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1.
Blair ML Mickelsen D 《American journal of physiology. Regulatory, integrative and comparative physiology》2006,291(3):R742-R750
Lesions of the lateral parabrachial nucleus (LPBN) impair blood pressure recovery after hypotensive blood loss (Am J Physiol Regul Integr Comp Physiol 280: R1141, 2001). This study tested the hypothesis that posthemorrhage blood pressure recovery is mediated by activation of neurons, located in the ventrolateral aspect of the LPBN (VL-LPBN), that initiates blood pressure recovery by restoring sympathetic vasomotor drive. Hemorrhage experiments (16 ml/kg over 22 min) were performed in unanesthetized male Sprague-Dawley rats prepared with bilateral ibotenate lesions or guide cannulas directed toward the external lateral subnucleus of the VL-LPBN. Hemorrhage initially decreased mean arterial pressure (MAP) from approximately 100 mmHg control to 40-50 mmHg, and also decreased heart rate. In animals with sham lesions, MAP returned to 84 +/- 4 mmHg by 40 min posthemorrhage, and subsequent autonomic blockade with hexamethonium reduced MAP to 53 +/- 2 mmHg. In contrast, animals with VL-LPBN lesions remained hypotensive at 40 min posthemorrhage (58 +/- 4 mmHg) and hexamethonium had no effect on MAP, implying a deficit in sympathetic tone. VL-LPBN lesions did not alter the renin response or the effect of vasopressin V1 receptor blockade after hemorrhage. Posthemorrhage blood pressure recovery was also significantly delayed by VL-LPBN infusion of the ionotropic glutamate receptor antagonist kynurenic acid. Both VL-LPBN lesions and VL-LPBN kynurenate infusion caused posthemorrhage bradycardia to be significantly prolonged. Bradycardia was reversed by hexamethonium or atropine, but did not contribute to posthemorrhage hypotension. Taken together, these data support the hypothesis that stimulation of VL-LPBN glutamate receptors mediates spontaneous blood pressure recovery by initiating restoration of sympathetic vasomotor drive. 相似文献
2.
A 2 min sample of an intracellular recording of in vivo synaptic activity from a vasomotor C-neuron in a bullfrog sympathetic ganglion was converted to a series of stimulus pulses. This physiologically derived activity was used to stimulate preganglionic C-fibres of similar ganglia studied in vitro. Intracellular recordings were made from exocrine B-cells within the ganglia. Although they do not receive fast, nicotinic synaptic input from preganglionic C-fibres, B-cell excitability was profoundly increased by stimulation of C-fibres with physiologically derived activity. Also, subthreshold depolarizing current pulses that failed to generate action potentials in B-cells under control conditions almost always generated action potentials whilst C-fibres were activated. These effects were attenuated or prevented by the luteinizing hormone releasing hormone antagonist, [D-pyro-Glu1,D-Phe2,D-Trp3,6]-LHRH (70 microM). The physiological release of luteinizing hormone releasing hormone from C-fibres therefore causes an interaction between vasomotor and exocrine outflow within a paravertebral sympathetic ganglion. 相似文献
3.
The nuclei of unfixed isolated rabbit neurons cleared on incubation with DNAse (10 mg/ml), but not RNAse (10 mg/ml). The nuclei stained for DNA with eight chromosomal or nuclear stains more intensely than the cytoplasm, and less intensely after treatment with DNAse (10 mg/ml). On the other hand, when the whole tissue was embedded and sectioned, DNA did not appear to be stained in the nucleus; the nucleolus and the cytoplasm were more heavily stained than the nucleoplasm. Possible explanations for this apparent anomaly are considered. It was concluded that DNA diffused out of the nucleus during embedding and sectioning, and that the colouration of the nucleolus and cytoplasm with the eight staining systems used was due to other nucleotides present. 相似文献
4.
