Nitric oxide (NO) is a gaseous neurotransmitter that may mediate a decrease in sympathetic output to the periphery. This implication predicts that NO-producing neurons in the brain are activated in animals experiencing increased levels of sympathetic activity. To test this prediction, we subjected t
Noradrenaline up-regulates the neuronal and the inducible nitric oxide synthase isoforms in magnocellular neurons of rat brain slices
✍ Scribed by Valérie Grange-Messent; Danièle Raison; Bernard Dugas; André Calas
- Publisher
- John Wiley and Sons
- Year
- 2004
- Tongue
- English
- Weight
- 686 KB
- Volume
- 78
- Category
- Article
- ISSN
- 0360-4012
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Nitric oxide (NO) and noradrenaline (NA) are suggested to be implicated in the regulation of neuropeptide secretion in the supraoptic nuclei (SON) and the paraventricular nuclei (PVN) of the hypothalamus. Our study demonstrates short‐term interactions between NA and the activity and expression of NO synthase (NOS) in magnocellular neurons, by using an ex vivo model of hypothalamic slices. In the SON as well as in the PVN, total NOS activity exhibited a time‐dependant increase after an incubation with NA. In the SON, this increase of total NOS activity was in part the consequence of stimulation of the iNOS activity. Coimmunodetections showed that cells expressing the inducible form of NOS were not astrocytes but magnocellular neurons. Steady‐state levels of iNOS and nNOS mRNA were dramatically enhanced by NA, particularly in the SON. Consequently, we provide new evidence that iNOS could play an important role in multiple physiological functions, including extracellular fluid balance, lactation, and parturition. © 2004 Wiley‐Liss, Inc.
📜 SIMILAR VOLUMES
## Abstract Acrylamide (ACR) is a known industrial neurotoxic chemical. Evidence suggests that ACR neurotoxic effect is related to brain neurotransmission disturbances. Since nitric oxide (NO) acts as a neurotransmission modulator and is produced by nitric oxide synthase (NOS), the neuronal NOS (nN
## Abstract Water‐deprivation‐induced osmotic stress leads to activation of a number of adaptive responses. Nitric oxide (NO) has been implicated in the modulation of these responses, as the amygdala has been implicated in ingestive behavior and modulation of autonomic homeostatic functions. Here w
## Abstract This study was conducted to define the molecular mechanism by which dehydration induces expression of neuronal nitric oxide synthase (nNOS) in the hypothalamic paraventricular nucleus (PVN). Rats were deprived from water for 48 hr and then sacrificed immediately or 1 hr after ad libitum
Nitric oxide (NO) and purinergic ionotropic receptors (P2X) mediate cellular events in the central nervous system (CNS) under physiological conditions as well as during pathological events, and they have been recently proposed to interact in mediating CNS response to injury (Viscomi et al. [2004] Ne
## Abstract To ascertain the possible implications of the nitric oxide (NO^•^) producing system in striatal senescence, and by using immunohistochemistry and image‐processing approaches, we describe the presence of the enzyme nitric oxide synthase (NOS), the NADPH‐diaphorase (NADPH‐d) histochemical