The localization of the first synapse in the carotid sinus baroreceptor reflex pathway and its alteration of the afferent input

Seller, H.; Illert, M.

doi:10.1007/bf00586608

Cited by 229 publications

(63 citation statements)

References 32 publications

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“…The inhibitory phase which succeeds evoked vagal responses limits the effectiveness of single shocks and prevents effects from the second shock in temporally close pairs. Seller & Illert (1969) described limitations on transmission in cells in the nucleus of the tractus solitarius (the first synapse of the baroreceptor pathway) as the frequency of afferent stimulation increased above 1 Hz. Possibly, the post-excitatory inhibition described here was important for these effects.…”

Section: Discussionmentioning

confidence: 99%

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Excitation and inhibition of cardiac vagal motoneurones by electrical stimulation of the carotid sinus nerve.

McCloskey¹,

Potter²

1981

The Journal of Physiology

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SUMMARY1. The carotid sinus nerve was electrically stimulated in dogs anaesthetized with chloralose. Stimuli (1 ms, 1-10 V, < 1 Hz) evoked responses in single cardiac efferent fibres dissected from the cervical part of the vagus nerve. The mean latencies of these responses varied, from fibre to fibre, between 30 and 120 ms.2. Stimuli given during the expiratory phase of the respiratory cycle evoked vagal responses with a shorter latency than similar stimuli given only during the inspiratory phase of the respiratory cycle.3. Following the vagal response to carotid sinus nerve stimulation a period of inhibition of vagal activity, lasting 100-150 ms, occurred. Refractoriness of the responding vagal motoneurone following an action potential could not account for this post-excitatory depression.4. The inhibitory effects of electrical stimulation of the carotid sinus nerve were further studied by applying pairs of similar electrical stimuli to the carotid sinus nerve. The second stimulus of a pair had to be given 80-100 ms after the first to evoke a second response.5. Trains of electrical stimuli (30-100 Hz) were also studied. At low frequencies the inhibitory effect of successive stimuli on vagal responses became less marked, but at higher frequencies only the first and last stimulus of the train reliably evoked responses. For trains of stimuli at both low and high frequencies, the last stimulus of the train evoked a vagal response, which was succeeded by a period of inhibition of vagal firing: this inhibition was then followed by further excitation before vagal discharge returned to resting levels.

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Section: Discussionmentioning

confidence: 99%

“…The stimulating voltage used was the smallest necessary to evoke a maximal fall in blood pressure during the test stimulation at 30 Hz (cf. Seller & Illert, 1969). When required, such stimuli could be delivered in expiration only or in inspiration only.…”

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confidence: 99%

Excitation and inhibition of cardiac vagal motoneurones by electrical stimulation of the carotid sinus nerve.

McCloskey¹,

Potter²

1981

The Journal of Physiology

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“…The nucleus tractus solitarius (NTS) is the primary site of termination of afferent nerve fibers arising from arterial and cardiopulmonary mechanoreceptors (Crill and Reis, 1968;Murra and Reis, 1969;Seller and Illert, 1969;Jordan and Spyer, 1977;Ciriello and Calaresu, 198 1). Neurons in the NTS integrate these and other circulatory related afferent signals and are important in the production of appropriate patterns of cardiovascular, pulmonary, and other homeostatic responses (Spyer,198 1).…”

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confidence: 99%

Cardiovascular function is altered by picomole injections of glutamate into rat medulla

et al. 1988

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Local neural circuitry in the nucleus tractus solitarius (NTS) involved in cardiovascular control was studied by injecting nanoliter volumes of excitatory amino acids into the structure. Experiments were performed on urethane-anesthetized, artificially ventilated rats. Multibarrel micropipettes were used for pressure ejection of drugs or a dye for marking ejection sites. Ejected volumes, ranging from 200 pl to 25 nl, were directly monitored for every injection. Injections of as little as 200 fmol of L-glutamate in 200 pl into the medial and lateral NTS region rostral to the obex elicited marked, site-specific decreases in arterial pressure and heart rate. The majority of these responses were eliminated by blockade of parasympathetic and sympathetic neural outflow. At sites caudal to obex, in the commissural region of the NTS, L-glutamate injections produced marked elevations in heart rate and arterial pressure which were sympathetically mediated. Responses to L- glutamate were attenuated by concurrent injection of glutamic acid diethyl ester and DL-2-amino-4-phosphonobutyrate, or lidocaine. These results indicate a heterogeneity in the spatial organization of brain- stem circuitry underlying cardiovascular control that has not been previously described.

