Nitric oxide impairs spatial learning and memory in a rat model of Alzheimer's disease via disturbance of glutamate response in the hippocampal dentate gyrus during spatial learning.

Nitric oxide (NO)-dependent pathways may play a significant role in the decline of synaptic and cognitive functions in Alzheimer's disease (AD). However, whether NO in the hippocampal dentate gyrus (DG) is involved in the spatial learning and memory impairments of AD by affecting the glutamate (Glu) response during these processes is not well-understood. Here, we prepared an AD rat model by long-term i.

[Chronic stress increases dopamine levels in hippocampal dentate gyrus and impairs spatial learning and memory in rats].

The objective of this study was to elucidate the effect of chronic stress (CS) on dopamine (DA) level and synaptic efficiency in the hippocampal dentate gyrus (DG) during spatial learning and memory. Sprague Dawley (SD) male rats were randomly divided into control group and CS group (n = 10). CS group was treated with chronic mild unpredictable stress, and control group did not receive any treatments.

Norepinephrine in the dentate gyrus is involved in spatial learning and memory alteration induced by chronic restraint stress in aged rats.

The role of norepinephrine of the hippocampal dentate gyrus in spatial learning and memory alteration induced by chronic restraint stress (CRS, 3 h/day, 6 weeks) was investigated in aged rats. Spatial learning and memory were assessed by the Morris water maze (MWM), and the extracellular concentration of norepinephrine and amplitude of field excitatory postsynaptic potential (fEPSP) were measured in the dentate gyrus during MWM test in freely-moving rats. Next, the involvement of β-adrenoceptors in spatial learning and memory of CRS rats was examined by microinjection of its antagonist (propranolol) into the dentate gyrus.

Activation of β-adrenoceptor facilitates active avoidance learning through enhancement of glutamate levels in the hippocampal dentate gyrus.

Long-term potentiation (LTP) is widely accepted as the best studied model for neurophysiological mechanisms that could underlie learning and memory formation. Despite a number of studies indicating that β-adrenoceptors in the hippocampal dentate gyrus (DG) is involved in the modulation of learning and memory as well as LTP, few studies have used glutamate release as a visual indicator in awake animals to explore the role of β-adrenoceptors in learning-dependent LTP. Therefore, in the present study, the effects of propranolol (an antagonist of β-adrenoceptor) and isoproterenol (an agonist of β-adrenoceptor) on extracellular concentrations of glutamate and amplitudes of field excitatory postsynaptic potential were measured in the DG region during active avoidance learning in freely moving conscious rats.

α1-Adrenoceptors in the hippocampal dentate gyrus involved in learning-dependent long-term potentiation during active-avoidance learning in rats.

The hippocampus is the key structure for learning and memory in mammals and long-term potentiation (LTP) is an important cellular mechanism responsible for learning and memory. The influences of norepinephrine (NE) on the modulation of learning and memory, as well as LTP, through β-adrenoceptors are well documented, whereas the role of α1-adrenoceptors in learning-dependent LTP is not yet clear. In the present study, we measured extracellular concentrations of NE in the hippocampal dentate gyrus (DG) region using an in-vivo brain microdialysis and high-performance liquid chromatography techniques during the acquisition and extinction of active-avoidance behavior in freely moving conscious rats.

Propofol depresses cerebellar Purkinje cell activity via activation of GABA(A) and glycine receptors in vivo in mice.

Propofol is an intravenous sedative-hypnotic agen, which causes rapid and reliable loss of consciousness. Under in vitro conditions, propofol activates GABAA and glycine receptors in spinal cord, hippocampus and hypothalamus neurons. However, the effects of propofol on the cerebellar neuronal activity under in vivo conditions are currently unclear.

[Effect of 5-HT1A receptors in the hippocampal DG on active avoidance learning in rats].

Objective: To investigate the effects of serotonin (5-HTIA) receptors in the hippocampal dentate gyrus (DG) on active avoidance learning in rats.

