海马参与自主神经系统调控的研究进展

海马在解剖结构上属于边缘前脑皮质结构,它与下丘脑、杏仁核、脑干有着极其复杂的相互联系。研究发现,刺激海马对自主神经活动产生影响,可引起心率、呼吸、血压等变化;而刺激外周自主神经也影响海马的结构和功能。进一步研究发现,海马可能是通过下丘脑和脑干的核团（如下丘脑室旁核、孤束核等）、内分泌系统和神经递质等参与自主神经系统的调控。     

吗啡对电刺激缰核引起的心血管反应的影响

缰核(Hb)是前脑边缘结构至脑干的驿站,可整合来自前脑边缘结构的信息。Hb发出大量纤维组成后屈束到达脑干广大区域,调节和控制脑干的许多生理功能,其中包括对心血管活动的调节。激活内阿片肽系统可抑制防御性心血管反应,纳洛酮可翻转这种作用。本实验用静脉和侧脑室注射的方法观察了吗啡对电刺激Hb引起的心血管反应的影响。     

电损毁缰核对成年雌性大鼠生殖周期及生育力的影响

电损毁缰核对成年雌性大鼠生殖周期及生育力的影响马丽娜黄民王绍（白求恩医科大学生理教研室,长春１３００２１）边缘前脑至脑干背侧通路的枢纽—缰核（Ｈａｂｅｎｕｌａ,Ｈｂ）参与生殖功能活动的调节。研究资料表明,蟾蜍Ｈｂ的体积在春季生殖期明显增大;在雌兔的Ｈ...     

急性分离缰核神经细胞膜上外向整流钾通道的电生理特性

钾电流参与静息电位的形成及动作电位的复极过程 ,许多神经递质通过调节Ｋ 通道的活动而影响细胞膜的兴奋性。缰核 (Ｈｂ)是连接边缘前脑至脑干背侧通路的驿站 ,参与机体活动的调节。Ｈｂ内也存在多种神经递质 ,而这些递质对Ｋ 通道活动的影响知之甚少。且关于Ｈｂ神经细胞膜上Ｋ 通道的研究主要运用分子生物学的方法 ,电生理研究较少。本实验用膜片钳的方法探讨了Ｈｂ神经细胞膜上最常见的一种Ｋ 通道的电生理特性 ,为探讨Ｈｂ内神经递质的作用机制提供基础。1　材料和方法(1 )Ｈｂ神经细胞的急性分离　将 1 0～ 2 0ｄ的ＳＤ乳鼠断头取脑 ,…     

脑干升压和降压区调节血压的中枢机制及其与延髓头端腹外侧区的机能联系

以往对血压的中枢调节有大量的研究,但由于实验所采用的不同方法和条件存在某些缺点和局限性,使各实验室报道的某些结果不一致,甚室完全相反。本文综述了经方法学上改进或多种实验结果验证后的脑干重要升压的和降压区对血压的中枢调节机制。     

缰核、弓状核对大鼠痛阈和针刺镇痛的影响

形态学资料和电生理实验证明,缰核是前脑边缘结构至脑干的中间枢纽,它接受隔区、视前区、海马、伏隔核等的抑制性作用,进而对脑干的有关核团如中缝核、蓝斑核的活动进行调节,从而加强针刺镇痛效应。本实验以整体动物的甩尾阈值为指标,确定并衡量缰核对基础痛阈的影响和在针刺镇痛中的作用。     

电刺激大鼠隔后部对血压和心率的影响及其下行通路

心血管中枢广泛分布在脊髓至大脑皮层的各级水平。其中边缘系统对心血管活动的调节作用显得更为突出。隔后部(CS)是边缘系统成员之一。缰核(Hb)是前脑边缘结构至脑干的驿站,前脑边缘结构的许多部位都有纤维会聚到Hb,CS就是其中之一。本实验室已证明     

