Supraoptic Neurosecretory Neurons Research Articles

Involvement of N-methyl-D-aspartic acid receptor activation in oxytocin and vasopressin release after osmotic stimuli in rats.

The present study aimed to examine roles of N-methyl-D-aspartic acid (NMDA) receptors in oxytocin and vasopressin release after osmotic stimuli. A noncompetitive NMDA receptor antagonist, MK-801 (0.2 mg/kg body weight, i.p.), significantly decreased plasma concentrations of oxytocin and vasopressin after hypertonic saline injection (0.3 or 0.6 M NaCl, i.p., 20 ml/kg). By contrast, oxytocin release induced by injection of cholecystokinin octapeptide (20 microg/kg, i.p.) was not significantly changed by MK-801. Hypertonic saline injection increased the number of cells expressing Fos in the supraoptic nucleus and in the regions anterior and ventral to the third ventricle (AV3V) regions [the organum vasculosum of the lamina terminalis (OVLT) and median preoptic nucleus]. MK-801 decreased the number of cells expressing protein in these areas after hypertonic saline injection. A microdialysis method showed that a hypertonic saline injection (0.6 M NaCl, 20 ml/kg, i.p.) facilitated glutamic acid release in and near the OVLT. The results support the view that NMDA receptor in the AV3V region modulates in a facilitative fashion the AV3V inputs to the supraoptic neurosecretory neurones.

Involvement of N‐Methyl‐D‐Aspartic Acid Receptor Activation in Oxytocin and Vasopressin Release After Osmotic Stimuli in Rats

AbstractThe present study aimed to examine roles of N‐methyl‐D‐aspartic acid (NMDA) receptors in oxytocin and vasopressin release after osmotic stimuli. A noncompetitive NMDA receptor antagonist, MK‐801 (0.2 mg/kg body weight, i.p.), significantly decreased plasma concentrations of oxytocin and vasopressin after hypertonic saline injection (0.3 or 0.6 M NaCl, i.p., 20 ml/kg). By contrast, oxytocin release induced by injection of cholecystokinin octapeptide (20 µg/kg, i.p.) was not significantly changed by MK‐801. Hypertonic saline injection increased the number of cells expressing Fos in the supraoptic nucleus and in the regions anterior and ventral to the third ventricle (AV3V) regions [the organum vasculosum of the lamina terminalis (OVLT) and median preoptic nucleus]. MK‐801 decreased the number of cells expressing protein in these areas after hypertonic saline injection. A microdialysis method showed that a hypertonic saline injection (0.6 M NaCl, 20 ml/kg, i.p.) facilitated glutamic acid release in and near the OVLT. The results support the view that NMDA receptor in the AV3V region modulates in a facilitative fashion the AV3V inputs to the supraoptic neurosecretory neurones.

Excitatory peptides and osmotic pressure modulate mechanosensitive cation channels in concert.

Behavioral and neuroendocrine responses underlying systemic osmoregulation are synergistically controlled by osmoreceptors and neuropeptides released within the hypothalamus. Although mechanisms underlying osmoreception are understood, the cellular basis for the integration of osmotic and peptidergic signals remains unknown. Here we show that the excitatory effects of angiotensin II, cholecystokinin and neurotensin on supraoptic neurosecretory neurons are due to the stimulation of the stretch-inactivated cation channels responsible for osmoreception. This molecular convergence underlies the facilitatory effects of neuropeptides on responses to osmotic stimulation and provides a basis for the gating effects of plasma osmolality on the responsiveness of osmoregulatory neurons to peptidergic stimulation.

717 Expression of dna topoisomerase 11 β increases in the supraoptic neurosecretory neurons after water deprivation

717 Expression of dna topoisomerase 11 β increases in the supraoptic neurosecretory neurons after water deprivation

GABA receptor mediation of median preoptic nucleus‐evoked inhibition of supraoptic neurosecretory neurones in rat.

