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31.
The present investigation was conducted to determine whether norepinephrine or acetylcholine systems of the amygdala could be involved in two adaptive feeding behaviors in the rat: development of taste aversion and recovery from neophobia. In a taste aversion paradigm, a single bilateral injection of physostigmine directly into the amygdala at the onset of an apomorphine-induced illness experience produced a time-dependent attenuation in the development of taste aversion; in contrast, norepinephrine had no disruptive effects. In a neophobia paradigm, norepinephrine injected directly into the amygdala after a novel taste experience resulted in a time-dependent attenuation in recovery from neophobia; however, physostigmine produced no disruptive effects. Hence, acetylcholine appears to mediate taste-illness associations, while norepinephrine plays an important role in recovery from neophobia, i.e., taste-“learned safety” associations. 相似文献
32.
Robert N. Holdefer Barry L. Jacobs 《Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale》1994,100(3):444-452
Neurons in the locus coeruleus (LC) encode information related to behavioral state in a tonic pattern of firing and information
related to the occurrence of a sensory stimulus in a phasic pattern of firing. The effects of phasic stimulation of the LC
(6 pulses at 30 Hz), designed to approximate its physiological activation by sensory stimuli, were studied in the lateral
geniculate nucleus (LGN) of anesthetized rats. Phasic stimulation of the LC significantly increased neuronal firing in the
LGN with a mean latency 320 ms from onset of stimulation. Receiver operating characteristic analyses on a trial-by-trial basis
showed that phasic LC stimulation can result in a highly discriminable signal in the LGN. This increased neuronal firing rate
in the LGN was specific for the site of stimulation and was reduced by the norepinephrine synthesis inhibitor αmethyl-p-tyrosine
and by intravenous WB-4101 (α1-receptor antagonist). Neurons in the LGN have a singlespike firing mode when sensory information is faithfully relayed from
retina to cortex and a burst-firing mode when the transfer of this information is degraded. Phasic LC stimulation reduced
burst firing (2–5 ms interspike intervals, ISIs) at low frequencies ( ≤4 Hz) in the LGN, and for some neurons there was an
absolute decrease in burst-like ISIs after LC stimulation, despite an increase in mean firing rate. 相似文献
33.
Neuroendocrine and cardiovascular stress reactivity was studied in healthy middle-aged individuals whose parental history included essential hypertension and/or myocardial infarction and a control group without parental history of cardiovascular disease. All subjects completed a rest session (1 hour) and a stress session (1 hour). The stress session included behavioral (mirror image tracing, mental arithmetic, and the Stroop color word conflict test) and physical stressors (the cold pressor test and isometric exercise). Systolic and diastolic blood pressures and heart rate were recorded at baseline before and during all stressors. Specimens for determination of urinary catecholamines and cortisol were sampled after the rest and stress sessions respectively. Generally, a parental history of hypertension but not of myocardial infarction influenced neuroendocrine and cardiovascular stress reactivity. A family history of hypertension was associated with exaggerated epinephrine, norepinephrine, and cortisol excretion during stress and with enhanced heart-rate reactivity to behavioral (mental arithmetic and mirror image tracing) but not to physical stressors (isometric exercise or the cold pressor test). We conclude that individuals with a family history of hypertension tend to display exaggerated cardiovascular and neuroendocrine reactivity to stress. 相似文献
34.
We provide here 29 genetic variations, including 28 novel ones, in five genes that are potentially involved in the excitement
of cardiomyocytes: we found 4 in KCNA10, 2 in KCNK1, 8 in KCNK6, 11 in SLC18A1 (VMAT1), and 4 in SLC6A2 (norepinephrine transporter). We also examined their allelic frequencies in a Japanese population of long QT syndrome-affected
and nonaffected individuals. These data would be useful for genetic association studies designed to investigate acquired arrhythmias.
Received: May 22, 2001 / Accepted: June 8, 2001 相似文献
35.
