Oxytocin and vasopressin neurones: vive la différence!
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Animals↗
Biomedical subjects
G I Hatton
Publications and source records attributed to G I Hatton.
Ca2+ release from internal stores: role in generating depolarizing after-potentials in rat supraoptic neurones.
1. Influences of Ca2+ release from internal stores on the generation of depolarizing after-potentials (DAPs) were investigated in magnocellular neurones of rat supraoptic nucleus (SON) using whole-cell patch recording techniques in brain slices. 2. DAPs were recorded from more than half of the cells encountered, and following evoked single spikes had an amplitude of 3.00 +/- 0.19 mV (mean +/- S.E.M.) and lasted for 1.02 +/- 0.06 s. Their sizes usually increased with the number of preceding spikes, but could be reduced or eliminated when intervals between consecutive current pulses evoking tens of spikes were short. 3. DAPs were eliminated by removal of external Ca2+, and significantly reduced by bath application of nifedipine or omega-conotoxin. 4. Blockade of Ca2+ release from internal stores by perifusion with ryanodine or dantrolene, or direct diffusion of Ruthenium Red into cells suppressed DAP amplitudes by approximately 50% and shortened their durations. 5. Depletion of internal Ca2+ stores by perifusion with thapsigargin or cyclopiazonic acid also reduced DAP amplitudes by approximately 50% and eliminated phasic patterns of firing. 6. Caffeine, an agent known to enhance intracellular Ca2+ release, amplified DAPs and promoted phasic firing. 7. These results suggest that Ca2+ influx via high-voltage-activated Ca2+ channels in SON cells triggers ryanodine receptor-mediated Ca2+ release from internal stores. This process enhances DAPs and promotes phasic firing in SON cells, and would thus contribute to vasopressin release.
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Function-related plasticity in hypothalamus.
Physiological activation of the magnocellular hypothalamo-neurohypophysial system induces a coordinated astrocytic withdrawal from between the magnocellular somata and the parallel-projecting dendrites of the supraoptic nucleus. Neural lobe astrocytes release engulfed axons and retract from their usual positions along the basal lamina. Occurring on a minutes-to-hours time scale, these changes are accompanied by increased direct apposition of both somatic and dendritic membrane, the formation of dendritic bundles, the appearance of novel multiple synapses in both the somatic and dendritic zones, and increased neural occupation of the perivascular basal lamina. Reversal, albeit with varying time courses, is achieved by removing the activating stimuli. Additionally, activation results in interneuronal coupling increases that are capable of being modulated synaptically via second messenger-dependent mechanisms. These changes appear to play important roles in control and coordination of oxytocin and vasopressin release during such conditions as lactation and dehydration.
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Oscillatory bursting of phasically firing rat supraoptic neurones in low-Ca2+ medium: Na+ influx, cytosolic Ca2+ and gap junctions.
1. Whole-cell patch recordings were obtained from supraoptic nucleus (SON) neurones in horizontal brain slices of adult male rats. Low-Ca2+ or Ca(2+)-free perifusion medium induced oscillatory bursting activity in all sixty-nine cells displaying both phasic firing and depolarizing after-potentials (DAPs). In fifteen non-phasic cells without DAPs, Ca(2+)-free medium produced little or no oscillatory bursting. 2. Typical bursts started with rapid membrane depolarization, resulting in a plateau with superimposed action potentials, and ended several hundred milliseconds later in swift repolarization. Prominent bursting was observed at membrane potentials from -50 to -70 mV, with maximum amplitudes of 12.2 +/- 0.7 mV (mean +/- S.E.M.) around -70 mV. Development of oscillatory bursting was dependent on reduction of [Ca2+]o, with a threshold for the bursting < or = 1.2 mM Ca2+. 3. Bursting was abolished by addition of TTX, Co2+, Ni2+ or Mg2+ into the Ca(2+)-free medium, or by replacement of external Na+ with choline or Li+. Low concentrations of TEA or increased [K+]o prolonged burst durations and enlarged oscillation amplitudes. 4. Voltage-clamp techniques were used to examine the persistent Na+ current (INaP), and revealed that low [Ca2+]o shifted the threshold for INaP activation in a negative direction and enhanced the amplitude of this current. These changes in INaP were abolished by adding Co2+ or Mg2+ to Ca(2+)-free medium. 5. Direct diffusion of BAPTA or heparin into neurones or bath application of ryanodine suppressed bursting. Oscillations were also eliminated by the uncoupling agents heptanol, halothane or acidification. 6. CNQX, APV, bicuculline, CGP35348 (GABAB receptor antagonist), promethazine, atropine, d-tubocurarine and suramin had no obvious effects on oscillatory bursting. Blockers of transient Ca2+, or hyperpolarization-activating cation currents also did not alter bursting activity. 7. These results suggest that intrinsic burst activity in SON neurons perifused with low-Ca2+ or Ca(2+)-free medium involves enhanced Na+ influx through persistent Na+ channels, and requires the presence of rapid intracellular Ca2+ mobilization that might also explain the selective existence of oscillatory bursting in phasically firing cells. Intercellular communication through gap junctions appears to be important in determining neuronal activity of the neuroendocrine cells in low-Ca2+ medium.
