Metabotropic glutamate receptor inhibition of visceral afferent potassium currents

Hay, Meredith; Lindsley, Kathy A.

doi:10.1016/0006-8993(95)00889-x

Cited by 16 publications

(9 citation statements)

References 17 publications

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“…The most abundant and well-studied presynaptic glutamate receptors are metabotropic types (Petralia et al, 1996a,b;Shigemoto et al, 1996). Metabotropic glutamate receptors were not examined in the present study, although they are prevalent in the NTS and include both postsynaptic and presynaptic locations Miller, 1994, 1995;Vitagliano et al, 1994;Hay and Lindsley, 1995;Jones et al, 1998). Presynaptic metabotropic glutamate receptors in the NTS modulate the activity of synapses by facilitating (Jones et al, 1998) or inhibiting (Glaum and Miller, 1995) the release of neurotransmitters.…”

Section: Distribution In the Nucleus Of The Tractus Solitariusmentioning

confidence: 85%

Glutamate receptor subunits in the nucleus of the tractus solitarius and other regions of the medulla oblongata in the cat

et al. 1998

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The nucleus of the tractus solitarius (NTS) is a primary termination zone for laryngeal, gustatory, cardiovascular, respiratory, gastrointestinal, and other visceral afferents. Although considerable information is available on the neurochemical aspects of the NTS in general, very little is known about glutamate receptors that may underlie many of the different functions mediated by the NTS. In addition, most previous glutamate receptor distribution studies were performed in the rat, whereas the cat, the subject of many physiological experiments involving the NTS, has received little attention. In the present study, the immunohistochemical distribution of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)-selective glutamate receptor subunits (GluR1, GluR2/3, GluR4) and the N-methyl-D-aspartate (NMDA) receptor subunit NR1 in the cat caudal brainstem was investigated by using subunit-specific antibodies. In the NTS, statistically significant differences were seen in the distribution of each antibody. Highest labeling was seen for GluR2/3 in most subnuclei, whereas GluR1-immunoreactive neurons were found more frequently than were NR1- or GluR4-immunoreactive neurons. GluR1 immunolabeling was particularly high in the interstitial subnucleus, whereas GluR2/3 immunolabeling was particularly high in the intermediate subnucleus. Qualitatively, labeling for GluR4 was most common in glia. The present results indicate that glutamate receptors show different subunit distributions in the subnuclei of the NTS and in other adjacent structures. This finding suggests that neurons in these structures are designed to respond differently to excitatory input.

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Section: Distribution In the Nucleus Of The Tractus Solitariusmentioning

confidence: 85%

Glutamate receptor subunits in the nucleus of the tractus solitarius and other regions of the medulla oblongata in the cat

et al. 1998

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“…Norepinephrine or ␣ 1 -adrenoreceptor agonists has been shown to reduce the amplitude of an early transient outward current presumed to be an A current in neurons from CA1 hippocampus (43) and dorsal raphe nucleus (46), and in ventricular myocytes (47). The A-type current has also been shown to be inhibited by glutamate in visceral sensory neurons (48) and angiotensin II in hypothalamic and brainstem neurons (21). Future experiments should examine whether PHE attenuates the A current in VMN neurons.…”

Section: ␣1-adrenergic Effects On Vmnmentioning

confidence: 98%

Estradiol modulation of phenylephrine-induced excitatory responses in ventromedial hypothalamic neurons of female rats