R.D. Myers H.S. Swartzwelder J.M. Peinado T.F. Lee J.R. Hepler D.M. Denbow J.M.R. Ferrer 《Brain research bulletin》1986,17(4):583-597
The purpose of this investigation was to determine the functional relationship between putative satiety peptides and endogenous norepinephrine (NE) activity in the hypothalamus. Permanent guide cannulae for push-pull perfusion were implanted stereotaxically in Sprague-Dawley rats so as to rest above the medial or lateral hypothalamus (LH). Post-operatively, the animals were either satiated with food and water, both available ad lib, or fasted for 18-22 hr prior to an experiment. To perfuse a site in the LH, paraventricular (PVN) or ventromedial nucleus (VMN), a concentric 29-23 ga push-pull cannula system was lowered to a pre-determined site, in most cases after catecholamine stores had been pre-labeled with [3H]-NE. During control tests, an artificial CSF was perfused at a rate of 20-25 microliter/min for 5-8 min with a 5 min interval between each sample. The addition of cholecystokinin (CCK) in a concentration of 2.0-6.0 ng/microliter to the CSF perfused in PVN or VMN of the satiated rat enhanced the efflux of NE; however, in the fasted animal CCK often suppressed the catecholamine's release. Perfused in the LH, CCK exerted opposite effects, typically augmenting NE output when the rat was fasted but not affecting the amine's activity during the sated condition. Proglumide (1.2 micrograms/microliter) attenuated CCK's effect in releasing NE when the antagonist was perfused in the PVN of the satiated rat. Similar experiments in which neurotensin (NT) was perfused in the LH, PVN and VMN revealed virtually the same inverse effects on NE release in the fasted and satiated rat, which again were anatomically specific. Finally, insulin and 2-deoxy-D-glucose (2-DG) exerted similar state-dependent effects on the release of NE within LH and PVN. Overall, the results suggest that CCK or other neuroactive peptide could serve as a "neuromodulator" of the pre-synaptic release of NE within classical hypothalamic structures which are thought to underlie both hunger and satiety. The state-dependent nature of the peptides' activity on the noradrenergic feeding mechanism implies that these substances constitute a pivotal portion of the profile of factors which impinge functionally upon the hypothalamic neurons responsible for the feeding response and its cessation. 相似文献
36.
The effects of several antidepressants on the release of (3H)-norepinephrine (NE) from homogenates of rat cerebral cortex were studied. A continuous superfusion collection system was used in order to differentiate these effects from effects on reuptake. Amitriptyline, maprotiline, mianserin, and trazodone produced a statistically significant decrease in spontaneous tritium efflux when present in the superfusion medium at a concentration of 1.0 M. The other antidepressants studied had no effect. We used a buffer with the K+ concentration raised to 56 mM as a model of depolarization-induced release. Desipramine, fluoxetine, and iprindole (again at 1.0 M) caused a significant decrease in this measure. These results indicate that some of both the tricyclic and atypical antidepressants may alter spontaneous or depolarization-induced release of NE.This work was supported in part by a grant from the Pharmaceutical Manufactures Association Foundation-Medical Student Research Fellowship 相似文献
37.
微量去甲肾上腺素预处理对大鼠心肌延迟性保护效应的实验研究 总被引:2,自引:0,他引:2
卢彦珍!病理生理学教研室 《长治医学院学报》2000,(3)
目的 :通过在体大鼠心肌缺血 /再灌注 (I/R)模型探讨去甲肾上腺素预处理对I/R心肌的延迟性保护作用。方法 :将实验动物分为假手术、I/R和去甲肾上腺素预处理 (NEPC) 3组 ,分别测定心肌梗塞面积、左室功能 ,观察心肌超微结构及血清肌酸激酶 (CK)及乳酸脱氢酶 (LDH)活性的变化。结果 :预先注入去甲肾上腺素能明显减小I/R所致的心肌梗塞面积 ,改善左室功能 ,保护心肌超微结构 ,增强细胞稳定性减少细胞内蛋白酶的漏出。结论 :去甲肾上腺素预处理可介导延迟性心肌保护效应 ,鉴于该法简便且无明显创伤更易于临床推广应用。 相似文献
38.
Alterations in catecholamine levels and neurotransmission have been shown in depressive disorders. However, the exact sites of alterations and the relation between these alterations to the etiology of the disease and the effectiveness of antidepressant therapy are poorly understood. In this study, catecholamine levels and metabolism were measured in specific brain regions of a genetic rat model of depression [Flinders Sensitive Line (FSL) rats], and compared to normal Sprague-Dawley rats. Norepinephrine levels were found to be two to threefold higher in the nucleus accumbens, prefrontal cortex, hippocampus and median raphe nucleus of FSL rats as compared with control Sprague-Dawley rats. Dopamine levels were sixfold higher in the nucleus accumbens and twofold higher in the striatum, hippocampus and hypothalamus of FSL rats as compared with control Sprague-Dawley rats. After chronic treatment with the antidepressant desipramine, the immobility score in a swim test, as a measure of a behavioral deficit, as well as catecholamine levels of the FSL rats became normalized, but these parameters in the control rats did not change. The results indicate that the behavioral deficits expressed in the FSL model for depression correlate with increased catecholamine levels in specific brain sites, and further suggest the FSL rats as a model for elucidation of the molecular mechanism of clinically used antidepressant drugs. 相似文献
39.