Action Potentials↗
Differential responses of oxytocin and vasopressin neurons to the osmotic and stressful components of hypertonic saline injections: a Fos protein double labeling study.
Expression of Fos protein, detected immunocytochemically, was used to assess the relative responses of supraoptic nucleus (SON) oxytocin- (OX) and vasopressin- (VP) containing neurons to the osmotic vs. the osmotic plus stressful components of intraperitoneal hypertonic saline injections. The percentage of SON neurons showing Fos-like immunoreactivity (Fos-ir) was quantified for rats receiving general anesthesia only, anesthesia 1 h prior to either isotonic or hypertonic saline injection or no anesthesia prior to hypertonic injection. Hypertonic saline injection with and without anesthesia induced Fos-ir in 66% and 77% of SON neurons, respectively, whereas isotonic saline with anesthesia and anesthesia alone resulted in 15% and 13%, respectively, of cells showing Fos-ir. Double labeling for Fos-ir and either OX-ir or VP-ir resulted in quantitatively different responses to hypertonic injections with and without anesthesia in OX-ir and VP-ir neurons. The VP-ir neuronal response was similar under the two conditions: 49% and 48% of VP cells displaying Fos-ir with and without prior anesthesia, respectively. By contrast, a higher percentage of OX-ir neurons was found to exhibit Fos-ir without (68%) than with (53%) anesthesia. Thus, a greater percentage of neurons was induced to express Fos-ir when the stressful components of the hypertonic injection were unattenuated by anesthesia, and this difference was entirely due to increased numbers of responding OX neurons. These data indicate that, under these experimental conditions, SON OX neurons respond in larger numbers to the osmotic components of hypertonic saline injections and have a greater responsiveness than do VP neurons to the stressful components.
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Histamine-induced prolonged depolarization in rat supraoptic neurons: G-protein-mediated, Ca(2+)-independent suppression of K+ leakage conductance.
Ionic mechanisms responsible for histamine-induced prolonged depolarization in supraoptic nucleus neurons were investigated using whole-cell patch recordings in horizontally prepared brain slices from adult male rats. Bath application of histamine (1-10 microM) in control medium induced membrane depolarization in nine of 12 phasically firing, putative vasopressin cells, but not in continuous firing, putative oxytocin cells (none of five cells). Depolarization, usually accompanied by increased firing rate, started within 20 s after histamine reached the slices, lasting for 3-13 min, after which they repolarized, and this was repeatable upon washout. Chelation of intracellular Ca2+ with 11 mM 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetra-acetate and perfusion of slices with Ca(2+)-free medium blocked neither histamine-induced membrane depolarizations nor increased firing rates in 24 of 30 cells recorded. Depolarizations were always associated with decreases in membrane conductance. Following treatment with promethazine (H1 receptor antagonist) in six cells excited previously by histamine, subsequent application induced neither membrane depolarization nor increased firing. H1 receptor agonists mimicked histamine-induced depolarization (four of six cells) but the H2 receptor agonist, dimaprit (10 microM), had no effect (all of nine cells). In medium containing 0 mM Ca2+, 2 mM Co2+ and 1-2 microM tetrodotoxin, with internal Ca2+ chelation, bath application of histamine induced an apparent inward current in 15 of 20 supraoptic neurons tested. The peak of inward current evoked by 1-10 microM histamine at holding potentials around -50 mV varied from 10 to 50 pA (27.3 +/- 0.3 pA, mean +/- S.E.M.). Ramp voltage tests revealed that this inward current decreased as membrane potential was hyperpolarized and had a reversal potential of -90.1 +/- 3.8 mV (n = 10). Subtraction of current obtained before from that during histamine application revealed a current that was linear against membrane potential. Increasing external K+ concentration or introduction of K+ channel blockers in the medium attenuated or abolished histamine-induced inward current at membrane potentials close to -50 mV. When external Cl- concentration was reduced, histamine-induced inward current was still seen in five of seven supraoptic cells tested. Neither inward current nor change in conductance was observed following bath application of histamine in 11 of 12 neurons recorded using patch pipettes containing guanosine 5'-O-(2-thiodiphosphate), and in seven of eight neurons using pipettes containing guanosine 5'-O-(3-thiotriphosphate). These results suggest that histamine depolarizes supraoptic neurons, at least in part, by inhibiting a K+ leakage current mediated by H1 receptors linked to GTP-binding proteins and Ca(2+)-independent pathways. This study provides initial evidence for the second messengers regulating K+ leakage current.
