Function-Related Plasticity in Hypothalamus

Hatton, Glenn I.

doi:10.1146/annurev.neuro.20.1.375

Cited by 297 publications

(249 citation statements)

References 107 publications

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“…The slices were ethanol-dehydrated, cleared, and mounted on glass slides in methyl salicylate. LY-filled cells were located, counted, and photographed under epifluorescence, special attention being paid to dendrodendritic contacts, the sites of coupling between SON neurons (for review, see Hatton, 1997). Conventional intracellular recording procedures were used as in our previous coupling studies Hatton, 1987, 1988;Yang, 1994, 1996).…”

Section: Methodsmentioning

confidence: 99%

“…NMDA receptors (Meeker et al, 1994), as well as NOS (noted above), are upregulated by the physiological stimulation of the magnocellular system. This may account for the differential response of lactating versus virgin female or males rats to the extent that lactation, like dehydration, is a general activating stimulus in this system (see Hatton, 1997).…”

Section: Synaptic Modulation Of Couplingmentioning

confidence: 99%

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Nitric Oxide via cGMP-Dependent Mechanisms Increases Dye Coupling and Excitability of Rat Supraoptic Nucleus Neurons

Yang

Hatton

1999

J. Neurosci.

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Unlike many neuron populations, supraoptic nucleus (SON) neurons are rich in both nitric oxide synthase (NOS) and the NO receptor-soluble guanylyl cyclase (GC), the activation of which leads to cGMP accumulation. Elevations in cGMP result in increased coupling among SON neurons. We investigated the effect of NO on dye coupling in SONs from male, proestrus virgin female, and lactating rats. In 167 slices 263 SON neurons were recorded; 210 of these neurons were injected intracellularly (one neuron per SON) with Lucifer yellow (LY). The typically minimal coupling seen in virgin females was increased nearly fourfold by the NO precursor, L-arginine, or the NO donor, sodium nitroprusside (SNP). L-Arginine-induced coupling was abolished by a NOS inhibitor. In slices from male and lactating rats who have a higher basal incidence of coupling, SNP increased coupling by approximately twofold over control ( p Ͻ 0.03). SNP effects were prevented by the NO scavenger hemoglobin (20 M) and by the selective blocker of NO-activated GC, ODQ (10 M). These results suggest that NO released from cells within the SON can expand the coupled network of neurons and that this action occurs via cGMP-dependent processes. Because increased coupling is associated with elevated SON neuronal excitability, we also studied the effects of 8-bromocGMP on excitability. In both phasically and continuously firing neurons 8-bromo-cGMP (1-2 mM), but not cGMP, produced membrane depolarizations accompanied by membrane conductance increases. Conductance increases remained when depolarizations were eliminated by current-clamping the membrane potential. Thus, NO-induced cGMP increases SON neuronal coupling and excitability. Key words: gap junctions; guanylyl cyclase inhibition; hemoglobin; L-NAME; ODQ; sodium nitroprusside; 8-bromo-cGMPStudies of the distribution of neuronal nitric oxide synthase (NOS) have shown this enzyme to be abundant in the dendrites, somata, and axon terminals of the neurons constituting the magnocellular hypothalamo -neurohypophysial system (Bredt et al., 1990;Dawson et al., 1991). Neurons of this system synthesize, transport, and release either oxytocin or vasopressin, and NOS has been found to be colocalized with both of these peptides (Sanchez et al., 1994). NO is a membrane-permeant neuronal messenger that is produced from L-arginine by the activation of NOS. T ypically, NO release from one cell type finds its way to its receptor, soluble guanylyl cyclase (sGC), in nearby (within 200 M) target cells of another type, activating this enzyme and elevating intracellular cGM P levels (Southam and Garthwaite, 1993;Wood and Garthwaite, 1994). Magnocellular neurons of the paraventricular and supraoptic (SON) nuclei are atypical in that they are rich not only in NOS but also in both the ␣1 and ␤1 subunits of sGC (Furuyama et al., 1993). Because this situation allows for NO activation of sGC within the same neuron as well as between any nearby magnocellular neurons, it is possible that NO plays an autoregulatory role in at least some of th...

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Section: Methodsmentioning

confidence: 99%

Section: Synaptic Modulation Of Couplingmentioning

confidence: 99%

Nitric Oxide via cGMP-Dependent Mechanisms Increases Dye Coupling and Excitability of Rat Supraoptic Nucleus Neurons

Yang

Hatton

1999

J. Neurosci.

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“…The heterogeneity of astrocytic coverage across different brain regions suggests, however, that glutamate spillover is favored in certain areas and suppressed in others (Bernardinelli et al, 2014a; Lange et al, 2012; Oliet et al, 2008). For example, in the supraoptic nucleus (SON), astrocytes undergo extensive morphological changes in lactating rats (Hatton, 1997; Piet et al, 2004a; Theodosis and Poulain, 1993). Astrocytic coverage is reduced and this leads to an enhanced number of synapses and neurotransmitter spillover (Hatton, 1997; Piet et al, 2004a; Theodosis and Poulain, 1993).…”

