Quantitative mapping of glutamate presynaptic terminals in the supraoptic nucleus and surrounding hypothalamus

Meeker, Rick B.; Swanson, D.J.; Greenwood, Robert; Hayward, James N.

doi:10.1016/0006-8993(93)90408-f

Cited by 110 publications

(78 citation statements)

References 36 publications

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“…PAG expression has been used in a number of previous studies to visualize and quantify glutamate-transmitting neurons [1,[38][39][40]48,75]. Glutamate has been firmly established as the predominant excitatory transmitter in the hypothalamus [5,51,74], and it's activity has been extensively linked to aggression in a range of animal models, including rats, mice, cats, and fighting bulls [6,30,36,56,57,71,76], where it appears be positively associated with the aggressive behavioral phenotype. In preliminary studies, we have shown that PAG containing neurons in the AH express 5HT1B receptors (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Lasting changes in neuronal activation patterns in select forebrain regions of aggressive, adolescent anabolic/androgenic steroid-treated hamsters

Ricci

Grimes

Melloni

2007

Behavioural Brain Research

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Repeated exposure to anabolic/androgenic steroids (AAS) during adolescence stimulates high levels of offensive aggression in Syrian hamsters. The current study investigated whether adolescent AAS exposure activated neurons in areas of hamster forebrain implicated in aggressive behavior by examining the expression of FOS, i.e., the protein product of the immediate early gene c-fos shown to be a reliably sensitive marker of neuronal activation. Adolescent AAS-treated hamsters and sesame oil-treated littermates were scored for offensive aggression and then sacrificed 1 day later and examined for the number of FOS immunoreactive (FOS-ir) cells in regions of the hamster forebrain important for aggression control. When compared with non-aggressive, oil-treated controls, aggressive AAS-treated hamsters showed persistent increases in the number of FOS-ir cells in select aggression regions, namely the anterior hypothalamus and lateral septum. However, no differences in FOS-ir cells were found in other areas implicated in aggression such as the ventrolateral hypothalamus, bed nucleus of the stria terminals, central and/or medial amygdala or in nonaggression areas such as the samatosensory cortex and the suprachiasmatic nucleus. These results suggest that adolescent AAS exposure may constitutively activate neurons in select forebrain areas critical for the regulation of aggression in hamsters. A model for how persistent activation of neurons in one of these brain regions (i.e., the anterior hypothalamus) may facilitate the development of the aggressive phenotype in adolescent-AAS exposed animals is presented.

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Section: Discussionmentioning

confidence: 99%

Lasting changes in neuronal activation patterns in select forebrain regions of aggressive, adolescent anabolic/androgenic steroid-treated hamsters

Ricci

Grimes

Melloni

2007

Behavioural Brain Research

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“…The other major afferent input to OT and VP neurons uses glutamate as the neurotransmitter (24,25,38,47,90). Under basal conditions, glutamatergic synapses represent about 22% of all synapses in the rat SON; they are twice as numerous on dendrites than on somata (24,25).…”

Section: Neurochemical Identity Of Synapses Undergoing Remodelingmentioning

confidence: 99%

Remodeling of astrocytes, a prerequisite for synapse turnover in the adult brain? Insights from the oxytocin system of the hypothalamus

Theodosis¹,

Trailin²,

Poulain³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Theodosis, Dionysia T., Andrei Trailin, and Dominique A. Poulain. Remodeling of astrocytes, a prerequisite for synapse turnover in the adult brain? Insights from the oxytocin system of the hypothalamus. Am J Physiol Regul Integr Comp Physiol 290: R1175-R1182, 2006; doi:10.1152/ajpregu.00755.2005.-Neurons, including their synapses, are generally ensheathed by fine processes of astrocytes, but this glial coverage can be altered under different physiological conditions that modify neuronal activity. Changes in synaptic connectivity accompany astrocytic transformations so that an increased number of synapses are associated with reduced astrocytic coverage of postsynaptic elements, whereas synaptic numbers are reduced on reestablishment of glial coverage. A system that exemplifies activity-dependent structural synaptic plasticity in the adult brain is the hypothalamo-neurohypophysial system, and in particular, its oxytocin component. Under strong, prolonged activation (parturition, lactation, chronic dehydration), extensive portions of somatic and dendritic surfaces of magnocellular oxytocin neurons are freed of intervening astrocytic processes and become directly juxtaposed. Concurrently, they are contacted by an increased number of inhibitory and excitatory synapses. Once stimulation is over, astrocytic processes again cover oxytocinergic surfaces and synaptic numbers return to baseline levels. Such observations indicate that glial ensheathment of neurons is of consequence to neuronal function, not only directly, for example by modifying synaptic transmission, but indirectly as well, by preparing neuronal surfaces for synapse turnover.NEURONS, GLIA, AND SYNAPTIC inputs are not static elements because they undergo dynamic transformations. This can take place under normal physiological conditions and highlights the adult nervous system's remarkable capacity to undergo restructuring to meet particular functional requirements. A change in the morphology of neurons, and especially of afferent inputs controlling their activity, can have important consequences on their respective functions. These modifications are often accompanied by remodeling of adjacent glia, which has further impact on neuronal activity by modifying the immediate extracellular microenvironment, thereby influencing synaptic and volume transmission.The hypothalamo-neurohypophysial system (HNS), and in particular, its oxytocinergic component, is a familiar model for this kind of morphological neuronal and glial plasticity (57,76). Oxytocin (OT) neurons accumulate in well-defined regions in the hypothalamus, the supraoptic (SON), and paraventricular (PVN) nuclei, and release OT mainly from axon terminals in the neurohypophysis to act as a neurohormone in vital functions like parturition, lactation, and osmotic regulation. Critical for this systemic secretion is the concomitant exocytotic release of the peptide from somata and dendrites of OT neurons themselves in the SON and PVN. This central release facilitates the synchronous high-frequency activity of...

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“…At these sites, the modular protein-protein motif or PDZ domain of NOS, implicated in the signal transduction mechanism, links the synthase to protein complexes (19). Significantly, NOS and glutamate receptors are widely distributed in the hypothalamo-neurohypophyseal system (20) and circumventricular organs (21). Additionally, GABAergic innervation of magnocellular neurons is abundant (22) and presynaptic activation of glutamate receptors modulates release of GABA in these neurons (23).…”

Section: No's Influence On Electrical Activity Of Magnocellular Neuronsmentioning

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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Quantitative mapping of glutamate presynaptic terminals in the supraoptic nucleus and surrounding hypothalamus

Cited by 110 publications

References 36 publications

Lasting changes in neuronal activation patterns in select forebrain regions of aggressive, adolescent anabolic/androgenic steroid-treated hamsters

Lasting changes in neuronal activation patterns in select forebrain regions of aggressive, adolescent anabolic/androgenic steroid-treated hamsters

Remodeling of astrocytes, a prerequisite for synapse turnover in the adult brain? Insights from the oxytocin system of the hypothalamus

Nitric oxide modulation of the hypothalamo-neurohypophyseal system

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