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Connexin 32 mRNA levels in the rat supraoptic nucleus: up-regulation prior to parturition and during lactation.
Toward the end of pregnancy, mammalian mothers undergo a cascade of hormonal, neural and somatic events that culminate in birth and lactation. Milk ejection, the final step in lactation, is regulated by high-frequency, synchronized firing of oxytocinergic neurons in the magnocellular nuclei of the hypothalamus. This synchronization of neural activity may be regulated by an increase in the cell-to-cell coupling of magnocellular neurons by connexins. Direct intercellular channels between neurons are formed by the connexin 32 protein. The present study examined the pattern of connexin 32 mRNA levels using semiquantitative in situ hybridization histochemistry with isotopically labeled cRNA probes complementary to connexin 32 and connexin 43, found in neurons/oligodendrocytes and astrocytes, respectively. Connexin 32 mRNA levels were relatively low in the supraoptic nucleus of virgin females and were dramatically up-regulated during late pregnancy. Immediately after birth, connexin 32 mRNA levels dropped and were similar to levels in virgins. On the 13th day of lactation when dye-coupling between magnocellular neurons is high, connexin 32 message levels were again very high. Levels of the astrocytic connexin 43 were no different in lactating and virgin animals. These results demonstrate that there are two peaks of connexin 32 expression, one immediately preceding parturition and one during lactation. So far, only the second peak of connexin 32 is known to be related to an increase in dye-coupling of magnocellular neurons in the supraoptic nucleus, suggesting that in this case, the elevation of connexin 32 message levels leads to the subsequent increase in intercellular coupling.
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Synaptically released histamine increases dye coupling among vasopressinergic neurons of the supraoptic nucleus: mediation by H1 receptors and cyclic nucleotides.
Activating direct olfactory (glutamatergic) inputs to supraoptic nucleus (SON) neurons increases interneuronal coupling in slices from lactating but from not virgin or male rats. Studied here were influences on coupling of another monosynaptic input to SON, the histaminergic tuberomammillary nucleus (TM) projection, activation of which selectively excites phasically firing (putative vasopressin) cells. Effects of TM stimulation and its possible downstream consequences on Lucifer yellow (LY) dye coupling among putative vasopressin cells were determined in male rat SONs. In unstimulated slices, 12 LY injections (1 cell/SON) yielded eight single and four pairs of coupled neurons. In slices in which TM was stimulated for 10 min at 10 Hz, 13 injections yielded 4 single and 28 coupled cells, with groups of 2 to 4 cells coupled to the injected neuron, a threefold increase in the number of coupled cells per injection (p < 0.02). Bathing slices in medium containing 10 microM pyrilamine (H1 antagonist) blocked this stimulation-induced coupling increase, suggesting mediation by activation of guanylate cyclase-cGMP to which H1 receptors often are linked . Bathing slices in medium containing 0.5-1 mM 8-bromo-cGMP yielded results similar to those of TM stimulation, a 2.5-fold increase over control in the number of coupled cells per injection. Effects of TM stimulation on coupling also were blocked by bathing slices in a guanylate cyclase inhibitor (10 microM LY83583). In contrast to cGMP, 1 mM 8-bromo-cAMP significantly reduced coupling. We conclude that synaptically released histamine increases coupling via cGMP-dependent mechanisms.