Lee

Kyrozis

Chevaleyre

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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Estrogens act within the ventromedial nucleus of the hypothalamus (VMN) to facilitate lordosis behavior. Estradiol treatment in vivo induces ␣1b-adrenoreceptor mRNA and increases the density of ␣1B-adrenoreceptor binding in the hypothalamus. Activation of hypothalamic ␣1-adrenoceptors also facilitates estrogen-dependent lordosis. To investigate the cellular mechanisms of adrenergic effects on VMN neurons, whole-cell patch-clamp recordings were carried out on hypothalamic slices from control and estradiol-treated female rats. In control slices, bath application of the ␣1-agonist phenylephrine (PHE; 10 M) depolarized 10 of 25 neurons (40%), hyperpolarized three neurons (12%), and had no effect on 12 neurons (48%). The depolarization was associated with decreased membrane conductance, and this current had a reversal potential close to the K ؉ equilibrium potential. The ␣ 1b -receptor antagonist chloroethylclonidine (10 M) blocked the depolarization produced by PHE in all cells. From estradiol-treated rats, significantly more neurons in slices depolarized (71%) and fewer neurons showed no response (17%) to PHE. PHEinduced depolarizations were significantly attenuated with 4-aminopyridine (5 mM) but unaffected by tetraethylammonium chloride (20 mM) or blockers of Na ؉ and Ca 2؉ channels. These data indicate that ␣1-adrenoceptors depolarize VMN neurons by reducing membrane conductance for K ؉ . Estradiol amplifies ␣1b-adrenergic signaling by increasing the proportion of VMN neurons that respond to stimulation of ␣1b-adrenergic receptors, which is expected in turn to promote lordosis.estrogen ͉ norepinephrine ͉ ventromedial hypothalamus T he ventromedial nucleus of the hypothalamus (VMN) has estrogen-concentrating neurons and is known for its role in the expression of female sexual behavior (1). Estrogens act within in the ventrolateral portion of the VMN to facilitate female reproductive behavior. Estradiol treatment in vivo increases levels of mRNA encoding the ␣ 1b -adrenergic receptor and decreases levels of ␣ 2 -adrenergic receptor protein and mRNA (2, 3). ␣ 1 -Adrenergic transmission facilitates estrogendependent sexual behavior in rodents (4, 5). One brain area where norepinephrine is thought to have this effect is in the VMN. The VMN is innervated by noradrenergic nerve terminals that originate from the brainstem A1 and A2 cell groups (6).There is a considerable amount of evidence that noradrenergic inputs to the hypothalamus are involved in the neuroendocrine control of female reproductive behavior: (i) neurotoxininduced lesions of hypothalamic noradrenergic terminals impair lordosis behavior in ovariectomized, estrogen/progesteronetreated female rats (7), (ii) microinjection of norepinephrine or adrenergic receptor agonists directly into the VMN induces lordosis in ovariectomized, estrogen-primed female rats (8), (iii) implantation of the ␣ 1 -noradrenergic receptor antagonist prazosin into the ventrolateral VMN of ovariectomized, steroid primed rats inhibits lordosis (9), (iv) norepinephrine is released with...

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“…Receptors from all three subtype groups of mGluR have been identified within the DVC (20,79,102,103, 186–189, 255). Group I mGluR are predominantly located postsynaptically (212) while Group II and group III mGluR are predominantly at presynaptic sites and modulate synaptic transmission (20, 79, 102, 186, 188, 211, 546). The presence of and location of mGluR within central vagal neurocircuits suggests that the glutamate released from vagal afferent terminals, in addition to relaying vagal afferent information, may also exert a longer term, more modulatory role over the activity of vagal neurocircuits.…”

Section: Properties and Organization Of Vagal Efferent Motoneuronsmentioning

confidence: 99%

Central Nervous System Control of Gastrointestinal Motility and Secretion and Modulation of Gastrointestinal Functions

Browning

Travagli

2014

Comprehensive Physiology

449

388

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Although the gastrointestinal (GI) tract possesses intrinsic neural plexuses that allow a significant degree of autonomy over GI functions, the central nervous system (CNS) provides extrinsic neural inputs that regulate, modulate, and control these functions. While the intestines are capable of functioning in the absence of extrinsic inputs, the stomach and esophagus are much more dependent upon extrinsic neural inputs, particularly from parasympathetic and sympathetic pathways. The sympathetic nervous system exerts a predominantly inhibitory effect upon GI muscle and provides a tonic inhibitory influence over mucosal secretion while, at the same time, regulates GI blood flow via neurally mediated vasoconstriction. The parasympathetic nervous system, in contrast, exerts both excitatory and inhibitory control over gastric and intestinal tone and motility. Although GI functions are controlled by the autonomic nervous system and occur, by and large, independently of conscious perception, it is clear that the higher CNS centers influence homeostatic control as well as cognitive and behavioral functions. This review will describe the basic neural circuitry of extrinsic inputs to the GI tract as well as the major CNS nuclei that innervate and modulate the activity of these pathways. The role of CNS-centered reflexes in the regulation of GI functions will be discussed as will modulation of these reflexes under both physiological and pathophysiological conditions. Finally, future directions within the field will be discussed in terms of important questions that remain to be resolved and advances in technology that may help provide these answers.

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Metabotropic glutamate receptor inhibition of visceral afferent potassium currents

Cited by 16 publications

References 17 publications

Glutamate receptor subunits in the nucleus of the tractus solitarius and other regions of the medulla oblongata in the cat

Glutamate receptor subunits in the nucleus of the tractus solitarius and other regions of the medulla oblongata in the cat

Estradiol modulation of phenylephrine-induced excitatory responses in ventromedial hypothalamic neurons of female rats

Central Nervous System Control of Gastrointestinal Motility and Secretion and Modulation of Gastrointestinal Functions

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