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J D Vincent

Publications and source records attributed to J D Vincent.

At least 91 records · Page 5Linked to original sources
PubMed1990

Somatostatin increases voltage-dependent potassium currents in rat somatotrophs.

To study the modulatory effects of somatostatin on membrane K+ currents, whole cell voltage-clamp recordings were performed on identified rat somatotrophs in primary culture. In the presence of Co2+ (2 mM) and tetrodotoxin (1 microM) in the bath solution to block Ca2+ and Na+ inward currents, two types of voltage-activated K+ currents were identified on the basis of their kinetics and pharmacology. First, a delayed rectifier K+ current (IK) had a threshold of -20 mV, did not decay during voltage steps lasting 300 ms, and was markedly attenuated by extracellular application of tetraethylammonium (TEA, 10 mM). Second, a transient outward K+ current (IA) was activated at -40 mV (from a holding potential of -80 mV) and persisted despite the presence of TEA. This IA was blocked by 4-aminopyridine (2 mM). Somatostatin (10 nM) increased IK by 75% and IA by 45% without obvious effects on steady-state voltage dependency of activation or inactivation, and these effects were reversible. This increase in K+ currents may contribute in part to the inhibitory effect of somatostatin on growth hormone release.

4-Aminopyridine↗
PubMed1990

Plateau potentials recorded from lactating rat enriched lactotroph cells are triggered by thyrotropin releasing hormone and shortened by dopamine.

Enrichment of dispersed pituitary cells from normal lactating rats on a continuous BSA gradient permitted the isolation of two prolactin cell populations--light and heavy. Hormone release studies indicated that spontaneous prolactin (PRL) release of the heavy fraction cells was particularly sensitive to TRH stimulation (mean of 450%) and that this effect of TRH was totally inhibited by Ca2+ channel blockers (Co2+, Cd2+, Ni2+ and Mn2+). For this reason, the electrophysiological response to TRH was investigated on heavy fraction cells. Experiments performed on 264 cells after 4-12 days in culture showed that these cells could be divided into two groups. The first group, called high resting potential (HRP) cells, constituted 73% of the total and was characterized by a mean resting potential of -60 mV and a mean input membrane resistance of 700 M omega, and these cells displayed plateau potentials, which were triggered by application of brief (2 s), large (1 nA) depolarizing or hyperpolarizing current steps. The plateaux were characterized by a sustained depolarization at a potential near -20 mV and they were concomitant with an increase of the membrane conductance. The repolarization consisted of a slight, gradual hyperpolarization followed by a rapid return to the resting potential. The second group of cells (the remaining 27%; called low resting potential or LRP cells) was characterized by a mean resting potential of -45 mV and a mean input membrane resistance of 250 M omega. These cells were excitable, 30% of them displaying spontaneous activity but never showing plateaux. Electrophysiological experiments showed that the majority of the HRP cells (99%) responded to TRH but were insensitive to dopamine (DA) ejections (up to 10(-6) M) at resting potential. Ejection of TRH onto HRP cells induced a slow depolarization (10-15 mV) concomitant with a decrease of the membrane resistance. This led the cell membrane potential to a critical value (approximately -50 mV), at which the plateau response was triggered. The plateau lasted for about 10 s from potentials greater than -100 mV, and could reach 10 min from holding potentials close to the resting potential. The amplitude of the plateau varied according to the holding potential and the reversal potential was found to be -20 mV. Local application of tetraethylammonium chloride (TEA, 30 mM) only slightly affected the amplitude of the plateaux but they were shortened or totally blocked by Co2+, Cd2+ and Ni2+.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Effects of dopamine on voltage-dependent potassium currents in identified rat lactotroph cells.

