Synaptic cleft? nuerotransmitters and person hungry?
Answer:
Xenical (orlistat) doesn't really effect neurotransmitter. It works by inhibiting the incorporation of fats. It does this by inhibiting an enzyme call pancreatic lipase; this enzyme normally breaks fat down into fatty acids, which can be absorbed by the intestines. No lipase, heavy absorption (that's why society on xenical can't eat lots of solid, if they do, they have fatty fluid faeces).
Meridia (Sibutramine) is a different matter. It does work on the brain, in truth reducing hunger. It works by blocking the reuptake of the neurotransmitters serotonin and noradrenaline (AKA norephinephrine). These neurotransmitters are released by neurons that project from the brainstem into the rest of the brain. Once the neurotransmitters are released (not into a true synaptic cleft, but more into the interstial/extracellular fluid), they are removed by uptake by molecular transporters.
By inhibiting these transporters, meridia increases the levels of noradrenaline and serotonin within the brain. How these neurotransmitters then effect the neurons that produce the sensation of hunger is not really unspoken, but importantly, somehow noradrenaline and serotonin reduce hunger.
It is believed that an nouns of the brain called the hypothalamus is really important within controlled both energy intake and zest expenditure in the body. There are a huge number of neurotransmitters that somehow modify this pathway, but the exact roles they adjectives play is elusive. Important neurotransmitters surrounded by this pathway are ghrelin (a protein released by the stomach that increases hunger), Obestatin (which works as the inhibitor of ghrelin), leptin (produced by fat cell, inhibits hunger, animals with no leptin become massively obsese). Actually the index goes on and on; neuropeptide Y, agouti related peptide, melanocyte stimulating hormone, histamine orexin.
It's incredibly complicated.