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Book: Glial neuronal signaling

Hatton, Glenn I.

2004

Author's details	ed. by Glenn I. Hatton
Language	English
Size	XI, 441 S. : Ill.
Publisher	Kluwer
Publishing place	Boston u.a.
Publishing country	United States
Document type	Book
Accompanying material	1 CD-ROM (12 cm)
HBZ-ID	HT014047167
ISBN	1-4020-7936-2 ; 978-1-4020-7936-8
Database	Catalogue ZB MED Medicine, Health

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Article: Dynamic neuronal-glial interactions: an overview 20 years later.

Hatton, Glenn I

Peptides

2004 Volume 25, Issue 3, Page(s) 403–411

Abstract: After commenting on some perceived reasons why our review may have been relatively frequently cited, a brief overview is presented that first summarizes what we knew 25 years ago about the dynamic neuronal-astroglial interactions that occur in response ... ...

Abstract	After commenting on some perceived reasons why our review may have been relatively frequently cited, a brief overview is presented that first summarizes what we knew 25 years ago about the dynamic neuronal-astroglial interactions that occur in response to changes in the physiological state of the animal. The brain system in which these dynamic interactions were studied was the magnocellular hypothalamo-neurohypophysial system (mHNS) of the rat. The mHNS developed as and continues to be the model system yielding the most coherent picture of dynamic morphological changes and insights into their functional consequences. Many other brain areas, however, have more recently come under scrutiny in the search for glial-neuronal dynamisms. Outlined next are some of the questions concerning this phenomenon that led to the research efforts immediately following the initial discoveries, along with the answers, both complete and incomplete, obtained to those research questions. The basis for this first wave of follow-up research can be characterized by the phrase "what we knew we didn't know at that time." The final section is an update and brief overview of highlights of both "what we know now" and "what we now know that we don't know" about dynamic neuronal-astroglial interactions in the mHNS.
MeSH term(s)	Animals ; Cell Communication/physiology ; Humans ; Hypothalamus/physiology ; Neuroglia/physiology ; Neurons/physiology ; Pituitary Gland/physiology ; Pituitary Gland/ultrastructure ; Rats ; Supraoptic Nucleus/ultrastructure
Language	English
Publishing date	2004-03
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	769028-9
ISSN	1873-5169 ; 0196-9781
ISSN (online)	1873-5169
ISSN	0196-9781
DOI	10.1016/j.peptides.2003.12.001
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Article: Glial-neuronal interactions in the mammalian brain.

Hatton, Glenn I

Advances in physiology education

2002 Volume 26, Issue 1-4, Page(s) 225–237

Abstract: Recognition of the importance of glial cells in nervous system functioning is increasing, specifically regarding the modulation of neural activity. This brief review focuses on some of the morphological and functional interactions that take place between ...

Abstract	Recognition of the importance of glial cells in nervous system functioning is increasing, specifically regarding the modulation of neural activity. This brief review focuses on some of the morphological and functional interactions that take place between astroglia and neurons. Astrocyte-neuron interactions are of special interest because this glia cell type has intimate and dynamic associations with all parts of neurons, i.e., somata, dendrites, axons, and terminals. Activation of certain receptors on astrocytes produces morphological changes that result in new contacts between neurons, along with physiological and functional changes brought about by the new contacts. In response to activation of other receptors or changes in the extracellular microenvironment, astrocytes release neuroactive substances that directly excite or inhibit nearby neurons and may modulate synaptic transmission. Although some of these glial-neuronal interactions have been known for many years, others have been quite recently revealed, but together they are forming a compelling story of how these two major cell types in the brain carry out the complex tasks that mammalian nervous systems perform.
MeSH term(s)	Animals ; Astrocytes/physiology ; Brain/physiology ; Cell Communication ; Models, Neurological ; Neuroglia/physiology ; Neuronal Plasticity/physiology ; Neurons/physiology ; Pituitary Gland, Posterior/physiology ; Signal Transduction
Language	English
Publishing date	2002-12
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	1024917-5
ISSN	1522-1229 ; 1043-4046
ISSN (online)	1522-1229
ISSN	1043-4046
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Article ; Online: Astrocytic plasticity and patterned oxytocin neuronal activity: dynamic interactions.