The effects of dopamine (DA) on voltage-dependent potassium currents were investigated in rat lactotrophs maintained in primary culture. Lactotroph cells were identified using the reverse hemolytic plaque assay. Membrane currents and potentials of lactotroph cells were recorded using the patch-clamp recording technique in the 'whole-cell' configuration. In the presence of cobalt (2 mM), two types of voltage-dependent K+ currents were recorded, a voltage-activated delayed K+ current (IK) and a voltage-activated transient K+ current (IA). The current IK was activated at membrane potentials varying from -20 to +40 mV and did not inactivate during prolonged voltage steps (up to 25 s); it was blocked by tetraethylammonium (10 mM). The current IA was activated at membrane potentials higher than -45 mV and showed a voltage-dependent inactivation between -110 and -40 mV; it was slightly inhibited by 4-aminopyridine (5 mM). Under current-clamp conditions, the majority of the cells (60%) showed spontaneous Ca2(+)-dependent action potentials (APs) while silent cells (40%) were excitable by depolarizing current pulses. Bath application of 10 nM DA evoked a hyperpolarizing response, blocked spontaneous APs and decrease the amplitude of evoked APs. Only the hyperpolarizing response faded during the course of the whole cell recording experiments. Under voltage-clamp conditions, DA induced a reversible increase in both voltage-dependent outward K+ currents, without modifying their thresholds. Steady-state inactivation of IA was not affected by DA. These DA-induced responses were dose-dependent and they involved D2 receptor activation. They were mimicked by the specific D2 receptor agonist bromocriptine (10 nM) and blocked by the specific D2 receptor antagonist sulpiride (100 nM), the D1 antagonist SCH 23390 being ineffective. The ability of DA to increase voltage-dependent K+ currents cannot be observed without GTP in the recording pipette. It was pertussis-toxin-sensitive but was affected neither by bath application of 1 mM forskolin nor by the presence of 500 microM cyclic AMP with 500 microM 3-isobutyl-1-methylxanthine in the pipette solutions. We conclude that in lactotroph cells DA specifically increases two voltage-dependent K+ currents via a pertussis-toxin-sensitive guanine nucleotide regulatory protein and appears to be independent of intracellular cyclic AMP. This effect leads to a decrease in the excitability of the cell, explaining in part the inhibitory effect of DA on prolactin release.

4-Aminopyridine↗
PubMed1990

Dopamine inhibits two characterized voltage-dependent calcium currents in identified rat lactotroph cells.

The effects of dopamine (DA) on voltage-dependent Ca2+ currents were investigated in cultured rat lactotroph cells using the patch clamp recording technique. Each recorded cell was identified by the reverse hemolytic plaque assay. In the whole-cell configuration, two types of Ca2+ currents, L and T, were characterized on the basis of their kinetics, voltage sensitivity, and pharmacology. The L component had a threshold of -25 mV, showed little inactivation during a 150-msec voltage step, and was maximal at +10 mV. Cadmium ions (100 microM) significantly reduced its amplitude (75%). The T component was activated at a membrane potential close to -50 mV, was maximal at -10 mV, and showed a voltage-dependent inactivation between -90 and -30 mV. It was quickly inactivated during a maintained depolarization (time constant, 27 ms at -30 mV) and was strongly reduced (80%) by nickel ions (100 microM). Bath application of DA (10 nM) caused a markedly general depression of inward Ca2+ currents, acting differently on the T- and L-type currents. DA application shifted the voltage-dependence of the L-type current activation toward depolarization values (8 mV) without modifying its time- and voltage-dependent inactivation. In contrast, DA enhanced the inactivation of the T-type current by accelerating its time-dependent inactivation (25% decrease in the time constant of inactivation) and by shifting the voltage-dependence of the T-type current inactivation toward hyperpolarizing values (-63 mV in control vs. -77 mV in the presence of DA). These effects of DA were dose-dependent and involved the activation of a D2 receptor type. They were mimicked by bromocriptine application (10 nM), whereas sulpiride (100 nM) blocked the DA-evoked response. The D1 antagonist SCH 23390 was ineffective up to 100 microM. All of these DA-induced modifications in Ca2+ currents were abolished using a GTP-free pipette solution or after pretreatment of cells with pertussis toxin, suggesting that DA can regulate the function of Ca2+ channels through GTP-binding proteins (G-proteins). Our results show that DA acts simultaneously by reducing both voltage-dependent Ca2+ currents on lactotroph cells. Thus, DA reduces the entry of Ca2+ ions across the surface membrane and thereby influences electrical activity and the cytosolic free Ca2+ concentration involved in both basal and evoked PRL release.