γ-氨基丁酸与心血管活动的调节

γ-氨基丁酸(GABA)是脑内具有普遍抑制作用的一种神经介质,它涉及多种重要功能。近年来,不少报道说明GABA与心血管活动调节有密切关系。这方面的研究多采用药理学方法。由于所用药物和用药方法不同,常引致不同的实验结果。一、GABA的中枢作用GABA在中枢有降压作用,也有升压作用。从目前的资料看,GABA降压作用的报道较多。(一)GABA的降压作用1973年,Guertzenstein首先提出GABA作用于脑干,引起血压下降。其后,Antonaccio等报道,向猫脑室注射GABA受体激动剂异鹅羔胺(musci-mol),动物血压明显降低和心率减慢。脑室内注射GABA也得到类似结果。这些药物的     

下丘脑hypocretin神经元协调睡眠-觉醒功能

哺乳动物的生活实际上是由睡眠与觉醒、休息与活动、镇静与警戒组成的。上世纪早期的研究预示了在下丘脑后部有一促觉醒区 ,目前神经科学家已证实了上述预测。下丘脑的hypocretin(也称为orexin)神经元对于觉醒系统的调节起着决定性作用 ,该神经元的活动能使睡意减少 ,同时提高觉醒和警戒。Hypocretin神经元分泌兴奋性神经递质hypocretin 1和hypocretin 2 ,投射到参与睡眠 觉醒机制的脑干 ,脑干的这些结构各有自己主要的神经递质 (如缝核的 5 羟色胺、蓝斑的去甲肾上腺素、背侧被盖的乙酰胆碱、乳头结节核的组胺、内侧隔核与斜角带核的γ …     

雌二醇对缰核神经元电活动的影响

边缘系统参与机体生殖功能的调节,作为边缘前脑至脑干背侧通路的枢纽缰核(ｈａｂｅｎｕｌａｒｎｕｃｌｅｕｓ,Ｈｂ)与下丘脑之间互有紧密的双相联系,在功能上互为协调。Ｈｂ对生殖功能活动具有重要的调节作用。在不同性甾体激素水平下,Ｈｂ内单位电活动形式明显不同。本文以电活动为指标,直接观察Ｈｂ在不同性甾体激素水平时雌激素敏感性相关神经元的电变化及其与内侧视前区下丘脑前区(ｍＰＯＡＡＨＡ)的功能联系。1　材料和方法(1)动物　体重为250ｇ左右成年Ｗｉｓｔａｒ雌性大鼠41只。受光照14ｈ,水食任取,观察阴道涂片,鉴定动情周期。(2)…     

Modulation of blood pressure by substance P: opposite effects of N- and C- terminal fragments on anesthetized rats

Considerable evidence suggests that substance P (SP) may be a transmitter mediating the depressor effects of baroreceptor reflex activation within the brainstem, yet intracerebroventricular administration of SP is reported to result in a pronounced pressor effect. In this study, SP injected into the 4th cerebral ventricle produced a biphasic effect; a brief decrease in blood pressure followed by a lengthy increase. Similar injections of a carboxy-terminal fragment of SP produced only a pressor effect of long duration. Injection of an amino-terminal SP fragment produced only a brief, rapid depressor effect. These results suggest that the amino-terminal sequence of SP may be involved in mediating the depressor effects of baroreceptor activation.     

Cardiovascular effects of cocaine in anesthetized and conscious rats

This study examined the cardiovascular and respiratory effects of cocaine and procaine in anesthetized and conscious rats. Intravenous cocaine (0.16-5 mg/Kg) elicited a rapid, dose dependent increase in mean arterial pressure of relatively short duration. In pentobarbital anesthetized (65 mg/Kg, i.p.) animals, the pressor phase was generally followed by a more prolonged depressor phase. These effects on arterial pressure were generally accompanied by a significant tachypnea and at larger doses (2.5 and 5 mg/Kg, i.v.), bradycardia. Procaine (0.31 and 1.25 mg/Kg, i.v.) produced similar cardiovascular and respiratory effects (depressor phase, tachypnea) in pentobarbital anesthetized animals. In conscious-restrained animals, both cocaine and procaine (1.25 mg/kg, i.v.) produced pressor responses. The subsequent depressor response was, however, absent in both cases. The cardiovascular effects of cocaine (0.25-1 mg/Kg, i.v.) in urethane anesthetized (1.25 g/Kg, i.p.) animals were essentially similar to those observed in conscious animals. Procaine (1mg/Kg) did not produce any significant cardiovascular effects in urethane anesthetized animals, but did elicit tachypnea. Reserpine pretreatment (10 mg/Kg, i.p.) did not significantly attenuate the pressor response in urethane anesthetized animals. Phentolamine pretreatment (3 mg/Kg, i.v.) did significantly antagonize the pressor effect in urethane anesthetized animals. These results suggest that: the depressor phase is likely due to a interaction between local anesthetic activity (cocaine and procaine) and barbiturate anesthesia, the cardiovascular effects of cocaine in conscious animals are more similar to those observed in urethane anesthetized rats than in pentobarbital anesthetized rats and the pressor effect in urethane anesthetized rats is apparently due to a reserpine resistant catecholaminergic mechanism.     

