2,3,4,5- Tetrahydro- 7,8- dihydroxy- 1- phenyl- 1H- 3- benzazepine (SKF 38393)

01/01/1997 - "Bromocriptine/SKF38393 treatment ameliorates obesity and associated metabolic dysfunctions in obese (ob/ob) mice."
08/01/1999 - "Our previous studies have shown that the dopaminergic D1 receptor agonist SKF38393 (SKF) plus the D2 receptor agonist bromocriptine (BC) act synergistically to reduce obesity in obese C57BL/6J (ob/ob) mice. "
01/01/1997 - "Bromocriptine and SKF38393 individually produced moderate improvements in obesity, hyperglycemia, and hyperinsulinemia. "

05/01/1990 - "The compound is less effective in inducing catalepsy, and antagonising SKF-38393 (tetrahydro- 1-phenyl-1H-3-benzazepine-7,8-diol HCl)-induced circling in 6-OHDA-lesioned rats and it does not induce perioral movements in rats. "
03/21/1994 - "The catalepsy induced by the synthetic cannabinoid, measured as the descent latency in the bar test, was enhanced in male rats chronically treated with the dopamine D1 receptor agonist SKF38393 (8 mg kg-1, twice a day during 21 days). "
10/01/1993 - "Rats injected with reserpine alone (2.5 mg/kg i.p.) developed akinesia and ptosis within 60-90 min. The D1 agonist SKF 38393 (30 mg/kg i.v.) rapidly reversed ptosis and restored near-normal mobility when administered 24 h after reserpine and AMPT; catalepsy was reversed for 90 min, after which the drug effect wore off. "
02/01/1988 - "The catalepsy of D-2 blockade with molindone was not potentiated by the D-1 agonist, SKF 38393, which slightly disrupted the catalepsy of D-2 blockade. "
10/01/2001 - "The MF exposed rat with chemically induced dopamine neurons damage exhibited a reduction of irritability and oral activity when stimulated with SKF 38393 (the agonist of central dopamine D(1) receptor) and some increase of catalepsy after administration of SCH 23390(the antagonist of central dopamine D(1) receptor). "

05/31/1990 - "In mice treated with reserpine (5 mg/kg s.c.) 18 h before testing, which on its own caused intense hypothermia (10-12 degrees C), SK&F 38393 (1.87-30 mg/kg s.c.) induced a dose-dependent and more marked rise of body temperature (5-7 degrees C). "
01/01/1990 - "Colonic temperature was not changed after acute SKF 38393 while acute LY 171555 induced a hypothermia. "
07/01/1993 - "Following chronic reserpinization, however, apomorphine (0.25-1 mg/kg) produced a significant rise in body temperature, which was significantly enhanced upon co-administration with SKF38393 (5 mg/kg) but reversed to hypothermia when given in combination with B-HT920 (0.5 mg/kg). "
07/01/1993 - "In naive rats, the D2 dopamine agonist B-HT920 (0.25-1 mg/kg) produced hypothermia, an effect sensitive to blockade by the D1/D2 antagonist haloperidol (0.5 mg/kg) and to potentiation by the D1 agonist SKF38393 (5 mg/kg). "
01/01/1989 - "The selective D2 agonist quinpirole (LY 171555) also elicited dose-dependent hypothermia, whereas the selective D1 agonist SKF 38393 had no effect. "

09/01/1987 - "SKF 38393 (a partial D1 agonist) caused slight sedation, minimal oral dyskinesia and a significant reduction in D2 agonist-induced repetitive movements."
03/01/1999 - "In adulthood, P0/1-lesioned rats exhibited increases in oral dyskinesias and rearing behavior following treatment with the partial D1 receptor agonists, SKF38393 and SKF77434, whereas rats lesioned on P7 exhibited increases in grooming. "
05/01/1991 - "Chronic administration of SKF-38393 alone produced sensitization of the oral dyskinesia response elicited by a challenge injection of the agonist, but no significant change in the grooming response. "
08/24/1988 - "The partial D-1 agonist, SKF 38393, induced/aggravated oral dyskinesia and slight sedation, but no non-oral repetitive movements. "
08/30/1991 - "In contrast to the oral dyskinesia, this altered sensitivity to SKF-38393 returned to normal within 20 days after terminating the reserpine treatment, suggesting that these two behavioral responses involve different neural mechanisms. "

01/01/1992 - "These behaviors typically involved an oral component and included grooming and mouthing following SKF-38393 in depleted 10-day-old pups, mouthing following administration of either agonist to depleted weanlings, and probing and intense self-mutilation (forepaw and tongue biting) following the combined agonists in depleted weanlings. "
09/01/1999 - "At 94 days of age, animals were injected with either SKF-38393 (3.0 mg/kg, intraperitoneally (i.p.)), a dopamine D1 agonist, or m-chlorophenylpiperazine (m-CPP) (3.0 mg/kg, i.p.), a 5-HT2C agonist, in an attempt to evoke behaviors such as stereotypical chewing, head-nodding, self-biting and self-mutilation. "
02/01/1988 - "After systemic administration of SKF-38393 or L-dopa, central microinjection of the adenosine agonists, 2-chloroadenosine or 5'-N-ethylcarboxamide adenosine, were effective in preventing self mutilation induced by these dopamine agonists in neonatally lesioned rats. "
10/01/1989 - "Pretreatment with the 5-HT antagonist methysergide did not produce a change in apomorphine-induced locomotion and did not antagonize the self-mutilation or the other behaviors produced by L-DOPA or SKF-38393 in neonatally lesioned rats, suggesting that 5-HT hyperinnervation is not responsible for these drug-induced changes in neonatal 6-OHDA-lesioned rats."