpha(1C) (in heart and brain), alpha(1D) (mainly in brain, heart, and endocrine tissue), and alpha(1F) (retina). Neuroendocrine L-type currents have a significant role in the control of neurosecretion and can be inhibited by GTP-binding (G-) proteins. However, the subunit composition of the VDCCs underlying these G-protein-regulated neuroendocrine L-type currents is unknown. To investigate the biophysical and pharmacological properties and role of G-protein modulation of alpha(1D) calcium channels, we have examined calcium channel currents formed by the human neuronal L-type alpha(1D) subunit, co-expressed with alpha(2)delta-1 and beta(3a), stably expressed in a human embryonic kidney (HEK) 293 cell line, using whole cell and perforated patch-clamp techniques. The alpha(1D)-expressing cell line exhibited L-type currents with typical characteristics. The currents were high-voltage activated (peak at +20 mV in 20 mM Ba2+) and showed little inactivation in external Ba2+, while displaying rapid inactivation kinetics in external Ca2+. The L-type currents were inhibited by the 1,4 dihydropyridine (DHP) antagonists nifedipine and nicardipine and were enhanced by the DHP agonist BayK S-(-)8644. However, alpha(1D) L-type currents were not modulated by activation of a number of G-protein pathways. Activation of endogenous somatostatin receptor subtype 2 (sst2) by somatostatin-14 or activation of transiently transfected rat D2 dopamine receptors (rD2(long)) by quinpirole had no effect. Direct activation of G-proteins by the nonhydrolyzable GTP analogue, guanosine 5'-0-(3-thiotriphospate) also had no effect on the alpha(1D) currents. In contrast, in the same system, N-type currents, formed from transiently transfected alpha(1B)/alpha(2)delta-1/beta(3), showed strong G-protein-mediated inhibition. Furthermore, the I-II loop from the alpha(1D) clone, expressed as a glutathione-S-transferase (GST) fusion protein, did not bind Gbetagamma, unlike the alpha(1B) I-II loop fusion protein. These data show that the biophysical and pharmacological properties of recombinant human alpha(1D) L-type currents are similar to alpha(1C) currents, and these currents are also resistant to modulation by G(i/o)-linked G-protein-coupled receptors.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2002

New disguises for an old channel: MaxiK channel beta-subunits.

Ca(2+)-activated K(+) channels of large conductance (MaxiK or BK channels) control a large variety of physiological processes, including smooth muscle tone, neurosecretion, and hearing. Despite being coded by a single gene (Slowpoke), the diversity of MaxiK channels is great. Regulatory b-subunits, splicing, and metabolic regulation create this diversity fundamental to the adequate function of many tissues.

Amino Acid Sequence↗
PubMedDate not supplied

Hormones associated with non-maternal infant care: a review of mammalian and avian studies.

Hormonal changes during non-maternal infant care have been demonstrated in many cooperatively breeding bird species, some monogamous rodents and two species of New World primates. Coevolution of hormones and social traits may have provided for the different breeding systems that occur today. Several hormones have been shown to covary with the breeding systems of vertebrates. Elevated levels of the hormone prolactin with male parenting behaviours are common to many birds, rodents and the callitrichid monkeys Callithrix jacchus and Saguinus oedipus. In birds, prolactin may be elevated in both male and female breeders during various stages of nest building, egg laying, incubating and feeding of young. Testosterone levels appear to have an inverse relationship to prolactin levels during infant care in birds and rodents, but this relationship has not been examined for primates. In cooperatively breeding birds, helpers who remain at the nest also have elevated levels of prolactin when displaying parental care behaviours. Prolactin levels are elevated in helper callitrichid monkeys during the postpartum period. Monogamous male rodents demonstrate elevated prolactin levels with parental care behaviour but, in contrast to the birds, the mechanisms mediating prolactin increase appear to differ for male and female rodents. Two factors may influence male parental behaviours and hormonal changes: stimuli from the pregnant female and stimuli from the newborn pups; whereas maternal behaviours are influenced by the maternal hormones of the female and the pup stimuli. An experiential factor may also influence male parental behaviours. Neuropeptides such as oxytocin and vasopressin appear to be involved in male rodent parental care and there may be an interaction between a series of hormones and neurosecretions and stimuli from mates and pups. Studies of Saguinus oedipus, the cotton-top tamarin, suggest that prolactin levels are responsive to stimuli from contact with infants and the level of infant care experience influences the levels of prolactin with male infant care. Father tamarins also have elevated levels of prolactin before the birth of infants suggesting that cues from the pregnant female are important. Prolactin's role in parental care may have evolved from prolactin's role in other reproductive functions. Hormonal regulation of non-maternal care may occur due to a complex interaction of many hormones and neurotransmitters. Studies described here should provide the impetus for further work on parental care hormones in a wide variety of primates.

