-Subunit Composition of Nicotinic Acetylcholine Receptors in Neurons of the Rat Submandibular Ganglia

Purnyn, H. E.; Skok, Maryna; Rikhalsky, Oleg V.; Horn, John P.; Skok, V. I.

doi:10.1023/b:neph.0000008822.69875.b5

Cited by 2 publications

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“…His early pioneering endeavors include: (1) the first intracellular recording of spontaneous natural synaptic activity in sympathetic neurons in vivo [1,2]; (2) the first voltage-clamp recordings of nicotinic excitatory postsynaptic currents in sympathetic neurons [3], of nicotinic current fluctuations [4], and of the underlying single nicotinic channel currents [5]; (3) the first substantive evidence for voltage-dependent channel block as a mechanism of pharmacological inhibition of sympathetic transmission by drugs hitherto classified as "competitive antagonists" [6,7]; and, more recently, (4) the introduction of subunitspecific antibodies to identify functional nicotinic receptor subunits [8,9].…”

Section: The Legacymentioning

confidence: 99%

The Skok legacy and beyond: Molecular mechanisms of slow synaptic excitation in sympathetic ganglia

Brown

2007

Neurophysiology

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his colleagues did much of the pioneering work on fast excitatory synaptic transmission in sympathetic ganglia and on nicotinic acetylcholine receptors that mediate fast transmission. I and my colleagues (including Alex Selyanko, one of Vladimir's protégés) have studied the additional process of slow synaptic excitation that is mediated by the action of acetylcholine on muscarinic receptors. This results primarily from the closure of "M-channels," a subset of voltage-gated potassium channels composed of Kv7.2 and Kv7.3 channel subunits. These channels require membrane phosphatidylinositol-4,5-bisphosphate (PIP 2 ) for their opening, and their closure by muscarinic receptor activation is now thought to result from the reduction in PIP 2 levels that follows receptor-induced PIP 2 hydrolysis. The dynamics of these two forms of synaptic excitation are compared.

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Section: The Legacymentioning

confidence: 99%

The Skok legacy and beyond: Molecular mechanisms of slow synaptic excitation in sympathetic ganglia

Brown

2007

Neurophysiology

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“…Intracardiac ganglion neurons can express α 2 to α 9 and β 2 to β 4 subunits, assembled predominantly as α 3 /β 2 , α 3 /β 4 , α 3 /β 2 /β 4 , α 3 /β 2 /α 5 , α 3 /β 4 /α 5 , and monomeric α 7 . For example, the canine intracardiac ganglion expresses predominately α 3 /β 2 nAChRs, with a smaller levels of α7 nAChRs [9-12]. …”

Section: Introductionmentioning

confidence: 99%

Electrophysiological and pharmacological evaluation of the nicotinic cholinergic system in chagasic rats

Bonfante-Cabarcas

Hincapié

Hernández

et al. 2013

BMC Pharmacol Toxicol

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BackgroundTwo theories attempt to explain the changes observed in the nicotinic acetylcholine receptors (nAChRs) in chagasic cardiomyopathy. The neurogenic theory proposes that receptor changes are due to loss of intracardiac ganglia parasympathetic neurons. The immunogenic theory proposes that the nAChRs changes are the result of autoantibodies against these receptors. Both theories agreed that nAChRs functional expression could be impaired in Chagas disease.MethodsWe evaluated nAChRs functional integrity in 54 Sprague Dawley rats, divided in two groups: healthy and chronic chagasic rats. Rats were subjected to electrocardiographic studies in the whole animal under pentobarbital anesthesia, by isolation and stimulation of vagus nerves and in isolated beating hearts (Langendorff’s preparation).ResultsNicotine, 10 μM, induced a significant bradycardia in both groups. However, rats that had previously received reserpine did not respond to nicotine stimulation. β-adrenergic stimulation, followed by nicotine treatment, induced tachycardia in chagasic rats; while inducing bradycardia in healthy rats. Bilateral vagus nerve stimulation induced a significantly higher level of bradycardia in healthy rats, compared to chagasic rats; physostigmine potentiated the bradycardic response to vagal stimulation in both experimental groups. Electric stimulation (e.g., ≥ 2 Hz), in the presence of physostigmine, produced a comparable vagal response in both groups. In isolated beating-heart preparations 1 μM nicotine induced sustained bradycardia in healthy hearts while inducing tachycardia in chagasic hearts. Higher nicotine doses (e.g.,10 – 100 uM) promoted the characteristic biphasic response (i.e., bradycardia followed by tachycardia) in both groups. 10 nM DHβE antagonized the effect of 10 μM nicotine, unmasking the cholinergic bradycardic effect in healthy rats only. 1 nM α-BGT alone induced bradycardia in healthy hearts but antagonized the 10 μM nicotine-induced tachycardia in chagasic rats. In healthy but not in chagasic hearts, 10 μM nicotine shortened PQ and PR interval, an effect counteracted by MA, DHβE and αBGTConclusionOur results suggest that cholinergic function is impaired in chronic Chagas disease in rats, a phenomena that could be related to alteration on the nAChR expression.

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-Subunit Composition of Nicotinic Acetylcholine Receptors in Neurons of the Rat Submandibular Ganglia

Cited by 2 publications

References 0 publications

The Skok legacy and beyond: Molecular mechanisms of slow synaptic excitation in sympathetic ganglia

The Skok legacy and beyond: Molecular mechanisms of slow synaptic excitation in sympathetic ganglia

Electrophysiological and pharmacological evaluation of the nicotinic cholinergic system in chagasic rats

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