Acetylcholine Sensitivity of Cat's Medullary Neurons

Salmoiraghi, G. C.; Steiner, Felix

doi:10.1152/jn.1963.26.4.581

Cited by 128 publications

(48 citation statements)

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“…In the present experiments intravenously administered physostigmine (0.15-0.30 mg/kg) excited 11 of 21 and electrophoretic ACh excited 26 of 96 brainstem neurons which responded to stimulation of the SR nerve of either side at a supramaximal intensity for stimulating Aa afferent fibers and were located in the medial reticular area. This location is in fairly good agreement with that of ACh sensitive neurons determined by their spontaneous activity (5,6) and with that of neurons responding to SR nerve stimulation (9).…”

Section: Discussionsupporting

confidence: 84%

Brainstem Acetylcholine Sensitive Neurons Activated by Cutaneous Impulses in Cats

Iwata

Sakai

1978

Japanese Journal of Pharmacology

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Abstract-In order to determine the cholinoceptive mechanism associated with cu taneous inhibition of jaw-closing and lumbar motoneurons, the area related to the inhibition produced by stimulation of the superficial radial nerve was identified by a lesion within the pontomedullary reticular formation and effects of drugs upon neurons were studied within this area. The cutaneous inhibition, as tested by the inhibition of monosynaptic reflex activity of jaw-closing and that of hindlimb spinal motoneurons was completely abolished by lesion of the medial portion of the pontomedullary reticular formation, but was little affected by lesions of the lateral portion. Intravenously administered physostigmine (0.15-0.30 mg/kg) excited 11 of 21 neurons whereas electro phoretic ACh (90 nA) excited 26 and inhibited 4 of 96 brainstem neurons located in this area. Eight of 11 physostigmine, and 4 of 26 ACh excited neurons were reticulospinal neurons with axonal conduction velocities of 20-40 m/sec. From results presented here together with those reported previously, these physostigmine sensitive and ACh excited brainstem neurons, reticulospinal and non-reticulospinal neurons, could be cholinoceptive interneurons of the polysynaptic inhibitory pathway, from the superficial radial nerve to jaw-closing and hindlimb spinal motoneurons.A muscarinic cholinergic mechanism has been suggested to be involved in the postsyn aptic inhibition of jaw-closing motoneurons of the trigeminal nucleus (1) and of hindlimb spinal motoneurons (2) by forearm cutaneous impulses (cutaneous inhibition). Previous observations following lesioning indicated that the pontomedullary reticular formation was essential for the inhibition, not only of the jaw-closing but also hindlimb spinal moto neurons produced by stimulation of the superficial radial (SR) nerve (2, 3). It has been reported that spontaneously active, acetylcholine (ACh) sensitive neurons are located in the pontomedullary reticular formation (4-8) and also that cutaneously excited neurons are found in this area (9). All these data suggest that ACh sensitive neurons in the brainstem are involved in the polysynaptic inhibitory circuitry of the cutaneous inhibitions. In the present experiments, a study was made of the effects of intravenously administered physostigmine and electrophoretically administered ACh on neurons responsive to cutaneous impulses in this area. The objective was to demonstrate the possibility that ACh functions as a trans mitter in the pathway of cutaneous inhibitions of these motoneurons. MATERIALS AND METHODSThe experiments were performed on 53 adult cats which were either unanesthetized, after precollicular decerebration during ether anesthesia, or anesthetized with pentobarbi

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Section: Discussionsupporting

confidence: 84%

Brainstem Acetylcholine Sensitive Neurons Activated by Cutaneous Impulses in Cats

Iwata

Sakai

1978

Japanese Journal of Pharmacology

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“…There have been discrepancies in the results concerning the responsiveness of the medullary neurons to electrophoretically applied catecholamines and ACh (25)(26)(27)(28). In the present experiment, the pH of the solution for amines and AT,, was adjusted to about 6.0, because the larger the pH, the greater was the effect.…”

Section: Discussionmentioning

confidence: 68%

Effects of Angiotensin Ii on the Medullaryneurons and Their Sensitivity to Acetylcholine and Catecholamines