Cardiovascular responses to substance P in the nucleus tractus solitarii: microinjection study in conscious rats

The cardiovascular effects of substance P (SP) microinjections in the nucleus tractus solitarii (NTS) were evaluated in conscious rats. We chose this model because it is an effective way to access some of the cardiovascular effects of neurotransmitters in the NTS without the inconvenience of blunting pathways with anesthetic agents or removing forebrain projections by decerebration. The cardiovascular responses to SP injections were also evaluated after chronic nodose ganglionectomy. We found that, in conscious rats, SP microinjections into the NTS induced hypertension and tachycardia. Unilateral and bilateral SP injections into the NTS caused a slow increase in blood pressure and heart rate that peaked 1.5-5 min after injection and lasted for 20-30 min. Nodose ganglionectomy increased the duration of the pressor and tachycardic effects of SP and enhanced the pressor response. These data show that SP in the NTS is involved in pressor pathways. The supersensitivity to SP seen after nodose ganglionectomy suggests that vagal afferent projections are involved in those pressor pathways activated by SP in the NTS.     

Enhancement of anandamide formation in the limbic forebrain and reduction of endocannabinoid contents in the striatum of delta9-tetrahydrocannabinol-tolerant rats

Recent studies have shown that the pharmacological tolerance observed after prolonged exposure to synthetic or plant-derived cannabinoids in adult rats is accompanied by down-regulation/desensitization of brain cannabinoid receptors. However, no evidence exists on possible changes in the contents of the endogenous ligands of cannabinoid receptors in the brain of cannabinoid-tolerant rats. The present study was designed to elucidate this possibility by measuring, by means of isotope dilution gas chromatography/mass spectrometry, the contents of both anandamide (arachidonoylethanolamide; AEA) and its biosynthetic precursor, N-arachidonoylphosphatidylethanolamine (NArPE), and 2-arachidonoylglycerol (2-AG) in several brain regions of adult male rats treated daily with delta9-tetrahydrocannabinol (delta9-THC) for a period of 8 days. The areas analyzed included cerebellum, striatum, limbic forebrain, hippocampus, cerebral cortex, and brainstem. The same regions were also analyzed for cannabinoid receptor binding and WIN-55,212-2-stimulated guanylyl-5'-O-(gamma-[35S]thio)-triphosphate ([35S]GTPgammaS) binding to test the development of the well known down-regulation/desensitization phenomenon. Results were as follows: As expected, cannabinoid receptor binding and WIN-55,212-2-stimulated [35S]GTPgammaS binding decreased in most of the brain areas of delta9-THC-tolerant rats. The only region exhibiting no changes in both parameters was the limbic forebrain. This same region exhibited a marked (almost fourfold) increase in the content of AEA after 8 days of delta9-THC treatment. By contrast, the striatum exhibited a decrease in AEA contents, whereas no changes were found in the brainstem, hippocampus, cerebellum, or cerebral cortex. The increase in AEA contents observed in the limbic forebrain was accompanied by a tendency of NArPE levels to decrease, whereas in the striatum, no significant change in NArPE contents was found. The contents of 2-AG were unchanged in brain regions from delta9-THC-tolerant rats, except for the striatum where they dropped significantly. In summary, the present results show that prolonged activation of cannabinoid receptors leads to decreased endocannabinoid contents and signaling in the striatum and to increased AEA formation in the limbic forebrain. The pathophysiological implications of these findings are discussed in view of the proposed roles of endocannabinoids in the control of motor behavior and emotional states.     

