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 known as a spontaneous Ca spark. This increase in calcium within the cell then activates a sodium-calcium exchanger (NCX), which removes one Ca from the cell, and exchanges it for 3 Na into the cell (therefore removing a charge of +2 from the cell, but allowing a charge of +3 to enter the cell) therefore in-creasing the membrane potential. The calcium is later pumped back into the cell via calcium channels located on the cell membrane and SR membrane. The increase in membrane potential produced by these mechanisms, activates T-type calcium channels and then L-type calcium channels (which open very