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“…Since the cadiovascular responses of KA are similar to those produced by microinjection into NTS of the amino acid neurotransmitter glutamic acid, the study adds further support to the hypothesis that L-glutamate is the neurotransmitter released by baroreceptor afferent nerves. Circ Res 48: 292-298, 1981 ANATOMICAL and electrophysiological studies have established that the intermediate one-third of the nucleus tractus solitarii (NTS) is the principal site of termination of the primary afferent fibers of baroreceptor nerves (Crill and Reis, 1968;Miura and Reis, 1969;Seller and Illert, 1969;Jordan and Spyer, 1977). Electrical stimulation restricted to this area simulates baroreflexes by eliciting hypotension and bradycardia (Crill and Reis, 1968;DeJong et al, 1975).…”

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confidence: 99%

Acute hypertension after the local injection of kainic acid into the nucleus tractus solitarii of rats.

Talman¹,

Perrone²,

Reis

1981

Circulation Research

116

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SUMMARY Kainic acid (KA), an analogue of L-glutamate, was microinjected in 0.1 pi of saline into the nucleus tractus solitarii (NTS) of adult rats. In rats anesthetized with halothane or a-chloralose, KA injected unilaterally elicited hypotension, bradycardia, and apnea. The threshold dose was 0.1-0.2 ng (10~1 3 mol). Doses >0.2 ng blocked responses to subsequent injections for at least 30 minutes. Doses of KA >15 ng reduced the reflex bradycardia elicited by raising the arterial pressure with phenylephrine and produced arterial hypertension in rats anesthetized with a-chloralose or in other rats within 15 minutes of terminating halothane anesthesia. Bilateral injection of KA in doses >15 ng completely blocked baroreflexes and resulted in a dose-dependent elevation of arterial pressure (167 ± 9.4; P < 0.001) both in a-chloralose-anesthetized rats and in awake rats after the termination of halothane anesthesia. The hypertension rapidly led to pulmonary edema and death. Procaine microinjected also elicited fulminating hypertension; vehicle did not. Doses of KA producing hypertension caused no histological or biochemical evidence of neuronal death. The cardiovascular responses to KA were restricted to sites in the intermediate one-third of NTS and could not be elicited by injection into adjacent sites in brainstem. The results indicate that, in low doses, KA injected into NTS stimulates neurons which mediate the baroreflex, whereas, in higher doses, it produces baroreflex blockade and neurogenic hypertension. The results suggest that fulminating hypertension can be produced by nondestructive perturbations of neurochemical transmission in brain. Since the cadiovascular responses of KA are similar to those produced by microinjection into NTS of the amino acid neurotransmitter glutamic acid, the study adds further support to the hypothesis that L-glutamate is the neurotransmitter released by baroreceptor afferent nerves. Circ Res 48: 292-298, 1981 ANATOMICAL and electrophysiological studies have established that the intermediate one-third of the nucleus tractus solitarii (NTS) is the principal site of termination of the primary afferent fibers of baroreceptor nerves (Crill and Reis, 1968;Miura and Reis, 1969;Seller and Illert, 1969;Jordan and Spyer, 1977). Electrical stimulation restricted to this area simulates baroreflexes by eliciting hypotension and bradycardia (Crill and Reis, 1968;DeJong et al., 1975). On the other hand, restricted electrolytic lesions abolish baroreflexes and, in unanesthetized animals, result in neurogenic hypertension. In the rat the hypertension is fulminating (Doba and Reis, 1973;DeJong and Palkovits, 1976) whereas in the cat (Nathan and Reis, 1977) or dog (Carey et al., 1979;Schmitt and Laubie, 1979) it is chronic and labile. It is uncertain whether the hypertension produced by electrolytic lesions of NTS is a consequence of destruction of intrinsic neurons of the NTS or of interruption of the primary afferent baroreceptor fibers terminating in or passing

show abstract

The localization of the first synapse in the carotid sinus baroreceptor reflex pathway and its alteration of the afferent input

Cited by 229 publications

References 32 publications

Excitation and inhibition of cardiac vagal motoneurones by electrical stimulation of the carotid sinus nerve.

Excitation and inhibition of cardiac vagal motoneurones by electrical stimulation of the carotid sinus nerve.

Cardiovascular function is altered by picomole injections of glutamate into rat medulla

Acute hypertension after the local injection of kainic acid into the nucleus tractus solitarii of rats.

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