Wang, Yu-Feng / Hatton, Glenn I

The Journal of neuroscience : the official journal of the Society for Neuroscience

2009 Volume 29, Issue 6, Page(s) 1743–1754

Abstract: Astroglial-neuronal interactions are important in brain functions. However, roles of glial fibrillary acidic protein (GFAP) in this interaction remain unclear in acute physiological processes. We explored this issue using the supraoptic nucleus (SON) in ... ...

Abstract	Astroglial-neuronal interactions are important in brain functions. However, roles of glial fibrillary acidic protein (GFAP) in this interaction remain unclear in acute physiological processes. We explored this issue using the supraoptic nucleus (SON) in lactating rats. At first, we identified the essential role of astrocytes in the milk-ejection reflex (MER) by disabling astrocytic functions via intracerebroventricular application of l-aminoadipic acid (l-AAA). l-AAA blocked the MER and reduced GFAP levels in the SON. In brain slices, l-AAA suppressed oxytocin (OT) neuronal activity and EPSCs. Suckling reduced GFAP in immunocytochemical images and in Western blots, reductions that were partially reversed after the MER. OT, the dominant hormone mediating the MER, reduced GFAP expression in brain slices. Tetanus toxin suppressed EPSCs but did not influence OT-reduced GFAP. Protease inhibitors did not influence OT-reduced GFAP images but blocked the degradation of GFAP molecules. In the presence of OT, transient 12 mm K(+) exposure, simulating effects of synchronized bursts before the MER, reversed OT-reduced GFAP expression. Consistently, suckling first reduced and then increased the expression of aquaporin 4, astrocytic water channels coupled to K(+) channels. Moreover, GFAP molecules were associated with astrocytic proteins, including aquaporin 4, actin, and glutamine synthetase and serine racemase. GFAP-aquaporin 4 association decreased during initial suckling and increased after the MER, whereas opposite changes occurred between GFAP and actin. MER also decreased the association between GFAP and glutamine synthetase. These results indicate that suckling elicits dynamic glial neuronal interactions in the SON; GFAP plasticity dynamically reflects OT neuronal activity.
MeSH term(s)	Action Potentials/physiology ; Animals ; Astrocytes/physiology ; Female ; Neuronal Plasticity/physiology ; Neurons/physiology ; Oxytocin/physiology ; Rats ; Rats, Sprague-Dawley
Chemical Substances	Oxytocin (50-56-6)
Language	English
Publishing date	2009-02-05
Publishing country	United States
Document type	Comparative Study ; Journal Article
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.4669-08.2009
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Article ; Online: Neural mechanisms underlying the milk ejection burst and reflex.

Hatton, Glenn I / Wang, Yu-Feng

Progress in brain research

2008 Volume 170, Page(s) 155–166

Abstract: One of the more interesting and complex phenomena involving neurohypophysial hormones is the milk ejection reflex and the events surrounding it. Accordingly, many investigations over the years have taken up the challenge of elucidating its myriad aspects. ...

Abstract	One of the more interesting and complex phenomena involving neurohypophysial hormones is the milk ejection reflex and the events surrounding it. Accordingly, many investigations over the years have taken up the challenge of elucidating its myriad aspects. Much has been learned from in vivo preparations about the sequence of events that so regularly occurs: important priming by maternal behaviours, the intermittent rhythms, gating of bursting, synchrony of the oxytocin (OXT) neuronal bursts emitted intermittently in response to the continuous suckling of the young and the factors that influence the amplitude of the bursts/milk ejections (e.g. number of suckling pups). In vivo electrophysiological studies are constrained by the infeasibility of routinely recording transmembrane events and, therefore, cannot offer detailed membrane and/or synaptic analyses. Recent studies have developed an in vitro model of OXT neuronal bursting that has allowed more mechanistic analyses of these bursts as well as factors involved in their generation and structure. Here we review many of the cellular and molecular mechanisms that have been shown to underlie the milk ejection bursts, as revealed by in vitro analyses.
MeSH term(s)	Animals ; Animals, Suckling/physiology ; Astrocytes/physiology ; Axons/metabolism ; Female ; Humans ; Infant ; Lactation ; Mammary Glands, Animal/physiology ; Maternal Behavior/physiology ; Milk/metabolism ; Models, Animal ; Neurons/physiology ; Norepinephrine/physiology ; Oxytocin/metabolism ; Parturition/physiology ; Receptors, Oxytocin/physiology ; Reflex/physiology ; Signal Transduction ; Supraoptic Nucleus/physiology
Chemical Substances	Receptors, Oxytocin ; Oxytocin (50-56-6) ; Norepinephrine (X4W3ENH1CV)
Language	English
Publishing date	2008-07-04
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ISSN	1875-7855 ; 0079-6123
ISSN (online)	1875-7855
ISSN	0079-6123
DOI	10.1016/S0079-6123(08)00414-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: The puzzle of pulsatile oxytocin secretion during lactation: some new pieces.

