Inhibition of NMDA Receptor Activation in the Rostral Ventrolateral Medulla by Amyloid-β Peptide in Rats.

N-methyl-D-aspartate (NMDA) receptors, a subtype of ionotropic glutamate receptors, are important in regulating sympathetic tone and cardiovascular function in the rostral ventrolateral medulla (RVLM). Amyloid-beta peptide (Aβ) is linked to the pathogenesis of Alzheimer's disease (AD). Cerebro- and cardiovascular diseases might be the risk factors for developing AD.

Ovariectomy Exacerbates Acute Ethanol-Induced Tachycardia: Role of Nitric Oxide and NMDA Receptors in the Rostral Ventrolateral Medulla.

Ethanol consumption influences cardiovascular functions. In humans, acute consumption of ethanol causes dose-dependent tachycardia. Our previous study showed that ethanol-induced tachycardia might involve decreased nitric oxide (NO) signaling in the brain's medulla.

Activation of mGluR5 and NMDA Receptor Pathways in the Rostral Ventrolateral Medulla as a Central Mechanism for Methamphetamine-Induced Pressor Effect in Rats.

Acute hypertension produced by methamphetamine (MA) is well known, mainly by the enhancement of catecholamine release from sympathetic terminals. However, the central pressor mechanism of the blood-brain-barrier-penetrating molecule remains unclear. We used radio-telemetry and femoral artery cannulation to monitor the mean arterial pressure (MAP) in conscious free-moving and urethane-anesthetized rats, respectively.

Involvement of metabotropic glutamate receptor 5 in ethanol regulation of NMDA receptor activity in rat substantia gelatinosa neurons.

Aims: Glutamatergic receptors are important targets of ethanol. Intake of ethanol may produce analgesic effects. The present study examined the effects of ethanol on the activity of ionotropic glutamate receptors in spinal cord substantia gelatinosa (SG) neurons, critical neurons involved in nociceptive transmission.

Potentiation of NMDA-Mediated Responses by Amyloid-β Peptide 1-40 in Rat Sympathetic Preganglionic Neurons.

The abnormal accumulation of amyloid-β peptides (Aβ) is one of the main characteristics of Alzheimer's disease (AD). Cerebro- and cardiovascular diseases may be the risk factors for developing AD. The effect of Aβ on central sympathetic control of cardiovascular function remains unclear.

Roles of cocaine- and amphetamine-regulated transcript peptide in the rostral ventrolateral medulla in cardiovascular regulation in rats.

Cocaine- and amphetamine-regulated transcript peptide (CARTp) is present in neurons and varicose fibers in the rostral ventrolateral medulla (RVLM) that is crucial in the control of cardiovascular function. Prior research indicated that intracisternal administration of CARTp evokes hypertension and accumulation of Fos in the RVLM. Despite the interaction among CARTp, cardiovascular effect, and the RVLM, no studies have directly examined whether CARTp participates in cardiovascular regulation in the RVLM.

Spontaneously hypertensive rats exhibit higher sensitivity to ethanol-induced hypotensive effects: Role of NMDA receptors and nitric oxide in rostral ventrolateral medulla.

Intake of ethanol (alcohol) affects cardiovascular function. Acute ethanol intake has been shown to lower blood pressure (BP) in hypertensive patients. The present study was undertaken to examine the effects and mechanisms of acute administration of ethanol on BP in hypertensive and normotensive rats.

Involvement of NMDA Receptors, Nitric Oxide, and GABA in Rostral Ventrolateral Medulla in Acute Ethanol-Induced Cardiovascular Responses in Rats.

Background: Consumption of ethanol (EtOH) (alcohol) has many effects on physiological functions, particularly those in the central nervous system (CNS) and cardiovascular system. Acute excessive intake of EtOH (alcohol intoxication) may cause hypotension and tachycardia. In this study, we examined the mechanistic involvement of glutamatergic N-methyl-d-aspartate (NMDA) receptors, nitric oxide (NO), and γ-aminobutyric acid (GABA) pathways in the CNS in acute EtOH-induced cardiovascular effects.

Role of neuronal nitric oxide synthase (nNOS) at medulla in tachycardia induced by repeated administration of ethanol in conscious rats.

Background: Intake of ethanol (alcohol) has been shown to influence cardiovascular function; the underlying brain mechanism remains unclear. Noting that nitric oxide (NO) system in the CNS is involved in the regulation of cardiovascular function, the present study examined the role of NO in medulla in ethanol-induced cardiovascular changes.

Methods: Ethanol was administered by oral gavage at dose of 3.

Dual regulation by ethanol of the inhibitory effects of ketamine on spinal NMDA-induced pressor responses in rats.

Background: Acute exposure of ethanol (alcohol) inhibits NMDA receptor function. Our previous study showed that acute ethanol inhibited the pressor responses induced by NMDA applied intrathecally; however, prolonged ethanol exposure may increase the levels of phosphorylated NMDA receptor subunits leading to changes in ethanol inhibitory potency on NMDA-induced responses. The present study was carried out to examine whether acute ethanol exposure influences the effects of ketamine, a noncompetitive NMDA receptor antagonist, on spinal NMDA-induced pressor responses.

Cocaine- and amphetamine-regulated transcript (CART) peptide activates ERK pathways via NMDA receptors in rat spinal cord dorsal horn in an age-dependent manner.

