Dissociation of active from immobility components of sexual behavior in female rats by central 6-hydroxydopamine: Implications for CA involvement in sexual behavior and sensorimotor responsiveness

Caggiula, Anthony R.; Herndon, James G.; Scanlon, Robert; Greenstone, Debra; Bradshaw, W. G.; Sharp, Donna

doi:10.1016/0006-8993(79)90582-1

Cited by 78 publications

(26 citation statements)

References 36 publications

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“…Similarly, more tyrosine hydroxylase immunoreactive cells were observed in VTA sections from E 2 +P- compared to E 2 -primed rats [48]. Following 6-hydroxydopamine lesions, there is an overcompensation in functioning of the remaining dopamine cells [49] and, among rats that received 6-OHDA lesions of the VTA, there is an exaggerated response to the facilitating effects of P on lordosis of E 2 -primed rats [50,51,52]. These findings suggest that P may have actions to increase tyrosine hydroxylase and dopamine within the VTA.…”

Section: Discussionmentioning

confidence: 99%

In the Ventral Tegmental Area, Progestins’ Membrane-Mediated Actions for Lordosis of Hamsters and Rats Involve Protein Kinase A

Petralia

Walf²,

Frye³

2006

Neuroendocrinology

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Progestin-facilitated lordosis of hamsters and rats is enhanced by activation of dopamine type 1 (D₁) or GABA_A/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 µg at h 0) + progesterone (P; 100 µg 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 µg 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, 5α-pregnan-3α-ol-20-one (3α,5α-THP; 100 or 200 ng/side), or β-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.

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Section: Discussionmentioning

confidence: 99%

In the Ventral Tegmental Area, Progestins’ Membrane-Mediated Actions for Lordosis of Hamsters and Rats Involve Protein Kinase A

Petralia

Walf²,

Frye³

2006

Neuroendocrinology

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“…Dopamine has also been proposed to exert inhibition on lordosis based on the results of studies which used peripheral administration of dopamine receptor agonists, antagonists and synthesis inhibitors [11,12,14]. Norepinephrine containing nerve endings may also partici pate in the control of lordosis since lesions of norepineph rine cell bodies facilitate [4,17] or inhibit [15] lordosis re sponding. Particular nuclei within the hypothalamus which may mediate the effect of pargyline on behavior cannot be deter mined from the results presented here.…”

Section: Discussionmentioning

confidence: 99%

“…Such studies indicate that serotonin and dopamine may ex ert inhibitory influences on lordosis [1, 11-14, 25, 33, 35]. Noradrenergic influences on lordosis behavior may be more complex than those of the other amines since conflicts Received: June 11, 1981 Accepted after revision: September 17,1981 exist between results obtained by both pharmacological [12,33,35] and lesion techniques [4,15,17], While considerable progress has been made in describ ing the neural basis of endocrine events, current pharmaco logical studies leave unanswered the questions of whether identified hormone-sensitive monoaminergic projection sites in the hypothalamus are responsible for changes in neuroendocrine function after peripheral drug treatment and which projection sites participate in particular aspects of gonadal hormone mediation of neuroendocrine events. One approach to answering these questions would be to perturb pharmacologically specific monoaminergic, hor mone-sensitive hypothalamic sites and ascertain the effect on neuroendocrine events.…”