Armstrong, William E / Hatton, Glenn I

American journal of physiology. Regulatory, integrative and comparative physiology

2006 Volume 291, Issue 1, Page(s) R26–8

MeSH term(s)	Animals ; Humans ; Lactation/metabolism ; Oxytocin/metabolism
Chemical Substances	Oxytocin (50-56-6)
Language	English
Publishing date	2006-07-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	603839-6
ISSN	1522-1490 ; 0363-6119
ISSN (online)	1522-1490
ISSN	0363-6119
DOI	10.1152/ajpregu.00879.2005
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Article ; Online: Interaction of extracellular signal-regulated protein kinase 1/2 with actin cytoskeleton in supraoptic oxytocin neurons and astrocytes: role in burst firing.

Wang, Yu-Feng / Hatton, Glenn I

The Journal of neuroscience : the official journal of the Society for Neuroscience

2007 Volume 27, Issue 50, Page(s) 13822–13834

Abstract: Neuronal firing patterns determine the manner of neurosecretion, the underlying mechanisms of which are poorly understood. Using supraoptic nuclei in brain slices from lactating rats, we examined the involvement of extracellular signal-regulated protein ... ...

Abstract	Neuronal firing patterns determine the manner of neurosecretion, the underlying mechanisms of which are poorly understood. Using supraoptic nuclei in brain slices from lactating rats, we examined the involvement of extracellular signal-regulated protein kinase 1/2 (ERK1/2) and filamentous actin (F-actin) in burst generation by oxytocin (OT) neurons. Blocking phosphorylation of ERK1/2 (pERK1/2) decreased miniature EPSCs and blocked OT-evoked bursts, as did intracellularly loading an antibody against pERK1/2. OT (10 pM) increased cytosolic pERK1/2 close to the cell membrane within the first 5 min, subsiding by 30 min, whereas OT elicited pERK1/2 nuclear translocation in closely associated supraoptic astrocytes. The increased pERK1/2 was tightly correlated with spatiotemporal actin dynamics. In OT neurons, OT initially increased F-actin, particularly at membrane subcortical areas, and then decreased it after 30 min. Both polymerization and depolymerization of actin cytoskeleton were associated with bursts, but only polymerization facilitated OT-evoked bursts. Blocking ERK1/2 activation blocked OT-evoked actin polymerization, whereas depolymerizing F-actin increased pERK1/2 expression. These changes were further identified in vivo. In intact animals, suckling increased ERK1/2 activation in the cytosol and membrane subcortical area F-actin formation in OT neurons, whereas it increased F-actin concentration in astrocytic somata. Coimmunoprecipitation showed that suckling increased molecular interactions between pERK1/2 and actin. Finally, two different blockers of ERK1/2 kinase injected intracerebroventricularly reduced suckling-evoked milk ejections. This is the first demonstration that OT mediation of suckling-evoked bursts/milk ejections is via interactions between pERK1/2 and actin cytoskeleton.
MeSH term(s)	Actins/metabolism ; Animals ; Astrocytes/metabolism ; Cytoskeleton/metabolism ; Enzyme Activation/drug effects ; Enzyme Activation/physiology ; Enzyme Inhibitors/pharmacology ; Female ; Injections, Intraventricular ; Lactation/drug effects ; Lactation/physiology ; Milk Ejection/drug effects ; Milk Ejection/physiology ; Mitogen-Activated Protein Kinase 1/antagonists & inhibitors ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/antagonists & inhibitors ; Mitogen-Activated Protein Kinase 3/metabolism ; Neurons/drug effects ; Neurons/metabolism ; Organ Culture Techniques ; Oxytocin/metabolism ; Oxytocin/pharmacology ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Supraoptic Nucleus/cytology ; Supraoptic Nucleus/metabolism ; Synaptic Transmission/drug effects ; Synaptic Transmission/physiology
Chemical Substances	Actins ; Enzyme Inhibitors ; Oxytocin (50-56-6) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24)
Language	English
Publishing date	2007-12-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.4119-07.2007
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Article: Mechanisms underlying oxytocin-induced excitation of supraoptic neurons: prostaglandin mediation of actin polymerization.

