Search PubMed⌕ Search

Biomedical subjects

D W Pfaff

Publications and source records attributed to D W Pfaff.

At least 343 records · Page 19Linked to original sources
PubMed1983

Estrogenic maintenance of lordotic responsiveness: requirement for hypothalamic action potentials.

Studies were conducted to determine the requirement for hypothalamic, sodium current-based action potentials in the performance of a stereotypic, estrogen-dependent reflex, the lordosis response. Intrahypothalamic infusion of local anesthetics (50% procaine or 0.5% bupivacaine) into conscious rats had no effect on lordotic responsiveness, and, in a separate group of urethane-anesthetized rats, depressed multiunit electrical activity temporarily. Intrahypothalamic infusion of tetrodotoxin into conscious rats, however, resulted in a dose-dependent, reversible decline in lordotic responsiveness. The first significant drop in lordotic responsiveness occurred 40 min after infusion; the minimum was reached 2-4 h after infusion. Recovery of lordotic responsiveness to preinfusion levels was complete by 12-24 h after infusion. Electrophysiological studies in a separate group of urethane-anesthetized rats revealed that intrahypothalamic tetrodotoxin infusion in most cases suppressed multiunit activity completely usually within 6 min, and this suppression lasted for at least several hours. These data indicate that large, prolonged decreases in electrical activity in the hypothalamus, where estrogenic action is necessary and sufficient to induce lordosis, result in a gradual, reversible decline in lordotic responsiveness. These data are consistent with a 'tonic' rather than a 'mount-by-mount' role of hypothalamic neurons in lordosis. Furthermore, since lordotic responsiveness declined only when hypothalamic electrical activity had been disrupted severely for at least 40 min, it is postulated that the neuroactive products released by lordosis-relevant, hypothalamic neurons may have a duration of action of at least several minutes.

Action Potentials↗
PubMed1983

Midbrain microinfusions of prolactin increase the estrogen-dependent behavior, lordosis.

Microinfusions of rat prolactin into the dorsal midbrain of estrogen-treated, ovariectomized rats increased lordosis behavior. Midbrain microinfusions of antiserum to prolactin into rats displaying maximum lordosis had the opposite effect. The distribution of a prolactin-like substance in the brain was studied immunocytochemically. The results suggest that a hypothalamic neuronal system projecting to the midbrain contains a prolactin-like substance that plays a role in facilitating this behavior and therefore may mediate some of the effects of estrogen on the brain. These data, together with others from studies of the prolactin gene and its regulation, indicate that it may be possible to analyze a sequence of molecular events in the brain that facilitate a behavioral response.

Adrenalectomy↗
PubMed1983

Actions of estrogens and progestins on nerve cells.

Estrogens and progestins alter electrical and chemical features of nerve cells, particularly in hypothalamus. Temporally, these events follow nuclear receptor occupation by these steroids, although not all effects have been proved to depend on translocation of receptors to the nucleus. Narrowing studies to focus on particular medial hypothalamic cells has been useful for understanding some of the actions of these steroids in brain. The variety of morphological, chemical, and electrical effects allow for a multiplicity in the cellular functions controlled by these hormones.

Animals↗
PubMed1983

Retrograde HRP identification of neurons in the rhombencephalon and spinal cord of the rat that project to the dorsal mesencephalon.

Neurons in the rhombencephalon and spinal cord of the rat that project to the dorsal midbrain were identified using the HRP retrograde neuroanatomical tracing method. Retrogradely labeled neurons were most numerous in the reticular formation, specifically in nucleus pontis oralis, caudalis, and gigantocellularis and in the sensory trigeminal complex. Neurons that project were also found in certain raphe nuclei, the parabrachial nuclei, the deep cerebellar nuclei, the vestibular cochlear complex, and the spinal cord. The diverse distribution of neurons that project to the midbrain is understandable in the context of the known diverse functions of the region, which include a role in sexual and other behaviors, nociception, and various autonomic functions.

Animals↗
PubMed1983

Effect of interruption of bulbospinal pathways on lordosis, posture, and locomotion.

The effect of interruption of descending bulbospinal projections arising from (i) the medial medullary reticular formation: nucleus reticularis gigantocellularis (NGC) and nucleus reticularis magnocellularis (NMC), (ii) nucleus raphe magnus, and (iii) nucleus subceruleus on the lordosis reflex, posture, and locomotion was examined. After interruption of descending NGC-NMC fibers, time-dependent deficits in lordosis were observed during the first two postoperative weeks with subsequent reflex recovery. A syndrome of postural and locomotor deficits occurred after NGC-NMC lesions. Postoperatively, postural reflexes were dominated by increased extensor tone which resulted in limb hyperextension. Specific time-dependent deficits in the control of extensor and flexor muscle groups involved in locomotion resulted in a motor syndrome that is detailed. After interruption of NMC fibers alone, no postural or locomotor deficits occurred and effects on lordosis were limited to the first few postoperative days. The NMC data suggested that the majority of the functional deficits seen after NGC plus NMC lesions were due to destruction of the NGC descending projections. Interruption of NSC bulbospinal fibers resulted in a significant depletion of spinal cord noradrenaline (NA) but not serotonin (5-HT). Functional deficits, when present, were limited to the first few postoperative days. Although interruption of descending NRM fibers resulted in a significant depletion of spinal cord 5-HT concentrations, greater depletions occurred in the NGC plus NMC group. No functional deficits were observed in the NRM group. These data suggest that interruption of NGC-NMC fibers destroyed the descending output from neurons which integrate the hormonal and sensory information necessary for lordosis.