Section: Implications Of Pap Morphogenesis For Synaptic Functionmentioning

confidence: 99%

“…For example, in the supraoptic nucleus (SON), astrocytes undergo extensive morphological changes in lactating rats (Hatton, 1997; Piet et al, 2004a; Theodosis and Poulain, 1993). Astrocytic coverage is reduced and this leads to an enhanced number of synapses and neurotransmitter spillover (Hatton, 1997; Piet et al, 2004a; Theodosis and Poulain, 1993). With the reduction of astrocytic synapse enwrapping also glutamate clearance is reduced which in turn leads to enhanced negative feedback on glutamate release and increased heterosynaptic depression of GABA release (Oliet et al, 2001; Piet et al, 2004b) and prolonged excitatory postsynaptic potentials (EPSPs) in the cerebellum (Iino et al, 2001).…”

Section: Implications Of Pap Morphogenesis For Synaptic Functionmentioning

confidence: 99%

Morphological plasticity of astroglia: Understanding synaptic microenvironment

Heller

Rusakov

2015

Glia

134

137

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Memory formation in the brain is thought to rely on the remodeling of synaptic connections which eventually results in neural network rewiring. This remodeling is likely to involve ultrathin astroglial protrusions which often occur in the immediate vicinity of excitatory synapses. The phenomenology, cellular mechanisms, and causal relationships of such astroglial restructuring remain, however, poorly understood. This is in large part because monitoring and probing of the underpinning molecular machinery on the scale of nanoscopic astroglial compartments remains a challenge. Here we briefly summarize the current knowledge regarding the cellular organisation of astroglia in the synaptic microenvironment and discuss molecular mechanisms potentially involved in use‐dependent astroglial morphogenesis. We also discuss recent observations concerning morphological astroglial plasticity, the respective monitoring methods, and some of the newly emerging techniques that might help with conceptual advances in the area. GLIA 2015;63:2133–2151

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“…These results indicate that NO production is enhanced during disturbances of fluid balance, presumably to meet the increasing demand for NO modulation of the magnocellular system. This enhanced action of NO occurs in parallel with morphological changes in the hypothalamo-neurohypophyseal system that are characterized by retraction of glia cells interposed among magnocellular neurons, resulting in formation of new synaptic connections that facilitate hormone release (16). Importantly, linkage between NO and plasticity of the nervous system has been demonstrated in the hippocampus, cerebellum (1) and neurohypophysis (17).…”

Section: Introductionmentioning

confidence: 99%

Nitric oxide modulation of the hypothalamo-neurohypophyseal system

Kadekaro

2004

Braz J Med Biol Res

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Nitric oxide (NO), a free radical gas produced endogenously from the amino acid L-arginine by NO synthase (NOS), has important functions in modulating vasopressin and oxytocin secretion from the hypothalamo-neurohypophyseal system. NO production is stimulated during increased functional activity of magnocellular neurons, in parallel with plastic changes of the supraoptic nucleus (SON) and paraventricular nucleus. Electrophysiological data recorded from the SON of hypothalamic slices indicate that NO inhibits firing of phasic and non-phasic neurons, while L-NAME, an NOS inhibitor, increases their activity. Results from measurement of neurohypophyseal hormones are more variable. Overall, however, it appears that NO, tonically produced in the forebrain, inhibits vasopressin and oxytocin secretion during normovolemic, isosmotic conditions. During osmotic stimulation, dehydration, hypovolemia and hemorrhage, as well as high plasma levels of angiotensin II, NO inhibition of vasopressin neurons is removed, while that of oxytocin neurons is enhanced. This produces a preferential release of vasopressin over oxytocin important for correction of fluid imbalance. During late pregnancy and throughout lactation, fluid homeostasis is altered and expression of NOS in the SON is down-and up-regulated, respectively, in parallel with plastic changes of the magnocellular system. NO inhibition of magnocellular neurons involves GABA and prostaglandin synthesis and the signal-transduction mechanism is independent of the cGMP-pathway. Plasma hormone levels are unaffected by icv 1H-[1, 2, 4]oxadiazolo-[4,3-a]quinoxalin-1-one (a soluble guanylyl cyclase inhibitor) or 8-Br-cGMP administered to conscious rats. Moreover, cGMP does not increase in homogenates of the neural lobe and in microdialysates of the SON when NO synthesis is enhanced during osmotic stimulation. Among alternative signal-transduction pathways, nitrosylation of target proteins affecting activity of ion channels is considered.

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Function-Related Plasticity in Hypothalamus

Cited by 297 publications

References 107 publications

Nitric Oxide via cGMP-Dependent Mechanisms Increases Dye Coupling and Excitability of Rat Supraoptic Nucleus Neurons

Nitric Oxide via cGMP-Dependent Mechanisms Increases Dye Coupling and Excitability of Rat Supraoptic Nucleus Neurons

Morphological plasticity of astroglia: Understanding synaptic microenvironment

Nitric oxide modulation of the hypothalamo-neurohypophyseal system

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