Wang, Yu-Feng / Hatton, Glenn I

Journal of neurophysiology

2006 Volume 95, Issue 6, Page(s) 3933–3947

Abstract: In nonneuronal tissues, activation of oxytocin receptors (OTRs), like other Galpha(q/11) type G-protein-coupled receptors (Galpha(q/11)/GPCRs), increase prostaglandin (PG) expression. This is not known for the OTRs expressed by central OT neurons. We ... ...

Abstract	In nonneuronal tissues, activation of oxytocin receptors (OTRs), like other Galpha(q/11) type G-protein-coupled receptors (Galpha(q/11)/GPCRs), increase prostaglandin (PG) expression. This is not known for the OTRs expressed by central OT neurons. We examined mechanisms underlying OT's effects on supraoptic nucleus (SON) OT and vasopressin (VP) neurons in hypothalamic slices from lactating rats. OT application (10 pM, 10 min) significantly increased firing rates of OT and VP neurons, both of which expressed OTRs. Indomethacin, an inhibitor of PG synthetases, blocked these increases. OTR (but not a V1 receptor) antagonist blocked OT effects without blocking the excitatory effect of PGE2. Tetanus toxin blocked OT effects on fast synaptic inputs and firing activity of SON neurons but not OT-evoked depolarization, suggesting involvement of both pre- and postsynaptic neurons. Indomethacin also blocked the excitatory effects of phenylephrine, another Galpha(q/11)/GPCR activating agent but not those of PGE2, a non-Galpha(q/11)/GPCR activating agent in the SON. OT or phenylephrine, but not glutamate or KCl, enhanced cyclooxygenase 2 expression at cytosolic loci in SON neurons and nearby astrocytes, as revealed by immunocytochemistry. This OT effect was not blocked by TTX. Western blot analyses showed that OT significantly increased cyclooxygenase 2 but not actin expression. OT promoted the formation of filamentous actin (F-actin) networks at membrane subcortical areas of both OT and VP neurons. Indomethacin blocked enhancement of F-actin networks by OT but not by PGE2. These results indicate that PGs serve as a common mediator of Galpha(q/11)/GPCR-activating agents in neuronal function.
MeSH term(s)	Actins/metabolism ; Animals ; Cells, Cultured ; Dimerization ; Female ; Hypothalamus/drug effects ; Hypothalamus/physiology ; Oxytocin/pharmacology ; Polymers/metabolism ; Prostaglandins/metabolism ; Rats ; Rats, Sprague-Dawley ; Supraoptic Nucleus/drug effects ; Supraoptic Nucleus/physiology ; Synaptic Transmission/drug effects ; Synaptic Transmission/physiology
Chemical Substances	Actins ; Polymers ; Prostaglandins ; Oxytocin (50-56-6)
Language	English
Publishing date	2006-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80161-6
ISSN	1522-1598 ; 0022-3077
ISSN (online)	1522-1598
ISSN	0022-3077
DOI	10.1152/jn.01267.2005
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Book: Glial neuronal signaling

Hatton, Glenn I / Parpura, Vladimir

2004

Author's details	edited by Glenn I. Hatton and Vladimir Parpura
Keywords	Neuroglia. ; Neurons. ; Neurotransmitters. ; Neurotransmitter receptors.
Language	English
Size	xi, 441 p. :, ill. ;, 24 cm. +
Publisher	Kluwer Academic Publishers
Publishing place	Boston
Document type	Book
Accompanying material	1 CD-ROM (4 3/4 in.)
ISBN	1402079362 ; 9781402079368
Database	NAL-Catalogue (AGRICOLA)

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Book: Glial neuronal signaling

Hatton, Glenn I / Parpura, Vladimir

2004

Author's details	edited by Glenn I. Hatton and Vladimir Parpura
MeSH term(s)	Neuroglia/physiology ; Signal Transduction/physiology ; Neurons/physiology ; Glutamic Acid/physiology
Language	English
Size	xi, 441 p. :, ill. ;, 24 cm. +
Publisher	Kluwer Academic Publishers
Publishing place	Boston
Document type	Book
Accompanying material	1 CD-ROM (4 3/4 in.)
ISBN	9781402079368 ; 1402079362
Database	Catalogue of the US National Library of Medicine (NLM)

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