The effects of noradrenaline on neurones in the rat dorsal motor nucleus of the vagus, in vitro.

Fukuda, Atsuo; Minami, Taketsugu; Nabekura, Junichi; Osuga, Yutaka

doi:10.1113/jphysiol.1987.sp016820

Cited by 74 publications

(62 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Anatomic studies have shown that the DMV receives massive projections from the NST (Rogers, Kita, Butcher & Novin, 1980). Since the synaptic inputs from the NST to the DMV were considered to be preserved in the slice preparations (Fukuda et al 1987), the transsynaptic effects of All on the DMV neurones mav be mediated bv its action on the neurones in the NST. However, involvement of interneurones within the DMV that have All receptors cannot be excluded.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of vasopressin and angiotensin II on neurones in the rat dorsal motor nucleus of the vagus, in vitro.

Katafuchi

Muratani

et al. 1992

The Journal of Physiology

View full text Add to dashboard Cite

SUMMARY1. Extracellular recordings were made from 297 spontaneously firing neurones in the dorsal motor nucleus of the vagus (DMV) in slice preparations of rat medulla oblongata. Some of the neurones recorded were identified to be vagal motoneurones by antidromic stimulation. The cells fired with a slow irregular pattern at an average rate of 1 1 + 041 spikes/s (mean + S.E.M.).2. Arginine vasopressin (AVP) was applied by perfusion in 196 of the 297 cells. Most of the neurones (190/196, 97 %) were excited by 10-6 M AVP with an increase in firing rate from the basal level of 11 + 0-1 to a maximum of 2-5 + 0-2 spikes/s. There was a dose-dependent relation between the concentration of AVP and the increased firing rate in all DMV neurones tested (n = 38). The threshold concentration of the peptide to produce changes in firing rate was assumed to be about 10-10 M. The remaining six neurones were not affected by application of AVP.3. Application of oxytocin (OXT, 10-6 M) increased the firing rate of all thirtyeight neurones tested. The effects of AVP and OXT on all neurones examined (n = 20 and 4, respectively) still persisted after blocking the synaptic transmission in a low-Ca2+ or Ca2+-free-high-Mg2+ solution, indicating the direct action of both AVP and OXT on the postsynaptic membranes.4. The AVP-induced excitatory responses were completely but reversibly blocked by the Vl-type receptor antagonists, [1-(,f-mercapto-/,,i-cyclopentamethylene-(n = 5) and Phaa-D-Tyr(Et)Phe-Gln-Asn-Lys-Pro-Arg-NH2 (n = 6), whereas a selective and reversible OXT receptor antagonist, desGly-NH2d(CH2)jTyr-(Me)2Thr4]ornithine vasotocin, which suppressed the OXT-induced excitation, did not block the responses to AVP (n = 11). 5. Application of angiotensin II (AII, 10-6 M) to 153 neurones increased the firing rates of 60 (39%) neurones. The firing rate was increased from the basal level of 1-0+041 to a maximum of 1-8+0-2 spikes/s (n = 60). The effect of All was completely abolished by an All receptor antagonist, [Sarl,lle8]angiotensin II (n = 6). There was a dose dependence of the excitatory response on All concentration in all of eleven neurones tested. The threshold concentration was assumed to be about MS 9206 Z -L. MO AND OTHERS 10-9 M. The activity of 5 (3 %) of 153 neurones was decreased, and the remaining 88 (58%) neurones were not affected by AII.6. After blocking synaptic transmission with low-Ca2+-high-Mg2+ medium, ten of sixteen neurones that had been excited by application of All in normal medium still responded to All, and the effects were abolished in the remaining six cells.7.Of fifty-nine cells tested with both AVP and AII applied at 10-6 M, responses of fifty-four (92 %) to AVP were excitation. Of these fifty-four, fifteen were also excited by application of All, one was inhibited, and All had no effect on the remaining thirty-eight (70 %).8. The excitatory responses induced by AVP were completely or partially blocked by simultaneous perfusion of All in normal medium, which were restored by [Sarl,lle8]AII, whereas the appli...

show abstract

Section: Discussionmentioning

confidence: 99%

“…9). However, DMV neurones were excited by noradrenaline through a1-receptors (Fukuda et al 1987). In addition, it has been generally accepted that a1-adrenergic activation induces inositol phospholipid breakdown.…”

Section: Discussionmentioning

confidence: 99%

Effects of vasopressin and angiotensin II on neurones in the rat dorsal motor nucleus of the vagus, in vitro.

Katafuchi

Muratani

et al. 1992

The Journal of Physiology

View full text Add to dashboard Cite

show abstract

“…Although a weak partial cu2-adrenergic agonist (Medgett et al, 1978) clonidine is remarkably effective in mimicking noradrenergic inhibition in several different regions in the nervous system, including the LC (Cedarbaum and Aghajanian, 1977;Reiner, 1985;Williams et al, 1985) the rat sympathetic ganglion (Brown and Caufield, 1979), substantia gelatinosa (North and Yoshimura, 1984) and dorsal motor nucleus of the vagus (Fukuda et al, 1987). A notable exception is the submucous plexus of the guinea pig ileum.…”

Section: Identification Of Cells Studied With Whole-cell Patch Clampmentioning

confidence: 99%

Noradrenaline hyperpolarizes identified rat mesopontine cholinergic neurons in vitro