Animals↗
PubMed1998

Diurnal rhythmicity of gonadotropin-releasing hormone gene expression in the rat.

The release of the decapeptide gonadotropin-releasing hormone (GnRH) from neuroterminals in the median eminence varies depending upon the stage of development, time of day, reproductive season, and day of the ovarian cycle. With respect to the biosynthetic events responsible for such alterations in GnRH release, we have reported that increases in GnRH mRNA occur concomitantly with or precede the proestrous GnRH/LH surge in female rats, and the pubertal increase in GnRH. Because a hallmark of puberty is the development of nocturnal increases in gonadotropin/GnRH release, in the present study, we examined whether a rhythm in GnRH gene expression occurs that may be responsible for this rhythm of neurosecretion. Additionally, we extended the previous finding of diurnal rhythms of GnRH gene expression in cycling females to adult male rats. The mechanism for these changes, i.e. GnRH gene transcription, RNA processing or a posttranscriptional mechanisms was also elucidated. In experiment I, GnRH gene expression was measured in female rats at different stages of puberty [P25 (juvenile); approximately P37 (day of vaginal opening); and P45 (postpubertal)] at 10.00, 14.00, 18.00, 22.00, 2.00 and 6.00 h. GnRH mRNA levels increased significantly during pubertal development, independent of any changes in GnRH gene transcription or RNA processing, indicating a posttranscriptional mechanism. GnRH mRNA levels did not vary with time of day in these pubertal rats, indicating that the diurnal rhythm of GnRH release that develops during puberty is probably a posttranslational event. In experiment II, GnRH gene expression was measured in adult male rats at the same 4-hour intervals. GnRH mRNA levels varied significantly with time of day: they increased from 10.00 to 14.00 h, remained elevated through 22.00 h, then decreased significantly to the nadir at 10.00 h. The mechanism for these changes appears to involve processing or stability of the GnRH mRNA in the nucleus. These results indicate that GnRH mRNA levels are regulated differentially with time of day depending upon age and gender.

Age Factors↗
PubMedDate not supplied

The insect frontal ganglion and stomatogastric pattern generator networks.

Insect neural networks have been widely and successfully employed as model systems in the study of the neural basis of behavior. The insect frontal ganglion is a principal part of the stomatogastric nervous system and is found in most insect orders. The frontal ganglion constitutes a major source of innervation to foregut muscles and plays a key role in the control of foregut movements. Following a brief description of the anatomy and development of the system in different insect groups, this review presents the current knowledge of the way neural networks in the insect frontal ganglion generate and control behavior. The frontal ganglion is instrumental in two distinct and fundamental insect behaviors: feeding and molting. Central pattern-generating circuit(s) within the frontal ganglion generates foregut rhythmic motor patterns. The frontal ganglion networks can be modulated in-vitro by several neuromodulators to generate a variety of motor outputs. Chemical modulation as well as sensory input from the gut and input from other neural centers enable the frontal ganglion to induce foregut rhythmic patterns under different physiological conditions. Frontal ganglion neurons themselves are also an important source of neurosecretion. The neurosecretory material from the frontal ganglion can control and modulate motor patterns of muscles of the alimentary canal. The current and potential future importance of the insect stomatogastric nervous system and frontal ganglion in the study of the neural mechanisms of behavior are discussed.

Animals↗
PubMed1978

[The mode of action of neurohormones on the central nervous system (author's transl)].

We tried to understand how hypophysiotropic polypeptides could be carried into some areas of the central nervous system. Granulations of neurosecretion in the ependymal cells and the presence of releasing hormones in the cerebrospinal fluid (CSF) suggest that CSF may transport these substances between the hypothalamus and other areas in the brain. Direct connections between the hypothalamus and other parts of the brain through secreting neurons are not necessary, the CSF transmitting to the cerebral hemispheres the hypothalamic polypeptides by the ventricles at the infundibulum.

Animals↗