title: [Significance of CRF and dopamine receptors in amygdala for reinforcing effects of opiates and opioids on self-stimulation of lateral hypothalamus in rats].
abstract: Bipolar electrodes were implanted in the lateral hypothalamus in a group of 44 Wistar male rats in order to study self-stimulation reaction in the Skinner box. Simultaneously, microcanules were implanted into the central nucleus of the amygdala to inject the drugs (1 microl per injection). The blockade of corticoliberin (CRF) receptors (astressin, 1 microg) or Na+influx currents (xycaine or lidocain 1 microg) by the intrastructural administration of drugs into the amygdala decreased self-stimulation reaction of the lateral hypothalamus in rats by 29-55%. The inhibition of D1 and D2 dopamine receptors in the amygdala with SCH23390 (1 microg) or sulpiride (1 microg) respectively, also reduced self-stimulation but to a lower degree. On the background of blockade of CRF (astressin) and dopamine (sulpiride) receptors as well as sodium influx ionic currents (lidocain) in the amygdala neurons, psychomotor stimulant amphetamine (1 mg/kg) and barbiturate sodium ethaminal (5 mg/kg) retained their psychoactivating effect on self-stimulation (+30-37%), while fentanyl (0.1 mg/kg) and leu-enkephaline (0.1 mg/kg) did not produce this effect. Fentanyl moderately activated self-stimulation only after the blockade of D1 dopamine receptors with SCH23390. After the blockade of CRF receptors, leu-enkephaline strengthened its depressant effect on self-stimulation reaction (-89%). Therefore, if the modulating action of amygdala on the hypothalamus is eliminated, the enhancing effects of opiates (fentanyl) and opioids (leu-encephaline) are blocked, but the effects of psychomotor stimulant amphetamine and barbiturate sodium ethaminal are retained.
authors: P D
authors: PD
authors: Shabanov
authors: A A
authors: AA
authors: Lebedev
authors: A V
authors: AV
authors: Liubimov
authors: V A
authors: VA
authors: Kornilov
mesh_terms: D000661:Amphetamine / Q000494:pharmacology; D000679:Amygdala / Q000187:drug effects* / Q000502:physiology; D000701:Analgesics, Opioid / Q000494:pharmacology; D000818:Animals; D001552:Benzazepines / Q000494:pharmacology; D002404:Catheterization; D003346:Corticotropin-Releasing Hormone / Q000494:pharmacology; D004298:Dopamine / Q000494:pharmacology; D018492:Dopamine Antagonists / Q000494:pharmacology; D004567:Electrodes, Implanted; D005283:Fentanyl / Q000494:pharmacology; D007031:Hypothalamus / Q000187:drug effects* / Q000502:physiology; D008297:Male; D009294:Narcotics / Q000494:pharmacology; D010446:Peptide Fragments / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D018019:Receptors, Corticotropin-Releasing Hormone / Q000037:antagonists & inhibitors / Q000378:metabolism*; D011954:Receptors, Dopamine / Q000378:metabolism*; D012653:Self Stimulation / Q000502:physiology*; D013469:Sulpiride / Q000494:pharmacology
chemical_list: D000701:Analgesics, Opioid; D001552:Benzazepines; D018492:Dopamine Antagonists; D009294:Narcotics; D010446:Peptide Fragments; D018019:Receptors, Corticotropin-Releasing Hormone; D011954:Receptors, Dopamine; C534628:SCH 23390; C104416:astressin; D013469:Sulpiride; D003346:Corticotropin-Releasing Hormone; D000661:Amphetamine; D005283:Fentanyl; D004298:Dopamine