K Iigaya FC Müller-Ribeiro J Horiuchi LM McDowall E Nalivaiko MA Fontes RA Dampney 《American journal of physiology. Regulatory, integrative and comparative physiology》2012,303(6):R599-R610
The superior and inferior colliculi are believed to generate immediate and highly coordinated defensive behavioral responses to threatening visual and auditory stimuli. Activation of neurons in the superior and inferior colliculi have been shown to evoke increases in cardiovascular and respiratory activity, which may be components of more generalized stereotyped behavioral responses. In this study, we examined the possibility that there are "command neurons" within the colliculi that can simultaneously drive sympathetic and respiratory outputs. In anesthetized rats, microinjections of bicuculline (a GABA(A) receptor antagonist) into sites within a circumscribed region in the deep layers of the superior colliculus and in the central and external nuclei of the inferior colliculus evoked a response characterized by intense and highly synchronized bursts of renal sympathetic nerve activity (RSNA) and phrenic nerve activity (PNA). Each burst of RSNA had a duration of ~300-400 ms and occurred slightly later (peak to peak latency of 41 ± 8 ms) than the corresponding burst of PNA. The bursts of RSNA and PNA were also accompanied by transient increases in arterial pressure and, in most cases, heart rate. Synchronized bursts of RSNA and PNA were also evoked after neuromuscular blockade, artificial ventilation, and vagotomy and so were not dependent on afferent feedback from the lungs. We propose that the synchronized sympathetic-respiratory responses are driven by a common population of neurons, which may normally be activated by an acute threatening stimulus. 相似文献
5.
Convergence of different preganglionic fibers on antidromically identified vasomotor neurons was studied by intracellular recording from neurons of ganglia L3 and L4 of the sympathetic chain, isolated from their rostral and caudal commissures, white ramus communicans, and muscular and cutaneous (mixed) twigs of the ventral branch and dorsal branch of the mixed nerve, in cats. Neurons activated antidromically by stimulation of these twigs were confidently considered to be vasomotor. Preganglionic fibers of only the B2 and C groups were shown to converge on the vasomotor neurons, by contrast with the rest. Discharges of neurons were evoked only by excitation of preganglionic fibers of the B2-group, arising mainly from higher segments of the spinal cord and entering through the rostral commissure. Vasomotor neurons also differ from the remaining ganglion cells in the properties of their axons, which conduct excitation at a significantly slower velocity (0.95±0.05 m/sec) than axons of other neurons (1.30±0.15 m/sec).I. P. Pavlov Institute of Physiology, Academy of Sciences of the USSR, Leningrad. A. A. Bogomolets Institute of Physiology, Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 9, No. 6, pp. 592–597, November–December, 1977. 相似文献
6.
Horiuchi J Killinger S Dampney RA 《American journal of physiology. Regulatory, integrative and comparative physiology》2004,287(6):R1335-R1343
The role of excitatory amino acid (EAA) receptors in the rostral ventrolateral medulla (RVLM) in maintaining resting sympathetic vasomotor tone remains unclear. It has been proposed that EAA receptors in the RVLM mediate excitatory inputs both to presympathetic neurons and to interneurons in the caudal ventrolateral medulla (CVLM), which then provide a counterbalancing inhibition of RVLM presympathetic neurons. In this study, we tested this hypothesis by determining the effect of blockade of EAA receptors in the RVLM on mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA), after inhibition of CVLM neurons. In anesthetized rats, bilateral injections of muscimol in the CVLM increased MAP, HR, and RSNA. Subsequent bilateral injections of kynurenic acid (Kyn, 2.7 nmol) in the RVLM caused a modest reduction of approximately 20 mmHg in the MAP but had no effect, when compared with the effect of vehicle injection alone, on HR or RSNA. By approximately 50 min after the injections of Kyn or vehicle in the RVLM, the MAP had stabilized at a level close to its original baseline level, but the HR and RSNA stabilized at levels above baseline. The results indicate that removal of tonic EAA drive to RVLM neurons has little effect on the tonic activity of RVLM presympathetic neurons, even when inputs from the CVLM are blocked. Thus the tonic activity of RVLM presympathetic neurons under these conditions is dependent on excitatory synaptic inputs mediated by non-EAA receptors and/or the autoactivity of these neurons. 相似文献
7.
