Active muscle vasodilatation produced by stimulation of the brain stem: its significance in the defence reaction

Abrahams, V. C.; Hilton, S. M.; Zbrożyna, A. W.

doi:10.1113/jphysiol.1960.sp006593

Cited by 461 publications

(160 citation statements)

References 23 publications

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“…In fact, the term, "defense reaction," was first used to describe the behavioral response evoked by electrical stimulation of the hypothalamus and other areas of the brain stem in the awake cat (Hess and Brtigger, 1943). Since that time, many studies have been conducted using electrical brain stimulation to map the neural pathways mediating defensive behavior and the associated pattern of sympathetic activation (Abrahams et al, 1960;Hilton and Zbrozyna, 1963;Flynn, 1967;Kaada, 1967;Fonberg, 1972Fonberg, , 1973Reis, 1972;Clemente and Chase, 1973;Hilton, 1975;Siegel and Edinger, 198 1). It is assumed in such work that the neural pathways underlying defense reactions elicited by brain stimulation overlap considerably, if not completely, with the pathways through which defense is expressed in response to natural (sensory) stimuli.…”

Section: Discussionmentioning

confidence: 99%

Different projections of the central amygdaloid nucleus mediate autonomic and behavioral correlates of conditioned fear

et al. 1988

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The purpose of the present study was to determine whether lesions of areas projected to by the central amygdaloid nucleus (ACE) would disrupt the classical conditioning of autonomic and/or behavioral emotional responses. The areas studied included 3 projection targets of the ACE: the lateral hypothalamic area (LH), midbrain central gray (CG) region, and bed nucleus of the stria terminalis (BNST). Lesions were made either electrolytically or by microinjection of ibotenic acid, which destroys local neurons without interrupting fibers of passage. Two weeks later, the animals were classically conditioned by pairing an acoustic stimulus with footshock. The next day, conditioned changes in autonomic activity (increases in arterial pressure) and emotional behavior (“freezing,” or the arrest of somatomotor activity) evoked by the acoustic conditioned stimulus (CS) were measured during extinction trials. Electrolytic and ibotenic acid lesions of the LH interfered with the conditioned arterial pressure response, but did not affect conditioned freezing. Electrolytic lesions of the rostral CG disrupted conditioned freezing but not conditioned changes in arterial pressure. Ibotenic acid injected into the rostral CG reduced neither the arterial pressure nor the freezing response. Injection of ibotenic acid in the caudal CG, like electrolytic lesions of the rostral CG, disrupted the freezing, but not the arterial pressure response. Injection of ibotenic acid into the BNST had no effect on either response. These data demonstrate that neurons in the LH are involved in the autonomic, but not the behavioral, conditioned response pathway, whereas neurons in the caudal CG are involved in the behavioral, but not the autonomic, pathway. Different efferent projections of the central amygdala thus appear to mediate the behavioral and autonomic concomitants of conditioned fear.

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Section: Discussionmentioning

confidence: 99%

Different projections of the central amygdaloid nucleus mediate autonomic and behavioral correlates of conditioned fear

et al. 1988

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“…The preparations for muscle, skin and submandibular salivary gland blood flow were those previously described (Hilton & Lewis, 1955;Abrahams, Hilton & Zbrozyna, 1960). Salivary secretion was recorded from the cannulated duct of one submandibular salivary gland: the gland was stimulated via a fluid electrode attached to the cut chordolingual nerve.…”

Section: Methodsmentioning

confidence: 99%

“…It was being used for this purpose, during experiments on the activation of cholinergic vasodilator nerves to skeletal muscle in decerebrate cats (Abrahams, Hilton & Zbrozyna, 1960), when it was found that the dose used to paralyse skeletal and respiratory muscles for 20 to 30 min also abolished the action of the vasodilator nerve fibres. Further experiments have shown that these doses of decamethonium affect transmission at a number of sites in the autonomic nervous system of the cat.…”

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confidence: 99%

Blocking Action of Decamethonium at Different Sites in the Autonomic Nervous System of the Cat