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Calbindin-D28k: role in determining intrinsically generated firing patterns in rat supraoptic neurones.
1. Physiological activation of rat supraoptic nucleus (SON) neurones leads to phasic firing in vasopressin neurones and fast, continuous firing in oxytocin neurones. Using whole-cell patch clamp methods in brain slices, we investigated the role of endogenous calbindin-D28k (calbindin) in determining these intrinsically generated patterns of firing. 2. Direct introduction of calbindin (0.1-0.2 mM) into twelve of twelve phasically firing neurones suppressed Ca(2+)-dependent depolarizing after-potentials (DAPs) and changed activity from phasic to continuous firing. Bovine calcium binding protein (0.3 mM), an analogue of calbindin, had similar effects on both DAPs and firing patterns in five of five cells tested. 3. Introduction of anti-calbindin antiserum (1:2000-5000) into thirteen of thirteen continuously firing neurones unmasked DAPs and converted continuous into phasic firing. Such effects could not be mimicked either by diffusion of normal rabbit serum or antibodies directed against glial fibrillary acidic protein or against neurophysin. 4. Immunocytochemical staining with antisera directed against calbindin revealed more intense staining in the dorsal, oxytocin-rich and less intense staining in the ventral, vasopressin-rich areas of the SON. 5. Elevated intracellular Ca2+ concentration ([Ca2+]i; 0.1 mM) induced DAPs and phasic firing in all twenty-nine SON cells recorded. During chelation of intracellular Ca2+ with (1.1-11 mM) BAPTA, fifty-eight of fifty-eight neurones recorded displayed regular continuous activity and had no DAPs. 6. These data suggest that firing activities in SON cells are dependent on [Ca2+]i and that calbindin, acting as an endogenous Ca2+ buffer, is involved in regulation of intrinsic firing patterns. It is likely that calcium binding proteins have a similar influence on the firing patterns of many neuronal types throughout the nervous system.
Action Potentials↗
NMDA and non-NMDA receptors on rat supraoptic nucleus neurons activated monosynaptically by olfactory afferents.
The recently discovered efferent projections from the main and accessory olfactory bulbs to the supraoptic nucleus (SON) were further investigated. Intracellular electrophysiological methods were used to determine (a) if these projections are monosynaptic, (b) which excitatory amino acid (EAA) receptor subtypes mediate responses to activation of these pathways and (c) whether the same receptor subtypes mediate responses of phasically firing (vasopressin) and continuously firing (putative oxytocin) neurons. Recordings were made from SON neurons in large explants and 500 microns thick horizontal slices, containing 2-6 mm of the piriform cortex and lateral olfactory tract (LOT). This allowed recording of synaptic responses to selective stimulation of the LOT. EPSPs in SON neurons faithfully followed stimulus frequencies of 50-100 Hz, indicating that these inputs were monosynaptic. Stimulus-evoked EPSPs were blocked by the non-specific EAA antagonist, kynurenate. Perifusion of the slice with Mg(2+)-free medium revealed the presence of NMDA receptors in addition to the non-NMDA receptors on both phasically and continuously firing cells, indeed, on all cells tested. Partial blockade of these EPSPs in Mg(2+)-free medium could be achieved with either the NMDA antagonist, AP5, or the non-NMDA antagonist, CNQX or NBQX. Full blockade of the stimulus-evoked EPSPs was effected by adding both types of antagonists to the medium, although spontaneous EPSPs were still observed in several cells. These results are consistent with prior studies showing both receptor subtypes in the SON. This is the first demonstration that afferent stimulation activates both subtypes in the same SON neuron regardless of its peptide content.
2-Amino-5-phosphonovalerate↗
Taurine immunoreactivity in the rat supraoptic nucleus: prominent localization in glial cells.