Animals↗
PubMed1983

A histochemical study of lateral longissimus muscle in rat.

Rat axial muscle previously has not been studied histochemically. We were interested in determining the fiber composition and fiber distribution in rat lateral longissimus (LL), the large epaxial dorsiflexor muscle active during sexual posturing in the female rat and to determine if estrogen replacement in ovariectomized rats would affect the histochemical profile. Staining for ATPase after acid preincubation at pH 4.5, pH 4.35, and after alkaline preincubation at pH 9.4 and staining for NADH-TR revealed that rat LL contains the three major types of fibers present in most mammalian hind limbs: fast-twitch glycolytic (FG); fast-twitch oxidative-glycolytic (FOG); and slow-twitch oxidative (SO). The muscle contains predominantly FG fibers; SO fibers are segregated superficially from L2--L6 where they comprise from 11 to 18% of the fiber population, and in an oxidative compartment in the medial deep region of L5 where they comprise 62% of all fibers. In the medial deep region of L5 most of the remaining fast fibers also contain oxidative enzyme. Spindles are most highly concentrated in this oxidative region of L5. Estrogen treatment did not affect the relative number, distribution, or diameter of the three muscle fiber types in rat LL. The concentration of SO and FOG fibers and spindles localized in the region of the lumbosacral joint is discussed by contrasting forceful movements (e.g., rump elevation during sexual behavior) with normal postural regulation.

Adenosine Triphosphatases↗
PubMed1983

Modulation of the lordosis reflex of female rats by LHRH, its antiserum and analogs in the mesencephalic central gray.

Effects of intracerebral infusion of LHRH and related compounds on the lordosis reflex were examined in ovariectomized, estrogen-treated female rats. Lordosis, triggered either by manual cutaneous stimulation or by male mounting, was facilitated by the infusion of LHRH dissolved in saline into the mesencephalic central gray at midcollicular levels (CG). Infusion of an anti-LHRH globulin into the CG disrupted lordosis. Pretreatment with estrogen was necessary to obtain the behavioral facilitation by LHRH infusion. In separate experiments, placement of cannulae containing LHRH in an agar-saline gel in the CG also facilitated lordosis behavior. LHRH analogs applied to the CG by this method showed a clear dissociation between their behavioral effects and their reported effects on LH release. Cellular mechanisms involved in the mediation of LHRH effect in midbrain for the facilitation of lordosis may be different from those in gonadotrophs for LH release.

Animals↗
PubMed1983

Immunocytochemical localization of luteinizing hormone-releasing hormone in male and female rat brains. Quantitative studies on the effect of gonadal steroids.

The peroxidase-antiperoxidase immunocytochemical method was used to determine quantitatively the effects of gonadal steroids on the immunoreactive luteinizing hormone-releasing hormone (LHRH) content in the brain of male and female rats. In the male rat, gonadectomy decreased both the number of cell bodies and optical density of staining in cell bodies containing immunoreactive LHRH; decreased the percentage of area covered by LHRH fibers in the middle and caudal aspects of the median eminence (ME) but not the organum vasculosum lamina terminalis (OVLT), and decreased the number of LHRH fibers localized in the midbrain central gray (MCG). Since others have shown previously that gonadectomy increases the LHRH content of portal blood in the male rat, the results suggest that the decreased somal accumulation of LHRH and decreased LHRH content in fibers in the ME and MCG measured in the present study following loss of testicular steroids reflect increased LHRH release from the ME and MCG into the portal blood and brain, respectively. Estrogen replacement in the gonadectomized female rat increased the optical density of staining in cell bodies but not the number of cell bodies containing immunoreactive LHRH, increased the percentage of area containing LHRH fibers in the caudal aspect of the ME but not the OVLT, and decreased the number of fibers containing LHRH in the MCG. Since others have shown previously that estrogen replacement to gonadectomized female rats decreases LHRH release into portal blood, the present results suggest that the estrogen-induced increases in somal accumulation of LHRH and increases in LHRH content in fibers in the ME reflect a decreased LHRH release from the ME into the portal blood. By analogous reasoning, the decreased LHRH fiber content measured in the MCG following estrogen replacement to gonadectomized females reflects an increased LHRH release into the MCG. This inference is consistent with a postulated role for LHRH in this brain site in the facilitation of lordotic responsiveness.