Animals↗
PubMed1989

Characterization of rat spinal cord receptors to FLFQPQRFamide, a mammalian morphine modulating peptide: a binding study.

An in vitro binding assay, using 125I-YLFQPQRFamide, a newly synthetized iodinated analog of FLFQPQRFamide, in which Phe1 (F) has been substituted by a Tyr (Y), was developed to demonstrate and characterize putative binding sites of this brain morphine modulating peptide. This radioligand bound in a time-dependent manner to rat spinal cord membrane preparation. This binding was dose-dependent, saturable and reversible. Both kinetic data and saturation measured at equilibrium lead to the existence of a homogenous population of high affinity binding sites with a Kd value of 0.09-0.1 nM and a maximal capacity Bmax of 14.5 +/- 2 fmol/mg protein. Results of competition experiments show that both FLFQPQRFamide and its analog YLFQPQRFamide had a similar capacity to inhibit the 125I-YLFQPQRFamide binding, suggesting that this radioiodinated analog is a good tool to study binding characteristics of FLFQPQRFamide receptors. The related octadecapeptide AGEGLSSPFWSLAAPQRFamide, another mammalian morphine modulating peptide competes for radioligand binding with similar potency. Our results also show that mu, delta and kappa opiate receptor agonists as well as the antagonist naloxone were not able to affect binding either in presence or in absence of 120 mM NaCl. Together, these data demonstrate that FLFQPQRFamide does not function as an endogenous opiate receptor antagonist and that is capacity to reduce opiate-induced analgesia is supported by specific binding sites.

Amino Acid Sequence↗
PubMed1989

Release of oxytocin within the supraoptic nucleus during the milk ejection reflex in rats.

To investigate the hypothesis that oxytocin may be released within the magnocellular nuclei in vivo, push-pull cannula perfusions were performed in anaesthetized lactating rats in one supraoptic nucleus of the hypothalamus while recording the intramammary pressure and/or the electrical activity of oxytocin cells in the contralateral supraoptic nucleus. Oxytocin content was measured in samples collected over 15 min, under various conditions: 1) with no stimulation; 2) during suckling and suckling-induced reflex milk ejections; 3) during electrical stimulation of the neuro-hypophysis by trains of pulses that mimicked oxytocin cell bursts; 4) under osmotic stimulation by i.p. injection of 2 ml of 1.5 M NaCl to evoke a tonic and sustained oxytocin release from the neurohypophysis. Oxytocin release within the supraoptic nucleus increased significantly during the milk ejection reflex and, to a lesser extent, during burst-like electrical stimulation of the neurohypophysis. In suckled rats, the increase started before the first reflex milk ejection occurred. There was no apparent correlation between the amount of oxytocin in the perfusates and the number of milk ejections and oxytocin cell bursts occurring during each perfusion period. The amount of oxytocin in the perfusates further increased-during facilitation of the milk ejection reflex by intraventricular injections of oxytocin or its analogue, isotocin. When suckling failed to evoke the milk ejection reflex, there was no change in intra-supraoptic oxytocin release. There was also no change after osmotic stimulation. When the push-pull cannula was positioned outside the supraoptic nucleus, there was no increase in the amount of oxytocin during the three types of stimulation tested. These results provide evidence for an endogenous release of oxytocin within the magnocellular nuclei in lactating rats. It is suggested that the increase in such a release induced by suckling is likely to be a prerequisite for the onset and the maintenance of the characteristic intermittent bursting electrical activity of oxytocin cells leading to milk ejections.

Animals↗
PubMed1989

Excitatory effect of serotonin on pacemaker neurons in spinal cord cell culture.

