The effect of central serotonergic stimulation on hippocampal and neocortical electrical activity and behavior was studied in freely moving rats by administering: (a)
tranylcypromine followed by
tryptophan, (b)
fluoxetine followed by
5-hydroxytryptophan, or (c)
p-chloroamphetamine alone. In all rats,
scopolamine-resistant hippocampal rhythmical slow activity (RSA), thought to be dependent on brain
serotonin, maintained its normal relation to behavior, occurring in close correlation with Type 1 behaviors (postural changes, turning of the head, walking). This RSA was generally absent during stereotyped behavior (head weaving, forepaw treading, hindlimb splaying and
tremor).
Scopolamine-resistant neocortical low-voltage fast activity (LVFA), also though to be dependent on brain
serotonin, was present during Type 1 behaviors and also during stereotyped behavior. Most rats that developed a full stereotyped behavior syndrome had behavioral and electrocortical
seizures which were associated with a reduction in the amplitude of hippocampal activity. These
seizures were suppressed by
methysergide or
benserazide.
Metergoline (and
methysergide to a lesser extent) suppressed the stereotypic behaviors of the
serotonin syndrome, resulting in a striking increase in the locomotion caused by central serotonergic stimulation. Such locomotion was accompanied by RSA and LVFA. It was concluded that increased serotonergic activity in the CNS causes an increase in motor activity and a correlated increase in
scopolamine-resistant hippocampal RSA and
scopolamine-resistant neocortical LVFA and suggested that
metergoline blocks
serotonin receptors mediating stereotyped behaviors, thereby permitting the expression of
serotonin-mediated locomotion.