Lau YE Galligan JJ Kreulen DL Fink GD 《American journal of physiology. Regulatory, integrative and comparative physiology》2006,290(1):R90-R95
Dai and colleagues (Dai X, Galligan JJ, Watts SW, Fink GD, and Kreulen DL. Hypertension 43: 1048-1054, 2004) found that endothelin (ET) stimulated O2- production in sympathetic ganglion neurons in vitro by activating ET(B) receptors. The objective of the present study was to determine whether activation of ET(B) receptors in vivo elevates O2- levels in sympathetic ganglia. Because ET(B) receptor activation increases blood pressure, we also sought to determine whether alteration in O2- levels was a direct effect of ET(B) receptor activation on sympathetic ganglia or an indirect consequence of hypertension. Male Sprague-Dawley rats received intravenous infusions of either the specific ET(B) receptor agonist sarafotoxin 6c (S6c; 5 pmol.kg(-1).min(-1)) or isotonic saline at 0.01 ml/min (control) for 120 min. To measure O2- levels, we removed the inferior mesenteric ganglion immediately after infusion and stained it with dihydroethidine (DHE). Mean arterial pressure increased 26.6 +/- 1.7 mmHg in the S6c-treated rats and 3.65 +/- 6 mmHg in control rats. Measurements of average pixel intensity revealed that the DHE fluorescence in ganglionic neurons and surrounding glial cells were 96.7% and 160% greater in S6c-treated than in control rats, respectively. To evaluate the effect of elevated blood pressure on O2- production, a separate group of rats received phenylephrine (PE; 10 mug.kg(-1).min(-1) iv) for 2 h. MAP increased 31 +/- 1.2 mmHg in PE-infused rats. The DHE fluorescence intensity in ganglia of PE-infused rats was significantly greater than that of control rats, 137.7% in neurons and 104.6% in glia but significantly lower than in ganglia from S6c rats. We conclude that ET(B) receptor activation in vivo significantly enhances O2- levels in sympathetic ganglia, due to both pressor effects and direct stimulation of ET(B) receptors in ganglion cells. 相似文献
8.
Excitatory and inhibitory responses of sympathetic discharge were recorded in single renal postganglionic neurons of rabbits anaesthetized with urethane and chloralose. The animals were vagotomized and had transected aortic nerves. Responses were elicited by single volleys in the aortic C-fibres. Excitatory responses consisted in short-lasting increase in the rate of ongoing sympathetic discharge and were followed by inhibitory responses. Excitatory effects together with inhibitory responses were seen in 68% of units (19/28). Only excitatory effects appeared in 2 neurons (7.1%) and only inhibitory effects in 7 neurons (25%). In renal neurons exhibiting both effects, the excitatory responses appeared after latency of 172 +/- 8 ms (x +/- S.D.) and had duration of 64 +/- 11 ms. Inhibitory effects had latency o f 257 +/- 10 ms and their duration amounted to 265 +/- 22 ms. In more than half of recordings the excitatory responses were separated from the inhibitory effects by discharge lasting 33 +/- 4 ms. Significant correlations between latencies of excitatory and inhibitory responses and between duration of excitatory and latency of inhibitory responses suggest interaction between both effects. Increase in the number of afferent volleys (1 through 5) evoked relatively small changes in duration of the excitatory effect indicating that temporal facilitation is of minor importance in generating this response. Temporal facilitation was found to play an important role in determining duration of the inhibitory response. Comparison of effects of unilateral and bilateral stimulation of the aortic C-fibres showed larger occlusion of durations of the excitatory than inhibitory responses. 相似文献
9.
Medullary raphé serotonergic neurons are chemosensitive in culture and are situated adjacent to blood vessels in the brain stem. Selective lesioning of serotonergic raphé neurons decreases the ventilatory response to systemic CO2 in awake and sleeping adult rats. Abnormalities in the medullary serotonergic system, including the raphé, have been implicated in the sudden infant death syndrome (48). In this study, we ask whether serotonergic neurons in the medullary raphé and extra-raphé regions are involved in the CO2 response in unanesthetized newborn piglets, 3-16 days old. Whole body plethysmography was used to examine the ventilatory response to 5% CO2 before and during focal inhibition of serotonergic neurons by 8-hydroxy-2-di-n-propylaminotetralin (8-OH-DPAT), a 5-HT1A receptor agonist. 8-OH-DPAT (10 or 30 mM in artificial cerebrospinal fluid) decreased the CO2 response in wakefulness in an age-dependent manner, as revealed by a linear regression analysis that showed a significant negative correlation (P < 0.001) between the percent change in the CO2 response and piglet age. Younger piglets showed an exaggerated CO2 response. Control dialysis with artificial cerebrospinal fluid had no significant effect on the CO2 response. Additionally, 8-OH-DPAT increased blood pressure and decreased heart rate independent of age (P < 0.05). Finally, sleep cycling was disrupted by 8-OH-DPAT, such that piglets were awake more and asleep less (P < 0.05). Because of the fragmentary sleep data, it was not possible to examine the CO2 response in sleep. Inhibition of serotonergic medullary raphé and extra-raphé neurons decreases ventilatory CO2 sensitivity and alters cardiovascular variables and sleep cycling, which may contribute to the sudden infant death syndrome. 相似文献
10.