Animals↗
PubMed1982

Characterization of estrogen-concentrating hypothalamic neurons by their axonal projections.

A method combining steroid autoradiography and fluorescent dye retrograde neuroanatomical tracing has been devised. This method makes it possible to demonstrate that some estrogen-concentrating cells in the ventrolateral subdivision of the ventromedial nucleus of the rat hypothalamus are neurons that send axons to the dorsal midbrain. Other cells only concentrate estrogen or only project to the midbrain. Estrogen-concentrating neurons in the ventromedial hypothalamus that project to the dorsal midbrain are likely to transmit hormone-influenced signals that regulate circuits for reproductive or other behaviors or autonomic functions.

Animals↗
PubMed1982

Intrahypothalamic colchicine infusions disrupt lordotic responsiveness in estrogen-treated female rats.

Since some estrogenic effects on lordotic responsiveness are mediated through hypothalamic protein synthesis, we conducted experiments to determine if axoplasmic transport in the hypothalamus is necessary for the induction and maintenance of this reflex by estrogen. Colchicine infusion into the hypothalamus, but not into the dorsal thalamus, of ovariectomized rats 24 h prior to administration of subcutaneous estrogen implants delayed the induction of lordotic responsiveness, as measured by the manual (cutaneous-pressure) method, by 2 days, as compared with vehicle-infused rats. In other experiments, colchicine infusion into the hypothalamus, but not into the dorsal thalamus, of conscious, ovariectomized, estrogen-implanted rats displaying maximal lordotic responsiveness resulted in a bimodal decline in lordotic responsiveness. An initial decline occurred 20-40 min after infusion, and was associated with general behavioral agitation and hyperactivity. A subsequent decline began 4 h after infusion and lasted for several days. Vehicle infusion did not decrease lordotic responsiveness. Colchicine infusion did not alter multiunit electrical activity recorded near hypothalamically directed cannulae tips over a period of several hours. Results suggest that axoplasmic transport within and/or from the hypothalamus is necessary for the estrogenic induction and maintenance of the lordosis reflex in rats.

Animals↗
PubMed1982

Autoradiographic identification of estradiol-concentrating cells in the spinal cord of the female rat.

The topography and number of estradiol (E)-concentrating cells in the lower lumbar and sacral segments of the spinal cord of the female rat have been examined by the steroid autoradiography method. A nuclear-saturating does of E was administered by intravenous infusion, which kept blood estrogen at or above proestrus levels for 3.5-4 h, much longer than usual for steroid receptor studies. The cord segments selected for examination are known to receive somatosensory information relevant for estrogen-dependent behavior, and to contain some of the motoneurons for epaxial muscles responsible for this behavior. Small numbers of E-concentrating cells were found in the dorsal portion of the gray matter of L4, L5, L6 and the sacral segments. These cells were found in lamina II, in the midline region which includes lamina X, and the medial portions of laminae III, IV and V when they cross in the midline. E-concentrating cells were also found in the lateral portions of laminae III, IV, and V, and in lamina VII. Virtually no E-concentrating cells were found in the ventral portion of the gray matter or in the white matter. The spinal cord had few E-concentrating cells compared to the hypothalamus.

Animals↗
PubMed1982

Responses of medullary reticulospinal and other reticular neurons to somatosensory and brainstem stimulation in anesthetized or freely-moving ovariectomized rats with or without estrogen treatment.

The medical medullary reticular formation (mMRF) is probably involved in controlling lordosis, a feminine mating reflex which requires both estrogen priming and appropriate somatosensory input(s). We have recorded single-unit activity of antidromically identified reticulospinal (RS) and unidentified (UI) neurons in mMRF of ovariectomized rats with or without estrogen treatment to investigate neurohormonal mechanisms regulating lordosis. The units were recorded in both acute and chronic preparations, the latter involving implanted "floating" wire electrodes to allow the influence of estrogen on a particular unit to be followed for several days. A substantial number of RS and UI units in both acute and chronic preparations were either excited or inhibited by a lordosis-eliciting somatosensory stimulation, indicating that the lordosis-eliciting sensory inputs did reach mMRF. The majority of these units responded promptly to the stimulation, and could participate in triggering the short-latency lordosis reflex. Electrical stimulation of several brainstem locations revealed that there was an extensive and specific convergence on mMRF neurons between inputs from the lordosis-eliciting stimulation and mesencephalic central gray, which has been shown to relay lordosis-inducing estrogen influence from hypothalamus to lower brainstem. Therefore, mMRF neurons can receive both the estrogen influence and the lordosis-eliciting inputs and integrate them. Although no apparent estrogen influence was detected in chronic preparations, statistical comparisons of results from acute preparations with or without estrogen treatment suggest that estrogen can increase the proportion of the neurons excited by the lordosis-eliciting stimulation and facilitate neuronal excitability. Both effects are consistent with the prevailing notion that the net lordosis-inducing influence of estrogen is facilitatory, and they may be mechanisms for making lordosis elicitable.

Animals↗