Suga

Suzuki

1979

Japanese Journal of Pharmacology

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Abstract-In order to elucidate the mechanism of the central hypertensive action of angiotensin II (ATzi), the effects of ATII on the medullary neurons of rabbits were studied by the technique of electrophoretic application.ATII gave rise to excitatory effect on some neurons of medulla and this effect was antagonized by a specific AT,, antagonist, 1-sarcosine-8-alanine-ATi1.The ATII sensitive medullary neurons showed no specific response to acetylcholine, norepinephrine or isoproterenol, but there was a significant increase in the excitatory response to norepinephrine in comparison with the ATrr non-sensitive neurons. The excitatory effect of AT,, was not blocked by atropine, phentolamine and propranolol.The ATII sensitive neurons in the medulla apparently do not have a topograhically or functionally characteristic distribution related to the central vasomotor control mechanisms. The neurons in the area postrema did not respond to electrophoretically applied ATII, while microinjection of ATII in this region produced remarkable hypertensive responses. These results suggest that the mechanism of the central hypertensive action of ATI i administered into the vertebral artery is primarily mediated by the chemoreception of the area postrema. The mecha nism of central cardiovascular effect of ATrr and of the effects of acetylcholine and catecholamines on the medullary neurons are discussed.Since the first observation of a central effect of angiotensin II (AT,,) in dogs (1), con siderable evidence has accumulated that at least some of the hypertensive effects of AT,, are mediated by an action on the central mechanisms of the autonomic nervous system (2).The lower medulla is considered by several investigators to be one of the sites of central

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“…However, it was controversial whether nAChRs contribute to regulation of respiratory circuits and whether activation of nAChRs is excitatory or inhibitory [63][64][65][66][67] , probably due to the variability (or lack of precise information) concerning recording locations and the states of anesthesia [68] . Bilateral injection of nerve agent sarin, a potent acetylcholinesterase inhibitor, into a compact area near the lateral reticular nucleus in the medulla of rabbit causes respiratory arrest, which can be reversed by atropine [69] .…”

Section: Activation Of Nachrs In the Prebötc Modulates Respiratory Rhmentioning

confidence: 99%

Central cholinergic regulation of respiration: nicotinic receptors

Shao

Feldman

2009

Acta Pharmacol Sin

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Nicotinic acetylcholine receptors (nAChRs) are expressed in brainstem and spinal cord regions involved in the control of breathing. These receptors mediate central cholinergic regulation of respiration and effects of the exogenous ligand nicotine on respiratory pattern. Activation of α4* nAChRs in the preBötzinger Complex (preBötC), an essential site for normal respiratory rhythm generation in mammals, modulates excitatory glutamatergic neurotransmission and depolarizes preBötC inspiratory neurons, leading to increases in respiratory frequency. nAChRs are also present in motor nuclei innervating respiratory muscles. Activation of post-and/or extra-synaptic α4* nAChRs on hypoglossal (XII) motoneurons depolarizes these neurons, potentiating tonic and respiratory-related rhythmic activity. As perinatal nicotine exposure may contribute to the pathogenesis of sudden infant death syndrome (SIDS), we discuss the effects of perinatal nicotine exposure on development of the cholinergic and other neurotransmitter systems involved in control of breathing. Advances in understanding of the mechanisms underlying central cholinergic/nicotinic modulation of respiration provide a pharmacological basis for exploiting nAChRs as therapeutic targets for neurological disorders related to neural control of breathing such as sleep apnea and SIDS.

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Acetylcholine Sensitivity of Cat's Medullary Neurons

Cited by 128 publications

References 0 publications

Brainstem Acetylcholine Sensitive Neurons Activated by Cutaneous Impulses in Cats

Brainstem Acetylcholine Sensitive Neurons Activated by Cutaneous Impulses in Cats

Effects of Angiotensin Ii on the Medullaryneurons and Their Sensitivity to Acetylcholine and Catecholamines

Central cholinergic regulation of respiration: nicotinic receptors

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