Intracellular recordings were made from fetal mouse spinal cord neurons in primary culture. One type of neuron, with large somata (40-50 microns diameter) and thick neurites exhibited endogenous bursting or beating pacemaker electrical activity. Noradrenaline depolarized this type of neuron by decreasing an M-like conductance. Micropressure application of serotonin (10(-5) M in the delivery pipette) onto the surface of pacemaker neurons evoked a depolarization of the membrane potential in a dose-dependent manner with an increased input resistance. No such response was observed with other types of spinal cord neurons in culture. The response to serotonin was partially voltage-dependent. The serotonin-induced depolarization reversed at holding potential close to -100 mV. However, the input resistance variation evoked by serotonin increased exponentially when membrane potential was depolarized. The reversal potential was modified by increasing extracellular K+ concentration and it was unaltered by increasing the intracellular Cl- concentration. The decrease in K+ conductance induced by serotonin was not suppressed by the application of tetraethylammonium (50 mM) or 4-aminopyridine (10 mM). Furthermore, application of Ba2+ (6 mM) or Cd2+ (0.1 mM) had no effect on this response, suggesting that the depolarization evoked by serotonin application was not calcium-dependent. The serotonin evoked increase in input resistance was mediated by activation of a 5-HT1A-like receptor site. Spiperone, a 5-HT1A antagonist reversibly blocked the response. Methiothepin, a 5-HT1-5-HT2 antagonist (10(-3) M); cocaine, a 5-HT3 antagonist (10(-3) M); ketanserin, a 5-HT2 antagonist (10(-3) M); and prazosin, an alpha 1 antagonist (10(-3) M) had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Characteristics and specific localization of receptors for atrial natriuretic peptides at non-neuronal cells in cultured mouse spinal cord cells.

Characteristics of atrial natriuretic peptide receptors were determined in cultured mouse spinal cord cells. Saturation and competition experiments demonstrated the presence of a single class of atrial natriuretic peptide binding sites with high affinity (KD = 0.054 nM) and a density of 1.92 fmoles/10(6) cells. A similar affinity (KD = 0.070 nM) was observed in rat spinal cord membrane preparations. These atrial natriuretic peptide binding sites were functional receptors since the treatment of cells with atrial natriuretic peptide increased cyclic guanosine monophosphate levels within these cells in a classical time-dependent manner. When atrial natriuretic peptide was applied onto the cell body of intracellularly recorded spinal cord neurons, this peptide did not evoke a change of the input resistance or of the resting membrane potential value. Light-microscopic autoradiography studies showed that no atrial natriuretic peptide binding could be detected on typical birefringent neurons but it could be located on astroglial and epithelial cells as identified by immunocytochemical markers. These results show that functional atrial natriuretic peptide receptors with high affinity exist in cultured mouse spinal cord cells and are not located on neurons. The presence of atrial natriuretic peptide receptors on astrocytes suggests that this neuropeptide might be a good candidate for neuron-glial communication. As the atrial natriuretic peptide binding sites previously shown in epithelia responsible for maintaining fluid and electrolyte gradients, the atrial natriuretic peptide receptors on epithelial cells in these spinal cord cultures may be involved in vivo in the control of water balance in the central nervous system.

Animals↗
PubMed1989

Electrophysiological responses to somatostatin of rat hypophysial cells in somatotroph-enriched primary cultures.