Taurine is an inhibitory amino acid that hyperpolarizes magnocellular neurosecretory neurons. To determine which cell types in the rat supraoptic nucleus contain taurine, we used a monoclonal antibody raised against a taurine conjugate. Preembedding immunocytochemistry was carried out at the light and electron microscopic levels using diaminobenzidine and gold-substituted silver-intensified peroxidase as markers. We report the presence of taurine in all cellular compartments of the supraoptic nucleus, except axons, with variable labeling intensities among the different compartments. Few cell bodies of magnocellular neurons were immunoreactive, but many distal dendrites and some proximal ones showed weak-to-moderate levels of immunoreactivity. Strong immunoreactivity was found over glial cell bodies and their processes, in particular in the ventral glial lamina of the supraoptic nucleus. Large astrocytic processes labeled with the taurine antibody included the endfeet participating in the glial limitans around capillaries and at the ventral surface of the hypothalamus. Other types of immunoreactive astrocytic profiles were found scattered within the neuropil where these processes participated in different interactions with the neuronal elements of the supraoptic nucleus. Immunoreactive glial expansions, sometimes even the main process of the glial cell, engulfed axonal boutons. Other labeled glial processes were found between two magnocellular perikarya or closely apposed to the membrane of axonal boutons contacting the neuronal cell bodies. The frequent finding of closely apposed glial and dendritic elements bearing different levels of taurine-like immunoreactivity suggests that exchange of taurine between those two compartments may occur. We propose that taurine could be released from supraoptic glia by a small decrease in osmolarity or by receptor-mediated mechanisms during conditions of low hormonal (vasopressin and/or oxytocin) needs. Such released taurine could then act on presynaptic or postsynaptic sites, or both, to exert its neuromodulatory actions.
3,3'-Diaminobenzidine↗
Effects of continuous environmental illumination on the albino rat hypothalamo-neurohypophysial system.
Continuous environmental illumination or constant light (LL) exposure causes a suppression of daily water intake, and long-term exposure of greater than 19 days produces a hypertrophy of magnocellular neuroendocrine cells (MNCs) in the hypothalamus. These findings led Glantz to hypothesize that LL increases the secretion of vasopressin (VP). We wanted to determine whether LL could trigger morphological changes within the hypothalamo-neurohypophysial system (HNS) seen with other manipulations that result in enhanced hormone release. The posterior pituitary of male albino rats that were exposed to LL for 24 or 48 h were examined ultrastructurally for evidence of enhanced hormone release. In addition, water intake, plasma VP levels, and MNC size within the supraoptic nucleus (SON) were measured. After LL exposure, the posterior pituitary morphology was different, suggesting enhanced hormone release. LL exposure did not affect plasma VP or the size of SON MNCs, but did suppress drinking behavior. These data show that posterior pituitary morphology is affected rapidly by LL exposure. The HNS response to LL exposure may consist of changes within the first 24 h of LL found within the posterior pituitary followed later by hypertrophy of the SON MNCs.
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Incidence of neuronal coupling in supraoptic nuclei of virgin and lactating rats: estimation by neurobiotin and lucifer yellow.
Dye coupling among neurons has been shown to reflect electrotonic coupling. Recent work in retina has revealed that the incidence of coupling is greater when estimated by neurobiotin (NB) transfer than by Lucifer yellow (LY). Several previous studies have shown that the incidence of LY coupling among supraoptic nucleus (SON) neurons of lactating rats is 2- to 4-fold higher than is observed in virgin females. We compared the incidence of coupling among SON neurons following simultaneous injections of LY and NB into the same cells in slices from virgin or lactating rats. As seen in previous studies, there were 4-fold more LY-coupled neurons per injection in lactating as compared to virgin rats. Under both conditions, the numbers of NB-coupled neurons per injection were 4-fold greater than was observed for LY; possible mechanisms are discussed. Individual NB-filled neurons were coupled to as many as 10 other cells distributed over a large area of the SON. These results confirm previous findings of more coupling in lactating than virgin SONs, and suggest that both the incidence and spatial extent of interneuronal coupling are greater and thus probably more important functionally than has been heretofore appreciated.
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Histamine mediates fast synaptic inhibition of rat supraoptic oxytocin neurons via chloride conductance activation.