A projection from the ventral tegmental area to the periaqueductal gray involved in cardiovascular regulation

Experiments were done in alpha-chloralose-anesthetized rats to determine a pathway mediating the cardiovascular depressor responses elicited from stimulation of the ventral tegmental area (VTA). The magnitude of the depressor responses elicited by glutamate stimulation (0.1 M/30 nl) of the VTA was examined after neuronal block produced by microinjections of lidocaine into ascending fiber bundles leaving the VTA to innervate the forebrain and thalamus. Bilateral microinjections of 1 microl of 4% lidocaine in the medial forebrain bundle (n = 6) and in the periventricular fibers of the midbrain (n = 5) did not attenuate the depressor response from stimulation of the VTA. Experiments were done using the anterograde tracer biotinylated dextran amine to identify descending projections from the VTA to cardiovascular centers in the brain stem. Examination of the nucleus of the solitary tract, ventrolateral medulla, and A5 catecholaminergic cell group revealed few or no fibers or terminals. Occasional fibers and some terminals were observed in the nucleus of raphe magnus, parabrachial nucleus, and locus ceruleus. A very dense bilateral projection was found to the ventrolateral periaqueductal gray (PAGvl) and dorsal raphe nucleus adjacent to the PAGvl. Bilateral injections of 4% lidocaine (n = 4) or 10 mM cobalt chloride (n = 5) into the PAGvl region attenuated the depressor responses elicited by stimulation of the VTA by approximately 50%. These experiments indicate that the depressor responses elicited from activation of the VTA are mediated in part by a pathway to a cardiovascular depressor area located in the PAGvl.     

Changes in the venous vessels capacitance in the cat forepaw in response to neurohumoral stimuli

The trend in changes of the cat forepaw vessels' capacity was found to practically not differ from the trend in shifts in the vena cava anterior basin's capacity: in both areas the capacity decreases in response to pressor neurogenic stimuli and decreases or increases under the effects of pressor and depressor humoral stimuli. The data obtained suggest that the trend in shifts of the vena cava anterior basin's capacity under the effects of pressor humoral stimuli mainly depends on the skin-muscular area's vessels, whereas the trend in shifts of the vena cava anterior basin's capacity under the effects of depressor humoral stimuli depends, apparently, on the shifts in the brain vessels' capacity function.     

Mechanisms underlying inhibition of nociceptive jaw-opening reflex produced by stimulating limbic structures

The comparative effectiveness of the inhibitory influence of tetanic (100 Hz) stimulation of the hypothalamus, amygdala, and limbic cortex on electromyograph (EMG) response in m. digastricus produced by electrical stimulation of tooth pulp afferents was investigated in cats anesthetized by a mixture of chloralose and Nembutal. It was found that the most pronounced inhibition of nociceptive EMG response was produced by stimulating the medial and lateral structures of the hypothalamus, a less intense response by stimulating central and medial amygdaloid nuclei, and the least reaction by stimulation of different areas of the limbic cortex. It was shown that mechanisms underlying inhibition of the jaw-opening reflex produced by hypothalamic tetanic stimulation is unconnected with the concomitant increase in blood pressure. The inhibitory action of hypothalamic tetanic stimulation following blood pressure stabilization persists; this would suggest a primary but not baroafferent mechanism underlying inhibition of activity in trigeminal nucleus nociceptive neurons. Pronounced and protracted depression of jaw-opening reflex takes place following long-term pressor response produced by injecting noradrenaline intravenously. The same pronounced and protracted pressor response occurs under the effects of angiotensin but without any noticeable change in the amplitude of nociceptive EMG response. Hypothalamic and noradrenergic mechanisms of pain sensitivity are discussed.L. A. Orbeli Institute of Physiology, Academy of Sciences of the Armenian SSR, Erevan. Translated from Neirofiziologiya, Vol. 19, No. 6, pp. 825–832, November–December, 1987.     

