INTRODUCTION

1. INTRODUCTION

The aim of the present study was to identify the underlying mechanisms behind neuromuscular junction synapses and muscle action potential (MAP) spread in a bullfrog model. This was accomplished by testing for the effects three drugs – verapamil, curare, and succinylcholine – have on MAP recruitment, facilitation, and synaptic delay.

It is already well established that verapamil is used to treat angina pectoris and hypertension in humans by blocking L-type Ca²⁺ channels and therefore the rapid influx of Ca²⁺ needed for muscle contraction. However, these mechanisms, as they apply to the bullfrog neuromuscular junction remain unclear. Since it is generally accepted that the sarcoplasmic reticulum (SR) in the ectothermic heart has little or no importance in supplying Ca²⁺ for contraction, whether or not verapamil has an effect on contraction may suggest an alternative mechanism for increasing intracellular calcium, or confirm that the same mammalian mechanistic response is used in frogs, except that they simply have little Ca²⁺ SR storage.

Likewise, the non-depolarizing nicotinic receptor blocker curare and depolarizing nicotinic receptor blocker succinylcholine are used in many anesthetic procedures as muscle relaxants. However, their effects on threshold potential and drug elimination in the bullfrog may differ from humans. The MAP studies performed will determine the types of receptors present and involved in the bullfrog neuromuscular contraction pathway, and may have advantages in medical studies on human patients.

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