Methods: Totally 36 SD rats were randomly divided into control group, antagonist group and agonist group(n = 12). Active avoidance learning ability of rats was assessed by the shuttle box.

Nitric oxide facilitates active avoidance learning via enhancement of glutamate levels in the hippocampal dentate gyrus.

The hippocampus is a key structure for learning and memory in mammals, and long-term potentiation (LTP) is an important cellular mechanism responsible for learning and memory. Despite a number of studies indicating that nitric oxide (NO) is involved in the formation and maintenance of LTP as a retrograde messenger, few studies have used neurotransmitter release as a visual indicator in awake animals to explore the role of NO in learning-dependent long-term enhancement of synaptic efficiency. Therefore, in the present study, the effects of l-NMMA (a NO synthase inhibitor) and SNP (a NO donor) on extracellular glutamate (Glu) concentrations and amplitudes of field excitatory postsynaptic potential (fEPSP) were measured in the hippocampal dentate gyrus (DG) region during the acquisition and extinction of active-avoidance behavior in freely-moving conscious rats.

Β-adrenoceptors in the hypothalamic paraventricular nucleus modulate the baroreflex in conscious rats.

The role of β-adrenoceptors of the hypothalamic paraventricular nucleus (PVN) in modulation of the baroreflex was investigated in conscious rats. The baroreflex was induced by intravenous injection of phenylephrine, and then the extracellular concentration of norepinephrine in the PVN region determined using microdialysis and high-performance liquid chromatography. Next, the role of the β-adrenoceptor in modulation of the baroreflex was investigated by perfusion of its antagonist or agonist into the PVN using microdialysis.

Intracerebroventricular injection of stresscopin-related peptide enhances cardiovascular function in conscious rats.

Stresscopin-related peptide (SRP), which is a member of the corticotropin-releasing factor (CRF) family, is a high-affinity ligand for the type 2 corticotropin-releasing factor receptor (CRF-R2) and is involved in stress-coping responses. Central treatment with SRP suppresses food intake, delays gastric emptying and decreases heat-induced edema, but the effects of central administration of SRP on the cardiovascular system are unclear. Here we examined the effects of intracerebroventricular (i.

Effects of stresscopin on rat hypothalamic paraventricular nucleus neurons in vitro.

The effects of stresscopin (SCP) on rat paraventricular nucleus (PVN) neurons were examined using whole-cell patch-clamp recordings and single-cell reverse-transcription multiplex polymerase chain reaction (SC-RT-mPCR) techniques. Under current-clamp conditions, bath application of SCP (100 nM) induced inhibition in 35.2% (37/105) of putative magnocellular neurons and 24.

[Cardiovascular change induced by central hypertonic saline are accompanied by GABA release in awake rats].

Aim: To investigate the possible involvement of gamma-aminobutyric acid (GABA) in the paraventricular nucleus (PVN) in cardiovascular responses induced by central salt loading.

Methods: Direct perfusion into PVN region with hypertonic saline (0.6 mol/L) was performed in conscious rats by using an in vivo brain microdialysis technique.

Changes of some amino acid concentrations in the medial vestibular nucleus of conscious rats following acute hypotension.

Microdialysis and high performance liquid chromatography (HPLC) were used to measure the changes of certain amino acids in the medial vestibular nucleus (MVN) of conscious rats in order to understand whether those amino acids are involved in the regulation of blood pressure. Acute hypotension was induced by infusing sodium nitroprusside (SNP) into the femoral vein. In the control group, glutamate (Glu) release increased, though gamma-aminobutyric acid (GABA) and taurine (Tau) release decreased in the MVN following acute hypotension.

[Changes of gamma-aminobutyric acid and glycine released in the medial vestibular nucleus following acute hypotension in conscious rats].

