Muscarinic antagonist brain, involving both increased levels of acetylcholine and degeneration of dopaminergic pathways (nigrostriatal pathway). Thus, in parkinsonism there is decreased level of dopaminergic activity. One method of balancing the neurotransmitters is through blocking central cholinergic activity using muscarinic receptor antagonists. Atropine acts on the M2 receptors of the heart and antagonizes the activity of acetylcholine. It causes tachycardia by blocking vagal effects on the sinoatrial node. Acetylcholine hyperpolarizes the sinoatrial node, which is overcome by MRA and thus increases the heart rate. If atropine is given by intramuscular or subcutaneous injection, it causes initial bradycardia. This is because by i.m/s.c
Sinoatrial node the 3 phases of a sinoatrial node action potential. In the ventricular action potential, there are 5 phases (labelled 0-4), however pacemaker action potentials don’t have an obvious phase 1 or 2. Phase 4 This phase is also known as the pacemaker potential. Immediately following an action potential, when the membrane potential is very negative (it is hyperpolarised) the voltage slowly begins to increase. This is initially due to the closing of potassium channels, which reduces the flow of potassium ions (I) out of the cell (see phase 3, below). Alongside the deactivation of the potassium channels, channels known as