1. Somatotroph cells were obtained from pituitaries of adult male rats by dissociation, separation and enrichment on a continuous gradient of bovine serum albumin at unit gravity. They were kept in culture for 7-15 days before electrophysiological experiments. 2. Immunofluorescent staining of the resulting gradient fractions (numbered F2 to F9) indicated that the majority of somatotrophs (75-85%) were located in the heavy fractions (F8 and F9). However, a small percentage (15-20%) of cells in these fractions were identified as lactotrophs. 3. Perifusion experiments indicated that on the one hand release of growth hormone from somatotroph-enriched fractions was stable at the level of 6 ng (2 min)-1 (10(6) cells)-1 and was markedly inhibited by somatostatin (1.9 ng (2 min)-1 (10(6) cells)-1) but not by dopamine. On the other hand, in the same cell preparations, basal prolactin release (1.6 ng (2 min)-1 (10(6) cells)-1) was significantly reduced by dopamine (0.08 ng (2 min)-1 (10(6) cells)-1) but remained unchanged by somatostatin treatment. 4. The inhibitory effect of somatostatin on growth hormone release was dose dependent. This effect was not abolished by tetraethylammonium (40 mM) or 4-aminopyridine (5 mM), but somatostatin decreased high-potassium-induced release. 5. In all the cells recorded (n = 187), 14% (n = 26) displayed a low resting potential (less than -30 mV) and poor membrane resistance (less than 50 M omega). The recording was unstable and resting potentials decreased regularly to 0 mV in less than 5 min. The other 86% of the cells displayed resting potentials varying from -45 to -65 mV and had a membrane resistance of more than 150 M omega. Only cells which displayed these membrane characteristics showed clear responses to somatostatin or dopamine, and were therefore chosen for experiments. 6. In all the cells selected for the experiments (n = 161), 78% (n = 126) showed either triggered or spontaneous action potentials. The action potentials remained insensitive to sodium-free bath solution, but were reversibly blocked by the calcium channel blockers cobalt (5 mM) or nickel (5 mM). 7. When the cells were at resting potential, somatostatin induced a hyperpolarizing response associated with a decrease of membrane resistance. During this response, spontaneous or triggered action potentials were inhibited. The hyperpolarizing response induced by somatostatin was dose-dependent.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1989

Effects of chronic icv infusion of vasopressin on sleep-waking cycle of rats.

The effect of arginine vasopressin (AVP) on the duration and the relative proportion of sleeping and wakeful periods has been investigated. Vigilance states were determined by visual scoring of polygraphic recordings from unrestrained rats. Animals were implanted with a cannula into the third ventricle through which AVP or related drugs, dissolved in artificial cerebrospinal fluid, were infused at a constant rate by an osmotic pump. Polygraphic data were collected 24 h/day from day 4 to day 9. Recordings were continued for 3 additional days during AVP recovery. AVP infusions significantly increased the amount of time spent in waking compared with control or recovery periods (12%). This effect was mimicked by an AVP agonist (2-phenylalanine, 8-ornithine oxytocin). Oxytocin, a peptide structurally close to AVP, induced a mild change in waking time. The infusion of an AVP antagonist, 1-desaminopenicillamine-2-(O-methyl)tyrosine-arginine vasopressin (dPTyr(Me)AVP), or of anti-AVP antibodies significantly decreased duration of waking. The infusion of antioxytocin antibodies did not modify the duration of waking. The effects of structural analogues of AVP relatively specific for each type of peripheral AVP receptor indicated the participation of a V1-like AVP receptor in the action of AVP on waking time. During infusion of anti-AVP antibodies and dPTyr(Me)AVP and during the first days of recovery from AVP infusion, the ultradian rhythmic distribution of sleep and wakefulness was still present, but the amplitude of the circadian rhythm was reduced.

Animals↗
PubMed1989

Electrophysiological responses of rat pituitary cells in somatotroph-enriched primary culture to human growth-hormone releasing factor.

The in vitro effects of human growth hormone releasing factor (hGRF, 1-44) were studied in somatotroph-enriched cultures (75-85%) obtained from adult male rat pituitaries. Cells perifused with hGRF showed an up to 800% increase in growth hormone (GH) release over basal values in a dose-dependent manner. Calcium current blockers (5 mM of Co2+, Ni2+ or Cd2+) completely inhibited this stimulating effect but sodium-free (choline) medium did not. Using a single-intracellular-electrode recording technique, it was found that hGRF induced a dose-dependent depolarizing response concomitant with a decrease in membrane resistance in 38% of the cells recorded (98 of 258 cells). The reversal potential of this response was close to -40 mV. This depolarizing response was recorded in both excitable and unexcitable cells with no marked difference. Co2+ and Ni2+ (5 mM) completely and reversibly inhibited the membrane response to hGRF. Application of hGRF and somatostatin (SRIF), a hormone that inhibits GH release, to the same cell cultures showed the existence of two subpopulations: one was responsive to both hGRF and SRIF (53%, n = 62), another was only responsive to SRIF (47%, n = 62). Human GRF did not affect prolactin release and did not modify the electrical properties of cells responding to dopamine and therefore considered as lactotrophs. These results suggest that (1) hGRF leads to an increase in growth hormone release and a modification of membrane electrical properties by means of an extracellular Ca2+-dependent pathway, and (2) according to their responses to SRIF and hGRF, there are at least two subpopulations of somatotrophs.

