This could be true, but it is an over-simplification of what is really going on. Truth is we don't know for certainty that this is what is going on. Several theories of the mechanism of LSD have been postulated. Each one presents a way in which LSD could affect behavior through activation of serotonergic neurons along with research to support it. However, each one has its weaknesses. In the end, it is difficult to determine how LSD actually alters behavior. The first theory is that LSD is a serotonin antagonist, specifically activating (or actually blocking) 5-HT2 receptors. This would prevent serotonin from having its normal effect. Support for this theory comes from studies that have shown that administration of some 5-HT2 antagonists do not decrease the effects of LSD, as you would expect if LSD was a serotonin agonist.
Activation of 5-HT2 receptors seems to cause serotonin to have an excitatory effect on some neurons. LSD prevents this action, thus having an antagonistic effect on the 5-HT2 serotonin system. However, even within this theory there are problems. The general theory of LSD as an antagonist is consistent with how it affects behavior. LSD seems to increase sensation, heart rate, and blood pressure, all of which are excitations of the nervous system. Because serotonin is an inhibitory neurotransmitter, antagonism of serotonin would result in an increase in neural activity. However, the fact that LSD is an antagonist to 5-HT2 receptors specifically makes this conclusion problematic. Because of the special action of 5-HT2 receptors, antagonism of serotonin at those receptors would result in a decrease in neural activity which would not explain the effects of LSD. If 5-HT2 receptors are in fact excitatory, one would expect antagonism of this system to have an inhibitory effect.
The next theory postulates that LSD is in fact a 5-HT agonist rather than an antagonist. One researcher was able to train rats to discriminate between LSD and saline based on it psychological effects. When the rats were given certain 5-HT2 antagonists, the rats lost the ability to discriminate between the two. Also, LSD has been shown to have a higher affinity for 5-HT receptors over all than serotonin but has a lower potency. Thus, while is more likely to bind to the receptors, it is not as likely to have an effect as serotonin. Even though LSD has some activity, it does not appear to be very strong. LSD may appear to be an antagonist even though by definition it is an agonist.
The last theory partially combines the last two theories. This theory postulates that 5-HT1 and 5-HT2 have an agonist/antagonist relationship. Thus substances that are agonistic to 5-HT1 receptors are antagonistic to 5-HT2 receptors. This is supported by the above research. LSD operates under this mechanism by enhancing serotonin activity at 5-HT1 receptors, while also blocking 5-HT2 receptors from the more effective activation of serotonin.