E M Penatti A V Berniker B Kereshi C Cafaro M L Kelly M M Niblock H G Gao H C Kinney A Li E E Nattie 《Journal of applied physiology》2006,101(4):1177-1188
Acute inhibition of serotonergic (5-HT) neurons in the medullary raphé (MR) using a 5-HT(1A) receptor agonist had an age-dependent impact on the "CO(2) response" of piglets (33). Our present study explored the effect of chronic 5-HT neuron lesions in the MR and extra-raphé on the ventilatory response to hypercapnia and hypoxia in piglets, with possible implications on the role of 5-HT in the sudden infant death syndrome. We established four experimental groups. Group 1 (n = 11) did not undergo any treatment. Groups 2, 3, and 4 were injected with either vehicle or the neurotoxin 5,7-dihydroxytryptamine in the cisterna magna during the first week of life (group 2, n = 9; group 4, n = 11) or second week of life (group 3, n = 10). Ventilation was recorded in response to 5% CO(2) (all groups) and 12% O(2) (group 2) during wakefulness and sleep up to postnatal day 25. Surprisingly, the piglets did not reveal changes in their CO(2) sensitivity during early postnatal development. Overall, considerable lesions of 5-HT neurons (up to 65% decrease) in the MR and extra-raphé had no impact on the CO(2) response, regardless of injection time. Postlesion raphé plasticity could explain why we observed no effect. 5,7-Dihydroxytryptamine-treated males, however, did present a lower CO(2) response during sleep. Hypoxia significantly altered the frequency during sleep in lesioned piglets. Further studies are necessary to elucidate the role of plasticity, sex, and 5-HT abnormalities in sudden infant death syndrome. 相似文献
11.
M Favilla B Ghelarducci A La Noce V Mais A Starita 《Bollettino della Società italiana di biologia sperimentale》1979,55(19):1960-1965
The characteristics of the control exerted by macular and ampullar vestibular receptors on oculomotor neurons (OMN) have been investigated by submitting unanesthetized, encéphale isolé rabbits to sinusoidal lateral tilts of varying frequencies (0.013-0.2 Hz). The phase of the response exhibited a progressive shift towards head velocity with increasing frequencies of tilt. The sensitivity of the OMN significantly increased at frequencies above 0.025 Hz, corresponding to peak accelerations suprathreshold for canals related vestibular neurons. The convergent action of macular and ampullar vestibular receptors in the control of vertical eye movements is discussed in relation with stimulus frequency. 相似文献
12.
Sandeep Sood Eric Raddatz Xia Liu Hattie Liu Richard L Horner 《Journal of applied physiology》2006,100(6):1807-1821
Although exogenous serotonin at the hypoglossal motor nucleus (HMN) activates the genioglossus muscle, endogenous serotonin plays a minimal role in modulating genioglossus activity in awake and sleeping rats (Sood S, Morrison JL, Liu H, and Horner RL. Am J Respir Crit Care Med 172: 1338-1347, 2005). This result therefore implies that medullary raphe neurons also play a minimal role in the normal physiological control of the HMN, but this has not yet been established because raphe neurons release other excitatory neurotransmitters onto respiratory motoneurons in addition to serotonin. This study tests the hypothesis that inhibition of medullary raphe serotonergic neurons with 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) suppresses genioglossus and diaphragm activities in awake and sleeping rats. Ten rats were implanted with electrodes to record sleep-wake states and genioglossus and diaphragm activities. Microdialysis probes were also implanted into the nucleus raphe obscurus (NRO). Experiments in 10 anesthetized and vagotomized rats were also performed using the same methodology. In anesthetized rats, microdialysis perfusion of 0.1 mM 8-OH-DPAT into the NRO decreased genioglossus activity by 60.7+/-9.0% and diaphragm activity by 13.3+/-3.4%. Diaphragm responses to 7.5% CO2 were also significantly reduced by 8-OH-DPAT. However, despite the robust effects observed in anesthetized and vagotomized rats, there was no effect of 0.1 mM 8-OH-DPAT on genioglossus or diaphragm activities in conscious rats awake or asleep. The results support the concept that endogenously active serotonergic medullary raphe neurons play a minimal role in modulating respiratory motor activity across natural sleep-wake states in freely behaving rodents. This result has implications for pharmacological strategies aiming to manipulate raphe neurons and endogenous serotonin in obstructive sleep apnea. 相似文献
13.