1. This study evaluated the influence of focal electrical and chemical microstimulation in the median preoptic nucleus (MnPO) on the excitability of putative vasopressin and oxytocin neurones recorded in the supraoptic nucleus of urethane- or pentobarbitone-anaesthetized rats. 2. In vasopressin neurones, single 1 Hz stimulation reduced the excitability of 120/139 cells. Trains of repetitive 5-30 Hz stimulation, or microinfusion of glutamate into the MnPO, similarly induced a cessation in spontaneous phasic or continuous firing in 17/18 and 17/20 vasopressin neurones, respectively. In 20/21 cells, locally applied bicuculline (100 microM) attenuated MnPO-evoked depressant responses whereas strychnine (100 microM) and timolol (20 microM) were without effect on 5/5 vasopressin neurones. In three cells, bicuculline applications were associated with marked increases in MnPO-evoked excitations. 3. In oxytocin neurones, single-pulse (1 Hz) electrical stimulation in MnPO evoked an increase in the excitability in 51/59 cells. However, in 6/7 oxytocin cells tested, glutamate microinfusions into MnPO induced prolonged suppression in firing. During trains of stimuli (5-30 Hz), 26/44 cells displayed an initial increase in firing associated with the first few impulses but this was then replaced by suppression of activity; another ten cells displayed excitation alone, and eight cells demonstrated only suppression. The depressant responses evoked during trains of MnPO stimulation were blocked by 100 microM bicuculline (6/6 cells tested) whereas strychnine was ineffective (2/2 cells tested). 4. These results suggest that the MnPO provides a mainly depressant influence on supraoptic vasopressin and oxytocin neurones, perhaps through the activation of postsynaptic GABAA receptors.

N-methyl- d-aspartate receptor antagonist ketamine selectively attenuates spontaneous phasic activity of supraoptic vasopressin neurons in vivo

Supraoptic neurosecretory neurons express a prominent N-methyl- d-aspartate receptor system. Recent in vitro evidence reveals that N-methyl- d-aspartate receptor activation dramatically alters the spontaneous discharge patterns of supraoptic neurons. In this study we evaluate whether N-methyl- d-aspartate receptors in vivo contribute to the development of characteristic phasic discharge patterns displayed by vasopressin-secreting neurons. Intravenous administration of ketamine hydrochloride, a non-competitive N-methyl- d-aspartate receptor antagonist, was used to examine whether N-methyl- d-aspartate receptor blockade influences patterned spontaneous discharge observed in supraoptic neuro-secretory neurons. Extracellular recordings were obtained from identified hypothalamic supraoptic neurons in pentobarbital-anaesthetized Long-Evans rats. Systemic administration of ketamine (≤1.5 mg/kg) potently suppressed spontaneous phasic discharge in 16/19 putative vasopressin-secreting cells. The ketamine-induced blockade was dose dependent, fully reversible and was associated with the complete blockade of activity evoked by local pressure application of N-methyl- d-aspartate, but not the activity evoked by α-amino-3-hydroxy-5-methyl-isoxazole-4-propionate receptor agonists (6/6 cells). Ketamine had no detectable effect on threshold or shape of antidromic action potentials. By comparison, the activity in 9/10 continuously active neurons (putative oxytocin-secreting) was unaffected by administration of identical doses of ketamine. These data suggest that N-methyl- d-aspartate receptors play an important role in regulating the onset and maintenance of spontaneous phasic activity patterns displayed by rat supraoptic vasopressin neurons in vivo.

Long-latency baroreceptor inhibition of supraoptic neurones in the cat.

Experiments were done to determine the central delay to inhibition of supraoptic neurosecretory neurones by carotid baroreceptors in chloralose-anaesthetised, paralysed cats. Fourteen out of 18 neurosecretory cells (identified by antidromic activation from the pituitary neural lobe) were tested for their response to inflation of the ipsilateral carotid sinus (prepared as a blind sac). This stimulus inhibited the spontaneous activity of 10 neurones, which were thus identified as putative vasopressin cells. Repetitive, precisely timed pressure pulses were delivered to the carotid sinus and used to construct post-stimulus histograms of this inhibition. The latency measured from the baroreceptor afferent barrage (recorded from the sinus nerve) to the onset of inhibition in supraoptic neurones was 251 +/- 58 ms (range 152-328, n = 10). The significance of this long latency for the neural pathways involved is discussed.

