Synapse and Junctional Transmission MCQs

Renshaw cells are the inhibitory interneurons present in spinal cord Renshaw cells are excited by a motor neuron. In turn, Renshaw cells inhibit the same motor neuron which excites it. This stabilize the firing rate of the motor neurons Also called as "negative feedback inhibition" Reference: Ganong, 25 th edition page no.122

Blocking K+ channels on the presynaptic membrane leads to accumulation of positively charged potassium ions inside, leading to depolarisation. Such depolarization leads to opening of the voltage gated calcium channels and neurotransmitter release. Reference: Ganong's Review of Medical Physiology, 25th Edition, Page Number-100.

Entry of calcium ions trigger the release of neurotransmitter stored in vesicles from the presynaptic ending Factors that decrease the presynaptic calcium levels, inhibits the release of neurotransmitter Reference: Ganong, 25 th edition page no.121

Even at rest, small quanta of acetylcholine are always released randomly at the synaptic cleft. This leads to a small potential called as miniature endplate potential, which is about 0.5 mV in amplitude. This small amount of Ach release varies directly with the Ca² + concentration and inversely with the Mg 2+ concentration at the endplate Reference: Ganong, 25th edition/page no. 108

Myasthenia gravis is characterized by auto antibodies developed against nicotinic Ach receptors Reference: Ganong, 25th edition page no.132

Coronary blood flow is directly related to the perfusion pressure (aortic diastolic pressure) and the duration of diastole. Because coronary flow drops to negligible values during systole, the duration of diastole becomes a limiting factor for myocardial perfusion during tachycardia. Coronary blood flow is inversely proportional to coronary vascular resistance. Resistance is determined mainly by intrinsic factors—including metabolic products and autonomic activity—and by various pharmacologic agents. Damage to the endothelium of coronary vessels has been shown to alter their ability to dilate and to increase coronary vascular resistance. Ref: Katzung B.G. (2012). Chapter 12. Vasodilators & the Treatment of Angina Pectoris. In B.G. Katzung, S.B. Masters, A.J. Trevor (Eds), Basic & Clinical Pharmacology, 12e.