Effect of intracerebral norepinephrine depletion on outcome from severe forebrain ischemia in the rat 总被引:3,自引:0,他引:3
Nellgård BM Miura Y Burkhard Mackensen G Pearlstein RD Warner DS 《Brain research》1999,847(2):174-269
Manipulations of plasma catecholamine concentrations influence outcome from ischemic brain insults. It has been suggested that these effects are mediated by influences on brain catecholamine concentrations. This study examined whether major changes in brain norepinephrine concentrations can alter outcome from severe forebrain ischemia. Sprague-Dawley rats were administered 50 mg/kg i. p. N-(chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) or were left untreated (control). One week later, these rats were subjected to either 7 or 8 min of normothermic forebrain ischemia (bilateral carotid occlusion and MABP=30 mmHg) and allowed to recover for 4 days. Histologic damage was then evaluated. In other control and DSP-4-treated animals, hippocampal microdialysate norepinephrine concentrations were measured before, during and after 8 min of forebrain ischemia. Norepinephrine concentrations were also determined in brain homogenates from non-ischemic DSP-treated and control rats. A 95% depletion of norepinephrine was observed in brain homogenates from non-ischemic DSP-4-treated rats compared with control. During ischemia, microdialysate norepinephrine concentrations increased in control but not in DSP-4-treated rats (P=0.002). For plasma, intra-ischemic epinephrine concentrations increased 8-10-fold and returned to baseline values post-ischemia with no differences between groups. Plasma norepinephrine values remained unchanged in both groups. Histologic damage resulting from either 7 or 8 min of ischemia in hippocampal structures, caudoputamen, and neocortex was similar between DSP-4-treated and control groups. This study could not identify any effect of major changes in brain norepinephrine concentrations on ischemic brain damage. These data indicate that peripheral catecholamine effects on near-complete forebrain ischemic outcome are unlikely to be mediated by effects on central catecholamine concentrations. 相似文献
40.
Rationale: Previous studies have demonstrated that anxiolytic-like anticonflict effects can be produced by either (1) acute administration
of traditional anti-anxiety compounds (benzodiazepines or barbiturates) or (2) chronic administration of tricyclic (TCA) or
monoamine oxidase inhibitor (MAOI) antidepressants. Objective: The present study determined the effects of noradrenergic neuronal depletion on these distinct anticonflict treatments.
Methods: After 3 weeks of training in a repeated measures drink suppression conflict paradigm, water-restricted rats consumed 11–14 ml
water/session (unpunished responding) and accepted 25–40 shocks/session (punished responding) during control (i.e., non-drug)
10-min test sessions. The noradrenergic neurotoxin DSP4 [N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine hydrochloride; 65 mg/kg, IP] or its vehicle (saline; 1 ml/kg) was administered after 3 weeks of
conflict testing. Conflict behavior was then evaluated for 8 weeks post-treatment. In separate groups of DSP4- and vehicle-pretreated
subjects, the effects of acute administration (10-min pretreatment) of phenobarbital (5–40 mg/kg) or alprazolam (0.3–2.5 mg/kg)
were determined. In a third experiment, the effects of chronic treatment with the TCA desipramine (DMI; 5 mg/kg, twice daily
for 8 weeks) or the non-selective MAOI phenelzine (4.0 mg/kg, twice daily for 8 weeks) on conflict behavior were determined
in additional groups of DSP4- or vehicle-pretreated subjects. Results: DSP4 treatment produced a modest yet statistically significant decrease in punished responding (i.e., anxiogenic-like effect)
relative to vehicle controls. DSP4 pretreatment did not alter the anticonflict effects of acute alprazolam or phenobarbital
treatment. In contrast, DSP4 treatment completely abolished the anticonflict effects produced by chronic DMI or chronic phenelzine
treatment. Conclusions: Thus, noradrenergic neuronal integrity appears to be required for the anxiolytic-like effects of chronic antidepressant
treatment, but not for the anxiolytic-like effects of acute treatment with barbiturates and benzodiazepines.
Received: 6 August 1998/Final version: 16 October 1998 相似文献