Apamin and d-tubocurarine block the afterhyperpolarization of rat supraoptic neurosecretory neurons.

Magnocellular neurosecretory cells (MNCs) were impaled in perfused explants of rat hypothalamus. Evoked bursts of spikes were followed by an afterhyperpolarization (AHP) lasting 1-2 s. In each of 22 cells this AHP was selectively suppressed by low nanomolar concentrations of apamin (IC50 = 1.3 nM) or micromolar concentrations of d-tubocurarine (IC50 approximately 40 microM). Blockade of the AHP was accompanied by a decrease in spike accommodation and an unmasking of the late depolarizing afterpotential which induces burst firing in MNCs. Modulation of the Ca2+-dependent K+ (AHP) conductance by an endogenous apamin-like ligand could play an important role in the control of firing rate and pattern in MNCs.

Characterization of spontaneous and evoked inhibitory postsynaptic potentials in rat supraoptic neurosecretory neurons in vitro

Intracellular recordings from 52 supraoptic nucleus neurosecretory neurons in perfused explants of rat hypothalamus revealed abundant spontaneous inhibitory postsynaptic potentials (sIPSPs) and a compound evoked inhibitory postsynaptic potential (eIPSP) following electrical stimulation in the diagonal band of Broca (DBB). These IPSPs were characterized in terms of the magnitude and ionic specificity of the underlying current and in terms of the transmitter responsible for their activation. sIPSPs rose rapidly to peak within 3-5 ms and decayed exponentially with a mean time constant of 20.2 +/- 1.9 ms (mean +/- SE), a value 1.6-fold greater than the mean cell time constant of 13.8 +/- 1.0 ms. The eIPSPs rose rapidly to peak within 3-10 ms and decayed exponentially over 60-100 ms with a mean time constant of 37.0 +/- 2.8 ms, which is 2.6-fold greater than the mean cell time constant. These features imply a brief persistence of the conductance underlying the IPSPs. In recordings with KAcetate-filled micropipettes, sIPSPs were hyperpolarizing at membrane potentials in the range of -50 to -70 mV and reversed polarity when the membrane was hyperpolarized beyond -80 mV. The mean reversal potential (EsIPSP) was -72.4 +/- 1.1 mV. eIPSPs were hyperpolarizing at resting membrane potential and could be reversed by membrane hyperpolarization beyond a mean reversal potential (EIPSP) of -67.4 +/- 1.4 mV. In recordings with KCl-filled micropipettes, sIPSPs were depolarizing at all membrane potentials more negative than -50 mV. Under these conditions, EsIPSP was estimated at -44 mV. sIPSPs were absent when chloride ions were removed from the perfusion medium. eIPSPs were depolarizing at all membrane potentials and often evoked action potentials; mean EeIPSP was 43.2 mV. Reversal potentials of spontaneous and evoked IPSPs were similar. At a given membrane potential, sIPSP amplitudes varied widely between 1 and 20 mV. The conductance increase underlying individual sIPSPs was estimated to vary between 0.17 and 3.0 nS (avg 0.6 nS) against a mean resting input conductance of 3.78 +/- 0.41 nS. Estimates of the conductance underlying eIPSPs varied widely between cells, from 0.8 to 22.0 nS (mean 72 nS). Accordingly, the ratio of evoked to spontaneous IPSP conductance varied from 1.6 to 43.7 (mean 13.1). The reversal potential of evoked IPSPs shifted with the extracellular concentration of Cl- ions ([Cl-]0) with a mean slope of 41 mV/log [Cl-]0.(ABSTRACT TRUNCATED AT 400 WORDS)

Non-synaptic depolarizing potentials in rat supraoptic neurones recorded in vitro.