Abrahams

Hilton

1962

British Journal of Pharmacology and Chemotherapy

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Doses of decamethonium sufficient to paralyse skeletal and respiratory muscles in the cat for 20 to 30 min can reversibly block transmission at several sites in the autonomic nervous system. The sympathetic vasodilator outflow to skeletal muscle was blocked at the post-ganglionic nerve endings, probably by preventing the release of acetylcholine. The effects of vagal stimulation on heart-rate and intestinal contraction were blocked in most experiments, possibly by an action on pre-ganglionic as well as post-ganglionic nerve endings. However, decamethonium did-not block all cholinergic nerve endings-for example, it did not diminish either the effects of stimulation of the chorda tympani on the submandibular salivary gland or those of pelvic nerve stimulation on the bladder.Decamethonium iodide is extensively used as a neuromuscular blocking agent in animal experiments. It was being used for this purpose, during experiments on the activation of cholinergic vasodilator nerves to skeletal muscle in decerebrate cats (Abrahams, Hilton & Zbrozyna, 1960), when it was found that the dose used to paralyse skeletal and respiratory muscles for 20 to 30 min also abolished the action of the vasodilator nerve fibres. Further experiments have shown that these doses of decamethonium affect transmission at a number of sites in the autonomic nervous system of the cat. METHODSThe experiments were performed on cats anaesthetized with chloralose (70 mg/kg) given intravenously after the induction of anaesthesia with ethyl chloride and ether.Regional blood flows were registered by the venous outflow technique using a transistorized drop recorder. The preparations for muscle, skin and submandibular salivary gland blood flow were those previously described (Hilton & Lewis, 1955;Abrahams, Hilton & Zbrozyna, 1960). Salivary secretion was recorded from the cannulated duct of one submandibular salivary gland: the gland was stimulated via a fluid electrode attached to the cut chordolingual nerve. The heart rate was recorded by means of a Statham strain gauge transducer connected to a cannula in one femoral artery, records being made with a high-speed pen recorder.Records of intestinal activity were made in situ by introducing a small rubber bag into a loop of small intestine through a small slit. About 1 ml. of normal saline was introduced into the rubber bag, which was then connected by polythene tubing to a Statham strain gauge. One vagus nerve was dissected free in the neck, divided, and the peripheral stump placed on platinum stimulating electrodes and immersed in liquid paraffin. Stimuli were supramaximal square waves, 10/sec, with a pulse width of 1 msec.

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“…Whereas in the dog and cat the existence of a cholinergic sympathetic vasodilator system is well established (Timms 1981, Schramm et al 1971, Bolme et al 1967, Abrahams et al 1960a, there is no evidence for such a mechanism in others species including the rabbit, the monkey and the rat.…”

Section: Introductionmentioning

confidence: 99%

Evidence for a role of nitric oxide in hindlimb vasodilation induced by hypothalamic stimulation in anesthetized rats

Ferreira-Neto

Possas

Lopes

et al. 2005

An. Acad. Bras. Ciênc.

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Electrical stimulation of the hypothalamus produces cardiovascular adjustments consisting of hypertension, tachycardia, visceral vasoconstriction and hindlimb vasodilation. Previous studies have demonstrated that hindlimb vasodilation is due a reduction of sympathetic vasoconstrictor tone and to activation of β 2 -adrenergic receptors by catecholamine release. However, the existence of a yet unidentified vasodilator mechanism has also been proposed. Recent studies have suggested that nitric oxide (NO) may be involved. The aim of the present study was to investigate the role of NO in the hindquarter vasodilation in response to hypothalamic stimulation. In pentobarbital-anesthetized rats hypothalamic stimulation (100 Hz, 150µA, 6 s) produced hypertension, tachycardia, hindquarter vasodilation and mesenteric vasoconstriction. Alpha-adrenoceptor blockade with phentolamine (1.5 mg/kg, iv) plus bilateral adrenalectomy did not modify hypertension, tachycardia or mesenteric vasoconstriction induced by hypothalamic stimulation. Hindquarter vasodilation was strongly reduced but not abolished. The remaining vasodilation was completely abolished after iv injection of the NOS inhibitor L-NAME (20 mg/kg, iv). To properly evaluate the role of the mechanism of NO in hindquarter vasodilation, in a second group of animals L-NAME was administered before α-adrenoceptor blockade plus adrenalectomy. L-NAME treatment strongly reduced hindquarter vasodilation in magnitude and duration. These results suggest that NO is involved in the hindquarter vasodilation produced by hypothalamic stimulation.

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Active muscle vasodilatation produced by stimulation of the brain stem: its significance in the defence reaction

Cited by 461 publications

References 23 publications

Different projections of the central amygdaloid nucleus mediate autonomic and behavioral correlates of conditioned fear

Different projections of the central amygdaloid nucleus mediate autonomic and behavioral correlates of conditioned fear

Blocking Action of Decamethonium at Different Sites in the Autonomic Nervous System of the Cat

Evidence for a role of nitric oxide in hindlimb vasodilation induced by hypothalamic stimulation in anesthetized rats

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