In the ventral tegmental area, progestins' membrane-mediated actions for lordosis of hamsters and rats involve protein kinase A.
Progestin-facilitated lordosis of hamsters and rats is enhanced by activation of dopamine type 1 (D1) or GABAA/benzodiazepine receptor complexes (GBRs) in the ventral tegmental area (VTA) and these effects involve G-proteins and second messengers, such as adenosine 3',5'-monophosphate (cAMP). We examined whether D1- and/or GBR-mediated increases in progestin-facilitated lordosis of female hamsters and rats involve the cAMP-dependent protein kinase, protein kinase A (PKA), in the VTA. In experiment 1, ovariectomized hamsters, primed with estradiol (E2; 10 microg at h 0) + progesterone (P; 100 microg at h 45), were first pre-tested for lordosis and motor behavior (h 48) and then infused with the PKA inhibitor, Rp-cAMP (100 ng/side), or vehicle. Thirty minutes later, hamsters were retested and then received infusions of the D1 agonist, SKF38393 (100 ng/side), the GBR agonist, muscimol (100 ng/side), or vehicle to the VTA. Hamsters were post-tested for lordosis and motor behavior 30 min later. In Experiment 2, ovariectomized rats, primed with E2 (10 microg at h 0), were first pre-tested for lordosis and then infused with Rp-cAMP (100 ng/side) or vehicle to the VTA at h 44. Immediately after testing, rats received infusions of SKF38393 (100 ng/side), muscimol (100 ng/side), or vehicle and were retested for lordosis. Rats were then infused with the neurosteroid, 5alpha-pregnan-3alpha-ol-20-one (3alpha,5alpha-THP; 100 or 200 ng/side), or beta-cyclodextrin vehicle and were post-tested for lordosis and motor behavior 10 and 60 min later. The enhancing effects of progestins or progestins plus D1 or GBR activation on lordosis of E2-primed hamsters and rats were blocked by the PKA inhibitor, Rp-cAMP. Thus, in the VTA, progestins' membrane actions involving D1 or GBRs are mediated, in part, by PKA.
Petralia
Sandra M
SM
Department of Psychology , The University at Albany, SUNY, Albany, NY 12222, USA.
Walf
Alicia A
AA
Frye
Cheryl A
CA
D015647:2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine / Q000494:pharmacology; D000818:Animals; D003350:Cortodoxone / Q000031:analogs & derivatives / Q000494:pharmacology; D006224:Cricetinae; D000242:Cyclic AMP / Q000031:analogs & derivatives / Q000494:pharmacology; D017868:Cyclic AMP-Dependent Protein Kinases / Q000187:drug effects / Q000378:metabolism*; D018491:Dopamine Agonists / Q000494:pharmacology; D005260:Female; D018755:GABA Agonists / Q000494:pharmacology; D009118:Muscimol / Q000494:pharmacology; D010052:Ovariectomy; D011187:Posture / Q000502:physiology*; D011372:Progestins / Q000502:physiology*; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D051381:Rats; D020318:Rats, Long-Evans; D011954:Receptors, Dopamine / Q000502:physiology; D011963:Receptors, GABA-A / Q000502:physiology; D012726:Sexual Behavior, Animal / Q000502:physiology*; D013873:Thionucleotides / Q000494:pharmacology; D017557:Ventral Tegmental Area / Q000502:physiology*
D018491:Dopamine Agonists; D018755:GABA Agonists; D011372:Progestins; D047428:Protein Kinase Inhibitors; D011954:Receptors, Dopamine; D011963:Receptors, GABA-A; D013873:Thionucleotides; C027460:dopamine-I receptor; C016957:adenosine-3',5'-cyclic phosphorothioate; D009118:Muscimol; D015647:2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine; C009412:tetrahydro-11-deoxycortisol; D000242:Cyclic AMP; D017868:Cyclic AMP-Dependent Protein Kinases; D003350:Cortodoxone