1993

View full text Add to dashboard Cite

Inhibition of brainstem cholinergic neurons by noradrenergic neurons of the locus ceruleus has long been suggested as a key mechanism of behavioral state control. In particular, the commonly held view is that noradrenaline (NA) plays a permissive role in rapid eye movement (REM) sleep generation by disinhibiting brainstem cholinergic neurons. While this notion has been supported by numerous investigations, the inhibition of cholinergic neurons by NA has never been directly demonstrated. The purpose of this study was to investigate the effects of NA upon identified cholinergic neurons in the rat mesopontine tegmentum. Using whole-cell patch-clamp recordings in slices, 175 cells were studied during bath application of 50 microM NA. Cholinergic neurons were positively identified by intracellular labeling with biocytin and subsequent staining with NADPH-diaphorase, a reliable marker for brainstem cholinergic neurons (Vincent et al., 1983). Successful intracellular labeling was obtained in 96 cells. Ninety-two percent (36 of 39) of cholinergic neurons hyperpolarized in response to NA, while noncholinergic cells (n = 57) exhibited mixed responses. Application of NA in a low-Ca2+, high-Mg2+ solution elicited the same hyperpolarizing effect as in normal solution, which indicated that the effect of NA on cholinergic neurons was direct. The noradrenergic hyperpolarization was mimicked by the alpha 2-adrenoceptor agonist UK- 14,304, and was blocked by the alpha 2-adrenoceptor antagonist idazoxan, which suggested an alpha 2-mediated response. Finally, voltage-clamp experiments revealed that NA activates the inwardly rectifying potassium current, IKG.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

“…In addition, amphetamine, an agent that releases noradrenaline, caused a depolarization that was blocked by prazosin, indicating that the release of endogenous noradrenaline increased the excitability of dorsal raphe neurons (Pan & Williams, 1989). The most commonly reported ionic mechanism that mediates the depolarization induced by a1-adrenoceptor activation is a decrease in potassium conductance (Yoshimura et al 1985;Fukuda, Minami, Nabekura & Oomura, 1987;Freedman & Aghajanian, 1987;McCormick & Prince, 1988; Legendre, Dupouy & Vincent, 1988;McCormick, 1992;Larkman & Kelly, 1992). There are several additional reports of noradrenaline acting on various conductances, ranging from an inhibition of the transient potassium conductance (Aghajanian, 1985;Wang, Wettwer, Gross & Ravens, 1991) to both augmentation (Freedman & Aghajanian, 1987) and depression.…”

mentioning

confidence: 99%

Alpha 1‐adrenoceptors in rat dorsal raphe neurons: regulation of two potassium conductances.

Pan

Grudt

Williams

1994

The Journal of Physiology

View full text Add to dashboard Cite

1. a -Adrenoceptor activation caused two separate effects in rat dorsal raphe neurons: a depolarization and an increase in the duration of the after-hyperpolarization following the action potential. The depolarization often resulted in repetitive action potentials.The al-adrenoceptor antagonists prazosin and WB 4101 blocked the depolarization induced by phenylephrine. The concentration-response curve to phenylephrine was shifted to the right by VWB 4101.2. Under voltage clamp, a,-adrenoceptor agonists caused an inward current at -60 mV, which often became smaller at negative potentials but rarely reversed polarity even at strongly negative potentials. Using whole-cell recording, the inward current reversed polarity at the equilibrium potential for potassium in the majority of cells. IntracellularCs' decreased or abolished the a1-mediated inward current. The inward current was dependent on external calcium, but not on the degree of internal calcium buffering. Removal of external calcium or addition of MgCl2, CoCl2 or CdCl2 reduced or blocked the effects of a1-adrenoceptor agonists. Barium and strontium supported and even augmented the inward current induced by ax-adrenoceptor agonists, whereas nifedipine and wo-conous toxin had no effect. In contrast, internal dialysis with the calcium chelator 1,2-bis(O-aminophenoxy)ethane-N,N,N'N'-tetraacetic acid (BAPTA) did not inhibit the inward current.3. The a,-induced depolarization was blocked (or occluded) by the inclusion of GTP-y-S (100 /SM) in the recording pipette. The phorbol-ester 4-phorbol 12,13-dibutyrate (PDBu) had no action on the membrane potential and depressed the phenylephrine-induced depolarization. This depression was reversed by the non-selective protein kinase inhibitor staurosporin. 4. Phenylephrine and noradrenaline increased a late component of the afterhyperpolarization (late-AHP) that followed a single action potential. The a,-sensitive late-AHP was blocked by apamine suggesting that it is a calcium-dependent potassium conductance. 5. Thapsigargin reduced the duration of the late-AHP and blocked the phenylephrinemediated prolongation. Caffeine also augmented the late-AHP and ryanodine blocked the augmentation induced by caffeine. The augmentation induced by phenylephrine was not occluded by caffeine and was still present after the caffeine-induced augmentation was blocked by ryanodine. 6. In slices pretreated with manoalide the depolarization induced by al-agonists was not changed; however, the late-AHP was reduced in duration and the a1-receptor-mediated augmentation of the late-AHP was decreased.7. The results suggest that the depolarization of dorsal raphe neurons by ac-adrenoceptor activation is through a decrease in potassium conductance that is independent of the activation of the phospholipase C pathway. The augmentation of the late-AHP is mediated by release of calcium from intracellular stores and may serve to regulate activity during the depolarization induced by a,-adrenoceptor activation.

show abstract

The effects of noradrenaline on neurones in the rat dorsal motor nucleus of the vagus, in vitro.

Cited by 74 publications

References 32 publications

Effects of vasopressin and angiotensin II on neurones in the rat dorsal motor nucleus of the vagus, in vitro.

Effects of vasopressin and angiotensin II on neurones in the rat dorsal motor nucleus of the vagus, in vitro.

Noradrenaline hyperpolarizes identified rat mesopontine cholinergic neurons in vitro

Alpha 1‐adrenoceptors in rat dorsal raphe neurons: regulation of two potassium conductances.

Contact Info

Product

Resources

About