Axons from the histaminergic neurons of the tuberomammillary nucleus project to both the anterior and tuberal portions of the supraoptic nucleus. Histamine is known to activate vasopressin neurons via a histamine receptor subtype 1 and to increase release of vasopressin, but effects on oxytocin neurons have been previously unexplored. Here we investigated the effects of tuberomammillary nucleus electrical stimulation as well as of histamine antagonists on supraoptic nucleus oxytocin and vasopressin neurons in slices of rat hypothalamus. Electrical stimulation evoked short constant latency (approximately 5 ms), fast (4-6 ms onset to peak) inhibitory postsynaptic potentials in oxytocin neurons and, as shown previously, fast excitatory postsynaptic potentials in vasopressin neurons. These synaptic responses followed paired-pulse stimulus frequencies up to 100 Hz and were, thus, probably reflecting monosynaptic connections. Inhibitory postsynaptic potentials were selectively blocked by histamine receptor subtype 2 antagonists (either cimetidine or famotidine) and by picrotoxin but not by histamine receptor subtype 1 antagonists or bicuculline. Similar synaptic responses to tuberomammillary nucleus stimulation were found in 16 of 16 neurons immunocytochemically identified as oxytocinergic and in seven putative oxytocin neurons. Perifusion of the slice with low chloride medium (4.8 mM) reversed stimulus-evoked inhibitory postsynaptic potentials. We conclude that histaminergic neurons monosynaptically contact both oxytocin and vasopressin cells of the supraoptic nucleus and inhibit the former via activation of chloride channels which can be blocked by the histamine receptor subtype 2 antagonists, famotidine and cimetidine.
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Systemic signals contribute to induced morphological changes in the hypothalmo-neurohypophysial system.
A systemic injection of hypertonic saline causes morphological changes in the supraoptic nucleus (SON) of the hypothalamus and the posterior pituitary, including withdrawal of astrocytic glial processes from among magnocellular neuroendocrine cells (MNCs) in the SON and increases in neural apposition with the basal lamina (BL) in the posterior pituitary. This study investigated whether systemic adrenalin provides a signal for these changes. Three groups of rats were given intraperitoneal injections of hypertonic (1.5 M) or normal (0.15 M) NaCl and were sacrificed 5 h after injection. One group was given no additional treatment, one group was anesthetized from prior to injection through perfusion, and one group was bilaterally adrenal-medullectomized several days prior to injections. Morphometric analysis of electron micrographs revealed rats given 1.5 M NaCl with no additional treatment showed expected changes in the SON and pituitary. Rats given 1.5 M NaCl and anesthetized showed diminished responses in the SON, and no changes in the pituitary compared to anesthetized rats given 0.15 M NaCl. No changes in withdrawal of glial processes from among MNCs or in neural apposition with the BL were seen in medullectomized animals. Thus, both anesthesia and adrenal-medullectomy interfere with signals for glial retraction and suggest that these responses are mediated by adrenalin.
Adrenal Medulla↗
Maternal behaviors: evidence that they feed back to alter brain morphology and function.
We review evidence suggesting that the brain of maternally behaving rats is altered as a result of the behavior of the animal towards her pups. Morphological changes seen in the supraoptic nucleus, which contains oxytocinergic neurons important for lactation, are observed not only in parturient, lactating animals but also in virgin animals induced by the presence of rat pups to behave maternally. The supraoptic nuclei of lactating and maternally behaving virgin animals have a higher incidence of dendritic bundling relative to non-maternal virgin animals. Also, stimulation of the lateral olfactory tract in in vitro brain slices elevates electrotonic coupling among supraoptic neurons only in maternally behaving animals and not in male or non-maternal virgins. In general the evidence presented supports the idea that maternal behavior in lactating and non-lactating animals, can have profound effects on the morphology and physiological functioning of oxytocinergic neurons in the hypothalamus.
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Morphological study of posterior pituitary in chronically dehydrated rats using an immunogold cytochemical label for vasopressin.
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Rapid synaptic changes and bundling in the supraoptic dendritic zone of the perfused rat brain.
In the dendritic region of the supraoptic nucleus of young adult rats we found ultrastructural evidence of rapid (< 30 min) morphological reorganization following transcardial perfusion of the anesthetized animals with high (325 mOsm), but not with normal, osmolality (302 mOsm) balanced salt solutions. The changes observed included significant increases in dendritic bundling and increased numbers of multiple axodendritic synapses (where one presynaptic terminal contacted two or more postsynaptic dendrites). In our initial experiments the perfusion medium contained tannic acid, but when the tannic acid was omitted in a separate set of experiments, the results were both similar and more striking. These studies indicate that the plasticity previously seen in this region under physiological conditions can occur rapidly and probably involves astrocytic process withdrawal from between adjacent dendrites. This change in the distribution of astrocytic processes allows previously single synapses access to additional postsynaptic dendritic membrane. Together, increased dendritic bundling and multiple synapses may facilitate the synchronization of cell firing and, thus, hormone release.
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