Animals↗
PubMed1988

Electrophysiology and ultrastructure of mouse hypothalamic neurons in culture: a correlative analysis during development.

The development of the electrical activity of hypothalamic neurons in dissociated cell cultures obtained from 14 day old mice foetuses was studied using patch extracellular and intracellular recording techniques. Electrophysiological data were compared with morphological observations obtained by electron microscopy. During patch recording, excitability of the cells was tested by the application of a 40 mM KCl solution. Tetrodotoxin (TTX, 10(-6) M in the delivery pipette) and Co2+ (10(-2) M in the delivery pipette) were applied to the recorded cell by pressure in order to study the involvement of sodium and calcium currents in the electrical activity during the in vitro development. From the first day of incubation, TTX and Co2+ were able to block reversibly the spontaneous electrical activity. However, only TTX application inhibited action potentials which suggests that calcium currents could be poorly involved in the action potential generation at the beginning of neuronal differentiation. Three different phases were found in the electrophysiological development of hypothalamic neurons in culture. The first phase (between the 1st and the 5th day of incubation) was characterized by an increase in the ratio of the spontaneously active cells (15% at day 1 and 90% at day 5). This increase paralleled the increase of the ratio of excitable cells. During this period no post-synaptic activity was detected. Morphologically, at 36 h, no synaptic contact was observed and growth cones were found to be very primitive. The second phase, between the 6th and the 9th day of culture, was characterized by a decrease in the ratio of spontaneously active cells and by the appearance, in a few cases, of a postsynaptic potential activity. During this phase the majority of the silent cells were excitable. At this stage neurons formed well differentiated neurites and growth cones. Synaptogenesis had already started and several stages of synapse formation could be seen. The third phase of the development, from 10 days of incubation, was characterized by an increase in post synaptic potential activity. During this period, numerous mature synapses could be observed although most of the synaptic contacts were located on neurites. In addition, some synapses were apposed onto degenerated structures. In conclusion, hypothalamic neurons in culture appear to differentiate in 3 steps: a primitive stage during which spontaneous electrical activity and excitability develop without any synaptic contact; a 2nd stage during which synaptic contacts develop, followed by a third stage of synapse maturation where mature synapses are formed whereas transient synapses degenerate.

Action Potentials↗
PubMed1988

A study of ionic conductances involved in plateau potential activity in putative vasopressinergic neurons in primary cell culture.

Vasopressin neurons in hypothalamic cell culture display regenerative calcium-dependent plateau potentials. The present study was undertaken to investigate the mechanisms underlying their time course and periodicity. Intracellular recordings showed that the duration of the plateaux was controlled by a progressive activation of a voltage- and calcium-dependent potassium conductance, but not by a progressive inactivation of calcium conductances. The refractory period appeared to be due to a calcium-dependent potassium conductance activated by membrane potential depolarization.

Animals↗
PubMed1988

Location of angiotensin II binding sites on neuronal and glial cells of cultured mouse spinal cord: an autoradiographic study.

Cultures of mouse spinal cord were used to visualize binding sites for [125I]angiotensin II (AII) by autoradiography. Visualization by light microscopy shows that neurones, but also glial cells possess angiotensin II binding sites which are located both on soma and processes. These findings open a new field of investigation for the understanding of the physiological significance of AII in the CNS.

Angiotensin II↗
PubMed1988

Excitatory effect of noradrenaline on pacemaker cells in spinal cord primary cultures.

