- Previous studies have suggested that the
syndrome of sedation and yawning behaviour in
the rat is dependent on stimulation of dopamine
autoreceptors - mainly because the syndrome is
produced by dopamine D-2 agonists given
systemically in low doses known to suppress the
release of endogenous dopamine.
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- However, exactly the same syndrome was found
after the local intracerebral injection of high
doses of dopamine agonists into the anterodorsal
region of the striatum, i.e. the D-2 agonist LV
171555 (5-10 ug), -NPA (1-2.5 µg),
N,N-propyl-5,6-ADTN (1-2.5 µg) and
apomorphine (10 µg), whereas the D-1
agonist SKF 38393 (5-10 ) was inactive. The
systemic injection of the D-2 antagonists
sulpiride and haloperidol produced total
antagonism of the sedation, yawning syndrome
induced by LV 171555 injected into the striatum,
whereas the D-1 antagonist SCM 23390 produced no
inhibition.
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- In support for the role of postsynaptic D-2
receptors, it was found that the depletion of
endogenous dopamine by the local injection of
6-OH-DA or systemic injection by reserpine +
cr-MT produced no inhibition of 10 µg LV
171555 injected into the striatum. The local
injection of sulpiride (50-100 ng) did not per
se induce the sedative/yasning syndrome.
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- Furthermore, a modulatory role of dopamine
D-l receptors iras found since the systemic
injection of SCM 23390 antagonized the
stereotyped behavioural stimulation by -NPA or
N,N-propyl-5,6-ADTN given systemically or
locally into intermediate ventromedial region of
striatum and changed the behaviour of the rets
into sedation and yenning activity.
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