To understand whether some amino acids in the medial vestibular nucleus (MVN) of conscious rats are involved in the regulation of blood pressure, microdialysis technique and high performance liquid chromatography (HPLC) were used to measure the changes of gamma-aminobutyric acid (GABA) and glycine (Gly) in this central area. Wistar rats (250-350 g) were randomly divided into three experimental groups: the control group with intact labyrinths; the ipsilateral MVN of unilateral labyrinthectomy (UL); contralateral MVN of the UL. Acute hypotension was induced by intravenous infusion of sodium nitroprusside (SNP).

[Facilitative effect of glycine on regulation of baroreflex in the hypothalamic paraventricular nucleus of conscious rats.].

The hypothalamic paraventricular nucleus (PVN) is a central site for integration of the endocrine system and the autonomic nervous system. Despite a number of studies have pointed out the importance of the PVN in the central regulation of cardiovascular functions, the chemical mediators in the PVN responsible for mediating baroreflex are not well understood. In the present study, we used the conscious rats to investigate the possible involvement of glycine (Gly) in PVN in the central regulation of baroreflex induced by intravenous injection of phenylephrine (0.

[Effect of antagonism of glutamate receptors in the PVN region on baroreflex in conscious rats].

Aim: To investigate the possible involvement of glutamate(Glu) in the paraventricular nucleus (PVN) in the central regulation of baroreflex.

Methods: The baroreflex was induced by intravenous injection of phenylephrine in conscious rats, and the extracellular concentration of Glu in the PVN region was measured by microdialysis and high performance liquid chromatography (HPLC) techniques. To determine whether the observed Glu release was involved in the baroreflex, NMDA and non-NMDA receptor antagonists, MK-801 and CNQX, were perfused in the PVN region during baroreflex.

Changes of amino acid concentrations in the rat medial vestibular nucleus following unilateral labyrinthectomy.

To understand the neurochemical mechanisms underlying the vestibular compensation, we determined the levels of amino acids such as aspartate, glutamate, glutamine, glycine, taurine, alanine in the medial vestibular nucleus (MVN) following unilateral labyrinthectomy (UL), by using in vivo brain microdialysis and high-performance liquid chromatography technique. Rats were pretreated by infusing 2% lidocaine 1.2 mL or 10 mg arsanilic acid into the tympanic cavity to obstruct uni-periphery vestibular organ, and then the levels of amino acids were determined in MVN of normal control and ipsilateral or contralateral lesional (ipsi-/contra-lesional) rats.

[Changes of glutamate and taurine released in the medial vestibular nucleus following acute hypotension].

In order to understand whether some special amino acids in the medial vestibular nucleus (MVN) of rats are involved in the regulation of blood pressure, we used microdialysis technique and high performance liquid chromatography (HPLC) to measure the changes of glutamate and taurine in this central area. Acute hypotension was induced by hemorrhage from the femoral artery. It was observed that the basal release of glutamate and taurine in the MVN was stable about 90 min after the beginning of microdialysis.

Enhanced cardiovascular alteration and Fos expression induced by central salt loading in a conscious rat transgenic for the metallothionein-vasopressin fusion gene.

The present study is an investigation of the responses of the cardiovascular system and Fos expression to intracerebroventricular (i.c.v.

[Effect of microinjection of atrial natriuretic peptide into the paraventricular nucleus on baroreflex sensitivity in conscious rats].

The role of atrial natriuretic peptide (ANP) in the central regulation of the circulation is known to be a neurotransmitter or a neuromodulator, but its actions on baroreceptor reflex function are not fully resolved. The present study examined the role of ANP (6, 60 ng/0.2 microl) by direct microinjection into the hypothalamic paraventricular nucleus (PVN) in conscious rats.

Possible involvement of nitric oxide in the central salt-loading-induced cardiovascular responses in conscious rats.

The objective of this study was to elucidate the possible involvement of nitric oxide (NO) in the cardiovascular responses induced by central salt loading. Direct perfusion of the hypothalamic paraventricular nucleus (PVN) region with hypertonic saline (0.3 or 0.