Abstract：
:The cataleptic activity of morphine and methadone was markedly potentiated in frontally decorticated rats with no apparent changes in the onset or duration of action. Enhancement of the opioid cataleptic response was not due to changes in the availability of the drugs in the brain. The potentiation of methadone-induced catalepsy in decorticated rats was mimicked in naive rats by intrastriatal (i.s.) application of 2-amino-7-phosphonoheptanoic acid (AP7), a potent and selective antagonist of N-methyl-D-aspartate (NMDA) receptors. Therefore, degeneration of glutamatergic synapses following decortication could be responsible for the changes in behavioral effects caused by opioids. The failure of AP7 to elicit an effect after injection into the n. accumbens fits with the possibility of a selective involvement of the striatum in this phenomenon. That the striatum plays a critical role in the expression of opioid-induced catalepsy was substantiated by the findings that: (1) naloxone, an opioid antagonist, injected i.s., prevents the potentiation of catalepsy induced by methadone and morphine in decorticated animals, (2) oxotremorine, a muscarinic agonist, injected i.s., reverses the enhancement of opioid-catalepsy in decorticated rats, (3) earlier studies by others showed that ablation of the striatum had a facilitatory action on opioid-induced catalepsy. In conclusion, evidence is given that the corticostriatal pathway exerts an inhibitory effect upon narcotic-induced cataleptic behavior. The possibility that this effect is mediated through striatonigral GABAergic output is discussed. The data further suggest that the neuronal mechanisms through which the corticostriatal pathway mediates narcotic catalepsy is operative through activation of NMDA receptors within the striatum.
journal_name
Brain Resjournal_title
Brain researchauthors
Consolo S,Forloni G,Ladinsky H,Palazzi Edoi
10.1016/0006-8993(88)91028-1subject
Has Abstractpub_date
1988-05-24 00:00:00pages
97-103issue
1-2eissn
0006-8993issn
1872-6240pii
0006-8993(88)91028-1journal_volume
449pub_type
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