Cardiorespiratory effects of μ and δ opiate agonists following third or fourth ventricular injections

The cardiorespiratory effects of prototype μ (morphine and β-casomorphine 1–4) and δ (D-Ala²-D-Leu⁵Enkephalin—DADLE) opioid ligands were compared following microinjection into third and fourth ventricular spaces in conscious and anesthetized rats. The direction of change in arterial pressure produced by ventricular opioid injections varied according to ligand, site of administration, and state of consciousness of the animal. In general, pentobarbital anesthesia blocked or reversed the pressor response to these opiate agonists; depressor responses became magnified following pentobarbital. Qualitatively, the predominant effect of third ventricular DADLE in anesthetized rats was to produce a depression of arterial pressure and pulse pressure, suggesting an involvement of hypothalamic δ opioid receptors in decreasing sympathetic outflow. By contrast, morphine exerted pronounced bradycardic effects following fourth ventricular administration, suggesting an action at μ opioid receptors which influence vagal parasympathetic activity. Both ligands lowered respiratory rates upon fourth ventricular injection, indicating a possible involvement of either opioid receptor subtype in the depression of brainstem respiratory centers. These depressant effects of opioids upon cardiorespiratory function were readily reversed by naloxone. The qualitative similarity between the cardiovascular effects of third ventricular DADLE administration and various forms of circulatory shock may indicate that both phenomena involve delta opioid receptors at hypothalamic sites.     

TRH: Cardiovascular and sympathetic modulation in brain nuclei of the rat

The cardiovascular and sympathetic effects of TRH in discrete cardiovascular-related brain nuclei were studied. Microinjections of TRH were made into the nucleus preopticus medialis (POM) of conscious rats and the nucleus tractus solitarius (NTS) of pentobarbitone-anesthetized, artificially respired rats. POM injections (1 μl, 0.8–80 nM) elicited dose dependent pressor and tachycardic responses which were accompanied by increased levels of norepinephrine (NE) and epinephrine (EPI) in the plasma. These pressor/tachycardic effects of TRH were also elicited in adrenal demedullated (ADM-x) rats, but completely abolished in ADM-x rats pretreated with bretylium (30 mg/kg, IA). NTS injections (0.1 μl, 30 and 150 nM) had a short depressor effect on blood pressure (BP) and a delayed increase in heart rate (HR). From these findings we suggest that the POM, a central nucleus in the AV3V region, may be an important forebrain site for autonomic regulation by TRH, mediated through the sympathetic nervous system.     

Neurocircuitry of stress integration: anatomical pathways regulating the hypothalamo-pituitary-adrenocortical axis of the rat

The hypothalamo-pituitary-adrenocortical (HPA) axis is recruitedby the organism in response to real or perceived threats tohomeostasis ("stress"). Regulation of this neuroendocrine systemis accomplished by modulation of secretory tone in hypophysiotrophicneurons of the medial parvocellular paraventricular nucleus.Excitation of these neurons is mediated by several sources:direct (and perhaps indirect) inputs from brainstem neuronsregulating autonomic tone/arousal; circumventricular organsmonitoring blood and CSF constituents; and local-circuit neuronswithin the hypothalamus and basal forebrain. The latter arepredominantly GABAergic; notably, these areas are targets fordescending GABAergic input from limbic structures, and may promotePVN secretory activity via disinhibition. Neurosecretory paraventricularnucleus neurons are inhibited by glucocorticoid–dependentand –independent mechanisms. Glucocorticoid negative feedbackappears to act both locally and in extrahypothalamic loci, andis likely integrated in a region- and stressor-specific manner.Inhibitory input to the medial parvocellular paraventricularnucleus emanate predominantly from the bed nucleus of the striaterminalis and hypothalamus, and are likely regulated by neuroendocrinehomeostats. Descending limbic inhibitory information appearsto act through excitation of these inhibitory inputs. Overall,integration of stressful information is a multi-faceted processintegrating prior experience and real or anticipated homeostaticdisruption into appropriate activation and deactivation of thehypothalamo-pituitary-adrenocortical axis.