Very good Q - I have not been asked this before.
The part of the sarcolemma where a motor efferent neurone meets the myocyte would be different for all three - in other ways the sarcolemma of smooth and striated muscle would be similar i.e. the receptors at the neuromuscular junction (on striated muscle) would be nicotinic Nm receptors on which acetylcholine will act whereas on smooth muscle, the postsynaptic receptors would be muscarinic receptors, the neurotransmitter being ACh again e.g. on the circular smooth muscle of bronchioles, contraction of which causes bronchoconstriction - OR the receptors at smooth muscle end organ could also be adrenergic e.g. beta-2 adrenoceptors on muscular arterioles mediating vasodilatation or alpha receptors on other arterioles, stimulation of which results in vasoconstriction (by the action of noradrenaline). Cardiac muscle exhibits intrinsity and automaticity i.e. it does not rely on neuronal input to depolarize, so has no receptors apart from the sino-atrial node myocytes which can respond to noradrenaline from sympathetic nerve input [causing tachycardia] or to acetylcholine from parasympathetic input (via the vagus nerve) causing bradycardia.
The crucial difference between smooth and striated muscle on the one hand against cardiac muscle on the other, is that cardiac muscle sarcolemmas of adjacent cells are connected to each other by gap junctions which allow movement of ions between adjacent myocytes to allow co-ordinated and harmonious contraction of the ventricles as a whole. The joint nature of cardiac myocytes is described as a syncytium [Greek syn/sym = together as in symphony/symbiosis/synchronous; cyto = cell].