Intracellular recordings obtained from eighty-two supraoptic nucleus neurones in perfused explants of rat hypothalamus revealed a mean resting membrane potential of -66 +/- 5 mV (S.D.) and spike amplitudes of 70-106 mV. When recorded with K acetate-filled micropipettes, non-spike membrane voltage fluctuations included spontaneous depolarizing and hyperpolarizing potentials. Spontaneous hyperpolarizing potentials peaked in 3-5 ms and decayed exponentially with a mean time constant of 20.2 +/- 0.1 ms, 1.6 times the membrane time constant of 13.8 +/- 0.1 ms. These potentials were identified as spontaneous inhibitory post-synaptic potentials, and all demonstrated a common reversal potential near -80 mV, a depolarizing shift of this reversal potential during intracellular Cl- accumulation, and reversible blockade by raising [Mg2+] to 15 mM in the perfusate. Depolarizing potentials with features typical of spontaneous excitatory post-synaptic potentials i.e. brief (8-20 ms) depolarizing transients, were rarely recorded with K acetate-filled micropipettes. Instead, most neurones demonstrated what are termed non-synaptic depolarizing potentials (n.s.d.p.s) lasting 20-125 ms (mean 86.4 +/- 8.6 ms (S.E. of mean)) with a rise time 21.1 +/- 2.8 ms and a decay time of 16.3 +/- 2.8 ms (n = 28 measured). Unlike typical spontaneous post-synaptic potentials, these events could sustain a constant peak amplitude for most of their duration. These n.s.d.p.s displayed a strong voltage-dependent behaviour and were detected only at membrane potentials within 5-7 mV of the threshold for spike initiation. Spontaneous slow depolarizing membrane shifts preceding or following phasic bursts, or any manipulation (e.g. current step, sinusoid, depolarizing after-potential) causing the membrane potential to enter this range of activation, prompted their appearance. N.s.d.p.s were completely insensitive to the presence of 15 mM-Mg2+ but they were reduced in size and frequency when Ca2+ were replaced with Co2+ or Mn2+. They were detected at a more positive membrane potential when Na+-dependent action potentials were blocked with tetrodotoxin. The size, voltage-dependent and non-synaptic nature of these depolarizing potentials raises the possibility that they reflect the activity of individual (or small clusters of) ionic channels carrying inward current. Their ability to serve as prepotentials to trigger spikes is deemed to be particularly important for promoting the onset of phasic bursts in supraoptic neurosecretory neurones.

Synergistic activation of rat supraoptic neurosecretory neurons by noxious and hypovolemic stimuli.

The effects of saphenous nerve stimulation on discharge activity of supraoptic neurosecretory (NS) cells were studied in anesthetized rats. Of 112 supraoptic neurosecretory cells, 62 exhibited a 'phasic' discharge pattern. The nerve stimulation transiently excited 46 of these 62 'phasic' units, as well as 35 of the 50 remaining 'non-phasic' units. No appreciable blood pressure change was noted using PSTHs with 1-ms resolution. Though the nerve stimulation also evoked a flexor reflex of the ipsilateral hind limb, blockage of the hind limb movement with gallamine did not alter the amplitude of the supraoptic cell excitation. The threshold of the nerve stimulation was higher for the excitation than for the flexor reflex. Effects of hypovolemic and hyperosmotic stimuli on discharge activity of 'phasic' cells during saphenous nerve stimulation were studied to find a possible interaction between these stimuli. Hemorrhage potentiated the transient excitation evoked by the nerve stimulation in all of the 8 'phasic' cells tested, while no such effect was seen after an injection of hypertonic sodium chloride solution in the 7 'phasic' cells tested. These electrophysiological data suggest that hypovolemic and noxious stimuli potentiate VP secretion in a synergistic manner but that hyperosmotic and noxious stimuli do not.