Activation of extracellular signal-regulated kinase (ERK) cascade in the spinal cord dorsal horn may contribute to pain hypersensitivity. Our recent study showed that cocaine- and amphetamine-regulated transcript peptide fragment 55-102 (CARTp) increased the levels of phosphoserine 896 and phosphoserine 897 on the N-methyl-d-aspartate (NMDA) receptor NR1 subunit (pNR1-ser896 and pNR1-ser897) via protein kinase A (PKA) and protein kinase C (PKC) signaling pathways leading to increases in NMDA receptor function in spinal cord dorsal horn neurons. Because NMDA receptor, PKC, and PKA signaling pathways may participate in ERK activation, we examined the effects of CARTp on ERK activation in spinal cord dorsal horn neurons in vitro.

Potentiation of spinal NMDA-mediated nociception by cocaine- and amphetamine-regulated transcript peptide via PKA and PKC signaling pathways in rats.

Our previous study showed that cocaine- and amphetamine-regulated transcript peptide fragment 55-102 (CARTp) specifically potentiated spinal N-methyl-D-aspartate (NMDA)-mediated nociceptive transmission in vivo and in vitro. The cellular mechanisms underlying CARTp potentiation of NMDA receptor function remains unclear. The present study was carried out to test the hypothesis that CARTp changes the phosphorylated state of NMDA receptors by activating intracellular signals and subsequently increasing the function of NMDA receptors.

The role of protein kinase A in acute ethanol-induced neurobehavioral actions in rats.

Background: cAMP-dependent protein kinase (PKA) signaling pathways are involved in the regulation of ethanol-induced sedative effects in knockout mouse models. In the present study, we examined the role of PKA on the behavioral action caused by ethanol in Sprague Dawley rats.

Methods: A loss of righting reflex (LORR) test was used to study the acute sedative effects of intraperitoneally injected ethanol.

Expression and activity of cocaine- and amphetamine-regulated transcript peptide(1-39) in the rat.

Cocaine- and amphetamine-regulated transcript (CART) peptide consists of a family of peptides. Expression of the peptide fragment CART(1-39) was explored in the rat using an antiserum directed against CART(1-39) of the short form of the human CART prohormone. CART(1-39)-immunoreactivity, herein referred to as irCART, was detected in the rat central and peripheral nervous tissues with a pattern similar to that labeled with the antiserum CART(55-102) or CART(79-102).

Ethanol inhibition of NMDA-induced responses and acute tolerance to the inhibition in rat rostral ventrolateral medulla in vivo: Involvement of cAMP-dependent protein kinases.

Our recent study showed that intravenous ethanol selectively inhibited the pressor effects elicited by the microinjection of N-methyl-D-aspartate (NMDA) into rostral ventrolateral medulla (RVLM) and acute tolerance to the inhibition was observed during prolonged application of ethanol in anesthetized Sprague-Dawley rats. In this study, we examined the role of the cAMP-dependent protein kinase (PKA) signaling pathway in acute tolerance to ethanol inhibition of NMDA-induced responses in rat RVLM. A significant increase in the level of PKA-regulated phosphoserine 897 on the NMDA NR1 subunit was found in the rostroventral medulla during acute ethanol tolerance.

Potentiation of spinal N-methyl-D-aspartate-mediated nociceptive transmission by cocaine-regulated and amphetamine-regulated transcript peptide in rats.

The present study examined the effects of cocaine-regulated and amphetamine-regulated transcript peptide (CARTp) fragment 55-102, on N-methyl-D-aspartate (NMDA)-mediated nociceptive transmission in vivo and in vitro. In-vivo experiments were conducted in Sprague-Dawley rats to evaluate the effects of CARTp on thermal hyperalgesia induced by NMDA or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA). Intrathecal NMDA (1, 2, 4 nmol) or AMPA (0.

Antioxidant activity of fermented soybean extract.

Free radicals are considered to be important causative factors in the development of cancer and cardiovascular diseases. This relationship has led to interest in evaluating the antioxidant capacities of many dietary supplements. Fermented soybean extract is produced by symbiotic fermentation of organic soybean with 20 types of Lactobacillus and yeast.

Acute tolerance to ethanol inhibition of NMDA-induced responses in rat rostral ventrolateral medulla neurons.

The present study was performed to examine the effects of acute ethanol exposure on N-methyl-D-aspartate (NMDA)-induced responses and the development of acute tolerance in rat rostral ventrolateral medulla (RVLM) in vivo and in vitro. Repeated microinjections of NMDA (0.14 nmol) into the RVLM every 30 min caused reproducible increases in mean arterial pressure in urethane-anesthetized rats weighing 325-350 g.

Inhibition by ethanol of NMDA-induced responses and acute tolerance to the inhibition in rat sympathetic preganglionic neurons in vitro and in vivo.

N-methyl-d-aspartate (NMDA) receptors have been demonstrated to be a pivotal target for ethanol action. The present study examined the actions of acute ethanol exposure on NMDA-induced responses and the acute tolerance to ethanol actions in rat sympathetic preganglionic neurons (SPNs) in vitro and in vivo. NMDA (50 microM) applied every 5 min induced reproducible membrane depolarizations of SPNs in neonatal spinal cord slice preparations.

Excitatory action of lead on rat sympathetic preganglionic neurons in vitro and in vivo.

Lead exposure elicited an increase in blood pressure and was considered to be a cardiovascular risk factor. The involvements of sympathetic nervous system and circulating catecholamines have been implicated in lead-induced hypertension. This study examined the effects of PbCl(2) on sympathetic preganglionic neurons (SPNs) in vitro and in vivo.