Horst Herbert 《Cell and tissue research》1992,270(1):149-156
Summary The anterograde tracer Phaseolus vulgaris-leucoagglutinin was injected into the medial nucleus of the solitary tract and into the rostral dorsomedial medulla. A sequential two-color immunoperoxidase staining was accomplished in order to demonstrate the co-distribution of presumed terminal axons with chemically distinct neurons in the dorsal raphe nucleus of the midbrain central gray, i.e., B7 serotonergic and A10dc dopaminergic neurons. Black-stained efferent fibers from the medial nucleus of the solitary tract and the rostral dorsomedial medulla intermingled with brown-stained serotonergic (5-hydroxytryptamine-immunoreactive) or dopaminergic (tyrosine hydroxylase-immunoreactive) neurons. Light microscopy revealed that the black-stained efferent axons exhibited numerous en passant and terminal varicosities that were often found in close apposition to brown-stained serotonergic and dopaminergic somata, and to proximal and distal dendrites and dendritic processes. The close association of immunoreactive elements suggests the presence of axo-somatic and axodendritic synaptic contacts of medullary fibers with serotonergic and dopaminergic neurons in the dorsal raphe nucleus. These projections could be involved in the modulation of dorsal raphe neurons, depending on the autonomic status of an animal. 相似文献
14.
E. Schürg-Pfeiffer C. Spreckelsen J. -P. Ewert 《Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology》1993,173(3):363-376
In freely moving toads, the temporal discharge patterns of tectal and medullary neurons were observed during prey-catching.
- Tectal T5.2 and T8.1 neurons displayed a premotor warming up firing that in the former was addressed specifically to prey orienting or snapping and in the latter generally to almost any kind of body movement.
- The temporal discharge patterns of T5.2 neurons during snapping were different from those during orienting toward prey. Snapping started in the peak phase of warming up; firing was immediately terminated during the snap; thereafter some rebound activity was observed. Orienting started after the premotor warming up in the declining phase whilst the neuron kept on firing during orienting and then settled when the orienting movement was completed.
- In toads which were not motivated to catch prey — comparabl to immobilized ones — the discharge frequency of T5.2 neurons toward a prey stimulus revealed no such warming up.
- Because it is known that prey-selective T5.2 neurons are controlled by pretectal inhibitory influences, the following experiment was conducted: during recording a T5.2 neuron a pretectal lesion was applied ipsilaterally to the recording site. After a few seconds, the neuron showed a strong premotor wanning up in response to any kind of moving object, followed by prey-catching.
- In the medulla oblongata, different H-type neurons of the hypoglossal nucleus displayed specific discharge patterns which resembled the tongue protractor and retractor muscle activities; a third type resembled the activity of the genio/sterno-hyoid muscle, which are suggested to stabilize the hyoid bone during snapping.
- There were medullary M8-type neurons with properties similar to T8.1.
- Snapping could be triggered by electrical stimulation of the optic tectum in the representation of the frontal visual field, but not by stimulation in the hypoglossal nucleus or the adjacent medial reticular formation.
- A concept of a neuronal circuit for the coordination of tongue muscle contractions in response to prey is proposed.
15.
16.
Endogenous opioid peptides appear to have neurotransmitter or neuromodulator functions in brain mediating a wide variety of effects. We have reported that intracisternal administration of synthetic human beta-endorphin increases plasma concentration of catecholamines, apparently by acting at unknown brain sites to increase sympathetic outflow to the adrenal medulla and sympathetic nerves. In the present study we examined the possibility that angiotensin II, acting in brain, modulates endorphin-induced catecholamine secretion. Simultaneous intracisternal administration of angiotensin II 1.0 nmol together with synthetic human beta-endorphin 1.45 nmol potentiated the plasma epinephrine, norepinephrine and dopamine responses to intracisternal beta-endorphin. In contrast, simultaneous intracisternal administration of the angiotensin II antagonist, [Sar1, Val5, Ala8]-angiotensin II (saralasin), 1.1 nmol together with beta-endorphin, blunted the plasma epinephrine, norepinephrine and dopamine responses to beta-endorphin. These data are consistent with the hypothesis that activation of angiotensin II receptors in brain potentiates the endorphin-induced stimulation of central sympathetic outflow. It remains to be demonstrated whether angiotensin II acting in brain to modulate activity of opioid neurons is synthesized in brain or is derived peripherally. 相似文献
17.