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confidence: 99%

Inhibition of Lordosis Behavior by Intrahypothalamic Implants of Pargyline

Luine¹,

Fischette²

1982

Neuroendocrinology

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Hypothalamic sites responsible for monoaminergic mediation of gonadal hormone-facilitated female sexual behavior (the lordosis response) were investigated. Pargyline, an irreversible inhibitor of monoamine oxidase, was applied stereotaxically to the hypothalamus of ovariectomized, estrogen-primed females 2 h prior to progesterone administration. Application of pargyline dorsal to or within the lateral aspect of the ventromedial nucleus led to a reduction in lordosis quotients and quality scores 5–7 and 29–31 h later. Implantation dorsal to or within the dorsomedial nucleus did not inhibit lordosis responding 5–7 h later but did inhibit the response 29–31 h later. In both implant sites, lordosis responding returned to prepargyline levels within 55 h after drug placement. The effects of the pargyline cannulae were verified biochemically by measuring activity of monoamine oxidase in preoptic-hypothalamic nuclei. Enzyme activity was inhibited to some extent in all nuclei sampled. The ability of the implants to antagonize lordosis responding was related to the extent to which they inhibited monoamine oxidase activity in the hypothalamus. Results suggest that localized perturbations in hypothalamic cells whose monoamine metabolism is known to be affected by gonadal hormones is sufficient to affect female sexual behavior.

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“…Cag giula and colleagues (180,181) found that intraventricular administration of 6-hydroxydopamine (6-0HDA) to rats primed with estrogen increased sexual receptivity, as measured by the lordosis quotient score, but not soliciting behavior. In animals made receptive with E2 + P, intraventricular .…”

Section: Dopamine: Ovulation and Feminine Sexual Behaviormentioning

confidence: 99%

Gonadal Steroid Action on the Brain: Neurochemistry and Neuropharmacology

McEwen¹,

Parsons²

1982

Annu. Rev. Pharmacol. Toxicol.

188

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INTRODUCTIONSteroid hormones of the gonads and adrenals influence the brain and alter the affective state as well as· overt behavior and neuroendocrine function. These actions are manifested in various ways and at various levels of obser vation and experimentation. For example, in female vertebrates of many species, estrogens prime the brain and pituitary gland and make possible the occurrence of ovulation and sexual receptivity. Androgens, On the other hand, facilitate male reproductive behavior including vocalizations (e.g. song in passerine birds, mate-calling in frogs), defense of territory and related aggressive displays, and copulatory behavior. At another level of analysis, estrogen treatment counteracts tardive diskinesia and L-DOPA induced diskinesia (1) and has antidepressant effects in women resistant to other kinds of antidepressant drug therapy (2). Moreover, changes in estro gen and progestin levels are often linked to the emotional lability associated with the premenstrual and postpartum periods (3, 4).Studies of the action of steroid honnones on the brain have progressed to a point where specific mechanisms and brain sites of action are now recognized. Especially important to the neurophannacologist are those aspects of mechanism which have begun to deal with hormonal modifica tion of properties and functions of synapses. Synaptic function and neuro transmission are indeed the common currency for the analysis of neuroendocrine events and honnone-regulated behaviors, as well as other aspects of brain function; and the study of drugs which modify neurotrans mission through blockade of synthesis, degradation, reuptake, and recep-555 0362-1642/82/0415-0555$02.00 Annu. Rev. Pharmacol. Toxicol. 1982.22:555-598. Downloaded from www.annualreviews.org Access provided by University of California -San Francisco UCSF on 02/04/15. For personal use only. Quick links to online content Further ANNUAL REVIEWS 556 MCEWEN & PARSONStors has produced a substantial literature implicating certain neuro transmitter candidates in those neuroendocrine and behavioral events. This article will summarize both hormone (especially gonadal steroid) action on synaptic properties and functions and the neuropharmacology of two well studied hormone-regulated events, the control of feminine sexual behavior and ovulation in rodents. Out of this summary will emerge, we hope, some generalizations which will help to guide future research.

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Dissociation of active from immobility components of sexual behavior in female rats by central 6-hydroxydopamine: Implications for CA involvement in sexual behavior and sensorimotor responsiveness

Cited by 78 publications

References 36 publications

In the Ventral Tegmental Area, Progestins’ Membrane-Mediated Actions for Lordosis of Hamsters and Rats Involve Protein Kinase A

In the Ventral Tegmental Area, Progestins’ Membrane-Mediated Actions for Lordosis of Hamsters and Rats Involve Protein Kinase A

Inhibition of Lordosis Behavior by Intrahypothalamic Implants of Pargyline

Gonadal Steroid Action on the Brain: Neurochemistry and Neuropharmacology

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