Intracellular recordings were made from dissociated fetal mouse spinal cord neurons in primary culture. One particular type of neuron, with a large cell body (40-50 micron) and three to five thick neurites, exhibited rhythmic electrical activity of two different types, consisting of either spontaneous burst discharges or tonic action potential firing. Both types of activity appeared to be triggered by an endogenous membrane potential oscillation. Micropressure application of noradrenaline (10(-5) M in the delivery pipette) onto the surface of such cells evoked, in a dose-dependent manner, an increase in the input resistance with a depolarization of the membrane potential. The response to NA was potential-dependent. The maximum change in input resistance was observed at membrane potential values between -60 mV and -45 mV and the response was suppressed at membrane potentials lower than -80 mV. No modification of the response was observed in the presence of 50 mM of tetraethylammonium. The extrapolated reversal potential, close to -90 mV, was modified by increasing extracellular K+ concentration and unaltered by increasing the intracellular Cl- concentration. The decrease in K+ conductance induced by noradrenaline was Ca2+-dependent and reversibly suppressed by Ba2+ (6 mM) and Cd2+ (0.1 mM). This response to noradrenaline was suppressed in the presence of muscarine (10 microM) suggesting that noradrenaline decreases a K+ conductance related to M current. The noradrenaline evoked increase in input resistance was mediated by activation of an alpha 1 receptor site. Prazosin, an alpha 1 antagonist and phentolamine, an alpha 1 alpha 2 antagonist, reversibly suppressed the response in a competitive manner. Yohimbine, a competitive alpha 2 antagonist, also blocked the response, but in a noncompetitive manner. Clonidine, an alpha 2 agonist, isoprenaline, a beta agonist and L-alprenolol, a beta antagonist, had no effect.

Action Potentials↗
PubMed1988

Synaptic and neuronal-glial plasticity in the adult oxytocinergic system in response to physiological stimuli.

Magnocellular oxytocinergic neurons in the hypothalamus offer a striking example of a mammalian neuronal system whose basic architecture and synaptic circuitry can be reversibly modified in adulthood. During parturition, lactation and prolonged osmotic stimulation, glial coverage of oxytocinergic neurons markedly diminishes and their surfaces are left in extensive juxtaposition; concurrently, there is formation of new synapses, which are predominantly GABAergic and which couple two or more oxytocinergic neurons simultaneously. These structural changes do not permanently modify the anatomy of the system since upon cessation of stimulation, neuronal juxtapositions and shared synapses disappear, to reappear upon new stimulation. At present, we can only speculate about the cellular mechanisms and factors responsible for these reversible neuroanatomical changes. However, oxytocin itself appears to be of primary importance since it can induce similar anatomical changes when chronically infused into the third ventricle.

Animals↗
PubMed1988

Role of central oxytocin in the control of the milk ejection reflex.

The neuropeptide oxytocin, synthetized by magnocellular neurons in the hypothalamus, is well known for its peripheral action after it is released into the bloodstream from axons in the neurohypophysis. Less familiar is the notion that it is also released centrally to control the activity of oxytocinergic neurons themselves. When injected into the third ventricle of lactating rats during suckling, oxytocin increases the basal firing rate of oxytocinergic neurons as well as their activity at the time of each reflex milk ejection. On the other hand, centrally administered oxytocin engenders the neuronal-glial and synaptic plasticity characteristic of the oxytocin system when it is physiologically activated. From numerous in vivo and in vitro observations, it appears that central oxytocin is released in the hypothalamic nuclei themselves. For example, the use of push-pull cannulae inserted into one supraoptic nucleus of suckled rats shows that oxytocin is released inside the nucleus specifically during milk ejection. Moreover, ultrastructural immunocytochemistry reveals synaptic terminals in the supraoptic nucleus where both the pre- and postsynaptic elements are oxytocinergic. Nevertheless, the mechanism of the central release of the neuropeptide has still to be determined, especially in view of electrophysiological observations indicating that the release process in the hypothalamus is different from that within the neurohypophysis.

Animals↗