Diagonal band neurons may mediate arterial baroreceptor input to hypothalamic vasopressin-secreting neurons

Diagonal band of Broca (DBB) neurons projecting to the hypothalamic supraoptic neurosecretory neurons were antidromically identified in pentobarbital-anesthetized male Long-Evans rats. Six of 12 DBB neurons tested for response to baroreceptor activation showed a consistent increase in firing. We propose that the established baroreceptor-induced inhibition of hypothalamic vasopressinergic neurons is mediated through DBB neurons.

Evidence for excitatory actions of histamine on supraoptic neurons in vitro: Mediation by an H 1-type receptor

The effects of histamine on the firing of supraoptic neurosecretory neurons in the rat were examined in vitro using acutely prepared, hypothalamo-neurohypophysial explants perifused with an artificial cerebrospinal fluid. Extracellular action potentials meeting the criteria of antidromic invasion from neurohypophysial stalk stimulation were recorded from 135 neurons in the tuberal portion of the supraoptic nucleus, which lies superficially along the tuber cinereum and consists of mostly vasopressincontaining neurons. Units could be classified as slow/silent (76.3%), phasic (21.5%) or continuous (2.2%) on the basis of their spontaneous activity. Histamine applied briefly to the perifusate excited approximately one-third of the slow silent neurons and approximately two-thirds of the phasic neurons, with a wide range (10 −3-10 −9) in the effective concentration across neurons. The H 1-receptor agonists 2-pyridylethylamine and 2-thiazolylethylamine mimicked these excitations in 10 of 12 and 3 of 6 neurons tested, respectively. The H 2-receptor agonists dimaprit (4 neurons) and impromidine (5 neurons) failed to excite any of the tested neurons previously excited by histamine. The H 1-receptor antagonist promethazine antagonized histamine's excitatory effect in 8 of 9 cells, while the H 2-receptor antagonist cimetidine had little effect on the 9 cells tested. Histamine also modified bursts of activity induced in some slow/silent neurons by antidromic stimulation without having an observable effect in the absence of an antidromic burst. In 10 of 18 neurons histamine produced an elongation of burst duration and a modest increase in intraburst firing rate when applied during an antidromically evoked burst. In an additional 5 of 17 neurons, which had neither previously responded to histamine nor shown an antidromically-evoked burst, the pairing of histamine application and antidromic shocks resulted in an antidromically evoked burst. The effects of histamine on evoked bursts also appeared to be mediated by an H 1-receptor. Histamine's excitation of supraoptic neurons is thus dependent on the electrical activity expressed by the neuron at the time of testing. Conductances activated by depolarization of the neuron may be modified by histamine or this compound may alter the threshold for burst generation. Considered with data showing H 1-receptor localization and histamine-immunoreactive fibers within the supraoptic nucleus, the present results, as well as those showing the potency of centrally applied histamine in releasing vasopressin, suggest histamine may act physiologically by altering the electrical activity of vasopressin-secreting neurons.

Calcium-dependent action potentials in rat supraoptic neurosecretory neurones recorded in vitro.

