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 slowly). These channels allow a flow of calcium ions (Ca) into the cell, making the membrane potential more positive. Phase 0 This is the depolarisation phase. When the membrane potential reaches a threshold value (around -20 to -50 mV), it begins to rapidly depolarise (become more positive). This is mainly due to the flow of Ca through the L-type calcium channels, which are now fully open. During this stage the T-type calcium channels and HCN channels deactivate. Phase 3 This phase is the repolarisation phase. This occurs due to the inactivation of the L-type calcium channels (preventing the movement of