Farnham MM Li Q Goodchild AK Pilowsky PM 《American journal of physiology. Regulatory, integrative and comparative physiology》2008,294(4):R1304-R1311
Pituitary adenylate cyclase-activating polypeptide (PACAP) is an excitatory neuropeptide present in the rat brain stem. The extent of its localization within catecholaminergic groups and bulbospinal sympathoexcitatory neurons is not established. Using immunohistochemistry and in situ hybridization, we determined the extent of any colocalization with catecholaminergic and/or bulbospinal projections from the brain stem was determined. PACAP mRNA was found in tyrosine hydroxylase-immunoreactive (TH-ir) neurons in the C1-C3 cell groups. In the rostral ventrolateral medulla (RVLM), PACAP mRNA was found in 84% of the TH-ir neurons and 82% of bulbospinal TH-ir neurons. The functional significance of these PACAP mRNA positive bulbospinal neurons was tested by intrathecal administration of PACAP-38 in anaesthetized rats. Splanchnic sympathetic nerve activity doubled (110%) and heart rate rose significantly (19%), although blood pressure was unaffected. In addition, as previously reported, PACAP was found in the A1 cell group but not in the A5 cell group or in the locus coeruleus. The RVLM is the primary site responsible for the tonic and reflex control of blood pressure through the activity of bulbospinal presympathetic neurons, the majority of which contain TH. The results indicate 1) that pontomedullary neurons containing both TH and PACAP that project to the intermediolateral cell column originate from C1-C3 and not A5, and 2) intrathecal PACAP-38 causes a prolonged, sympathoexcitatory effect. 相似文献
18.
Myofilament-polyribosome complexes in the conducting system of hearts from cow, rabbit, and cat 总被引:1,自引:0,他引:1
L E Thornell 《Journal of ultrastructure research》1972,41(5):579-596
19.
Dennis A. Przywara Sanjiv V. Bhave Anjali Bhave Pertha S. Chowdhury Taruna D. Wakade Arun R. Wakade 《The Journal of membrane biology》1992,125(2):155-162
Summary We studied the effects of lanthanum (La3+) on the release of 3H-norepinephrine(3H-NE), intracellular Ca2+ concentration, and voltage clamped Ca2+ and K+ currents in cultured sympathetic neurons. La3+ (0.1 to 10 m) produced concentration-dependent inhibition of depolarization induced Ca2+ influx and 3H-NE release. La3+ was more potent and more efficacious in blocking 3H-NE release than the Ca2+-channel blockers cadmium and verapamil, which never blocked more than 70% of the release. At 3 m, La3+ produced a complete block of the electrically stimulated rise in intracellular free Ca2+ ([Ca2+]
i
) in the cell body and the growth cone. The stimulation-evoked release of 3H-NE was also completely blocked by 3 m La3+. However, 3 m La3+ produced only a partial block of voltage clamped Ca2+ current (I
Ca). Following La3+ (10 m) treatment 3H-NE release could be evoked by high K+ stimulation of neurons which were refractory to electrical stimulation. La3+ (1 m) increased the hyperpolarization activated, 4-aminopyridine (4-AP) sensitive, transient K+ current (I
A
) with little effect on the late outward current elicited from depolarized holding potentials. We conclude that the effective block of electrically stimulated 3H-NE release is a result of the unique ability of La3+ to activate a stabilizing, outward K+ current at the same concentration that it blocks inward Ca2+ current. 相似文献
20.
de Souza Villa P Menani JV de Arruda Camargo GM de Arruda Camargo LA Saad WA 《Regulatory peptides》2008,150(1-3):14-20
The paraventricular nucleus (PVN) may be considered as a dynamic mosaic of chemically-specified subgroups of neurons. 5-HT(1A) is one of the prime receptors identified and there is expressed throughout all magnocellular regions of the PVN. Several reports have demonstrated that a subpopulation of the magnocellular neurons expressing 5-HT(1A) receptors are oxytocin (OT) neurons and activation of 5-HT(1A) receptors in the PVN increases the plasma OT. Increasing evidence shows that OT inhibits water intake and increases urinary excretion in rats. The aim of this study was to investigate the role of serotonergic 5-HT(1A) receptors in the lateral-medial posterior magnocellular region of the PVN in the water intake and diuresis induced by 24 h of water deprivation. Cannulae were implanted in the PVN of rats. 5-HT injections in the PVN reduced water intake and increased urinary excretion. 8-OH-DPAT (a 5-HT(1A) agonist) injections blocked the water intake and increased urinary output in all the periods of the observation. pMPPF (a 5-HT(1A) antagonist) injected bilaterally before the 8-OH-DPAT blocked its inhibitory effect on water intake and its diuretic effect. We suggest that antidipsogenic and diuretic responses seem to be mediated via 5-HT(1A) receptors of the lateral-medial posterior magnocellular region of the PVN in water-deprived rats. 相似文献