Intracellular recordings obtained from thirty-nine supraoptic nucleus neurones in perfused hypothalamic explants displayed a mean resting membrane potential of -69 mV and spike amplitude of 79 mV. Voltage-current plots were linear in the hyperpolarizing direction and revealed a mean slope resistance of 197 M omega. After Na+ channel blockade with tetrodotoxin (TTX; 0.3-16 microM), the voltage-current relationship did not change significantly for hyperpolarizing pulses. An increase in spike threshold in TTX permitted visualization of a reduction in slope resistance to depolarizing current pulses. This rectification was reduced by the addition of the Ca2+ channel blockers Cd2+, Co2+ or Mn2+. High threshold TTX-resistant spikes with amplitudes ranging between 25 and 64 mV were evoked in an all-or-none manner by brief intracellular current pulses applied above 1.0 Hz. Current pulses presented at lower frequencies (less than or equal to 0.5 Hz) evoked graded responses. In seventeen of nineteen cells, prolonged depolarizing current pulses elicited repetitive firing of TTX-resistant spikes with a progressive increase in their amplitude, rise and fall times and after-hyperpolarizations. TTX-resistant spikes were reversibly abolished when CaCl2 was replaced by equimolar amounts of EGTA or by the addition of either Cd2+, Co2+ or Mn2+ to the perfusion medium. In artificial medium containing EGTA, both the shoulder on the repolarization phase of the spike and the subsequent after-hyperpolarization were reversibly abolished. Tetraethylammonium (TEA; 2-5 mM) induced prolongation of mean action potential durations from 1.9 to 12.3 ms (nineteen cells); in TTX, TEA also prolonged the duration and increased the over-all peak amplitude of the TTX-resistant (Ca2+) spike. While TEA also enhanced the amplitude of the Na+ spike, no comparable prolongation in spike duration was observed. These data indicate that somatic action potentials of supraoptic nucleus cells arise from the co-activation of a low threshold Na+ conductance and a higher threshold Ca2+ conductance; the latter is expressed as a shoulder on the repolarization phase of the action potential.

Activity dependence of action potential duration in rat supraoptic neurosecretory neurones recorded in vitro.

Action potential durations, measured at one-third peak amplitude, were examined during intracellular recordings in 134 supraoptic nucleus neurones maintained in vitro in perfused hypothalamic explants. Spike durations ranged between 1.2 and 3.9 ms and were dependent on firing frequency. Shortest measurements (1.74 +/- 0.03 ms; mean +/- S.E. of mean) were obtained during relative quiescence, i.e. less than or equal to 0.5 Hz. A gradual increase in firing frequency through continuous injection of depolarizing current prolonged spike duration, with maximum levels (2.68 +/- 0.05 ms) achieved at 20 Hz. When interspike interval variability was eliminated and firing was more precisely regulated by brief 15-20 ms intracellular current pulses given at pre-determined frequencies, a proportional relationship between increasing spike duration and firing frequency was retained but the change in spike duration at frequencies between 2 and 10 Hz was less pronounced. Once action potentials had achieved the long duration configuration, their return to the shorter duration took place gradually during any succeeding silent interval with a time constant of 4.9 s. Action potential broadening occurred progressively and was most pronounced at the onset of spontaneous or current-induced bursts. In thirty-six phasically active neurones, spike broadening at the onset of a burst was concurrent with the presence of 5-10 consecutive short (less than or equal to 100 ms) interspike intervals; thereafter, despite a greater than 50% reduction in firing frequency, action potential durations remained prolonged throughout the burst. In all of nineteen cells tested, frequency-dependent changes in spike duration were reversibly decreased or blocked by Cd2+, Co2+ and Mn2+, or when CaCl2 was exchanged for equimolar amounts of EGTA in the perfusion medium. These observations indicate that a Ca2+ conductance contributes to frequency- and firing-pattern-dependent changes in spike duration in rat supraoptic nucleus neurones.

Ultrastrukturelle veränderungen des supraoptico-neurohypophysären systems nach läsion des hypophysenstiels bei der ratte

Fine structural changes occurring in the supraoptic nucleus and the neural lobe have been studied in rats following the electrolytic lesion of the hypophysial stalk. Supraoptic neurosecretory neurones undergo a typical chromatolytic reaction. In addition, proliferating microglial cells disconnect axosomatic synapses and phagocytose degenerating neurones. Surviving neurones show signs of structural restitution 3 to 4 weeks after surgery. In the neurohypophysis degeneration of secretory nerve endings started with the disintegration of secretory vesicles 3 to 4 d postoperatively. Degenerated axon terminals were engulfed by pituicytes. Signs indicative of axonal regeneration were not observed in the neural lobe up to the end of the 4th postoperative week.

α-Adrenergic activation of rat hypothalamic supraoptic neurons maintained in vitro

Extracellular recordings from 141 rat supraoptic nucleus neurons maintained in vitro in a perfused hypothalamic explant indicated that the excitability of 85% of cells was enhanced by the addition of 10–200 μM norepinephrine (NE) and the α-agonist methoxamine (MOXY), but not by isoproterenol, to the perfusion medium or by pressure application. Similar responses were observed from 7 cells maintained in synaptic isolation in medium containgng 15 mM Mg 2+. At the lowest effective concentration (10 μM), NE and MOXY induced bursting activity without an overall increase in firing frequency; at higher concentrations an initial increase in firing frequency was followed by the appearance of phasic activity patterns. The actions of NE and MOXY were reversibly blocked by administration of the α-adrenergic antagonists phenoxybenzamine (1–10 μM), yohimbine (> 10 μM) and irreversibly blocked by prazosin (10 nM−1 μM). These observations suggest that NE has a predominatly facilitatory role to enhance the excitability and promote bursting activity in supraoptic neurosecretory neurons through an α-1 adrenoreceptor mechanism.

Effect of cooling on supraoptic neurohypophysial neuronal activity and on urine flow in the rat.

The activity of antidromically identified supraoptic neurosecretory neurones was recorded in Sprague-Dawley rats under urethane or sodium pentobarbitone anaesthesia during cooling of the body with a cold pack. Of twelve phasic neurones studied during a complete cooling and rewarming cycle, six displayed an initial increase, followed by a depression in activity during the period of reduced body temperature. The remaining six phasic neurones did not alter their activity during cooling. Non-phasic neurohypophysial neurones displayed a reversible reduction (n = 8), or increase (n = 6) in activity during cooling, while seven neurones were unaffected by changes in body temperature. In four other anaesthetized Sprague-Dawley rats, urine flow was reduced by approximately 50% during cooling; this was followed by a diuresis after removal of the cold pack and return of body temperature to normal. The antidiuresis did not occur in homozygous Brattleboro rats which lack arginine vasopressin. The electrophysiological data from a proportion of the supraoptic neurohypophysial neurones correlate with the observed changes in urine flow.

Terminal degeneration in supraoptic nucleus following subfornical organ lesions: ultrastructural observations in the rat

A projection from the subfornical organ (SFO) to the supraoptic nucleus, recently identified in light microscopic studies, was examined at the ultrastructural level following lesions in SFO. After 18–36 h, axon terminal degeneration was identified in axosomatic contacts with supraoptic neurosecretory neurons, and in axodendritic contacts within and around the supraoptic nucleus. These observations confirm a monosynaptic pathway from SFO to supraoptic neurosecretory neurons that may participate in the release of vasopressin following activation of angiotensin II receptors in SFO.

Amygdalar inputs to ADH-secreting supraoptic neurones in rats.

Effects of amygdala stimulation on the discharge activity of antidromically identified supra-optic neurosecretory neurones were studied in male rats anaesthetized with urethane. Stimulation of the medial and the basal amygdala produced excitation or inhibition of discharge activity both in phasically firing ("phasic") and in continuously firing ("continuous") neurones. More "phasic" neurones were excited than were inhibited after medial amygdala stimulation. On the other hand, fewer "continuous" neurones were excited by stimulation of the either amygdala area than were inhibited. This difference of responsiveness between "phasic" and "continuous" neurones is statistically significant. Synaptic inputs to supraoptic neurosecretory neurones after amygdala stimulation were also observed in rats with a lesion of the stria terminalis. Supraoptic nucleus stimulation activated antidromically 14 of the 336 amygdala neurones tested. Since "phasic" neurones have been identified as ADH-secreting neurones, it is concluded that ADH-secreting neurones in the rat supraoptic nucleus receive predominantly excitatory synaptic inputs from the medial amygdala and these amygdalar synaptic inputs are mediated by pathways which are at least in part monosynaptic and are not included in the stria terminalis.