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PubMed1990

Analysis of the action of angiotensin II on the baroreflex control of heart rate in conscious rabbits.

There is considerable evidence that angiotensin II (Ang II) attenuates the baroreflex control of heart rate (HR), but the mechanism and site of this action have not been precisely defined. In the present study the effects of systemically and centrally administered Ang II on the baroreflex control of HR were investigated in conscious, chronically prepared rabbits. Baroreflex curves (HR vs. mean arterial pressure) were generated with iv infusions of phenylephrine or nitroprusside. Background infusion of Ang II at 10 ng/kg.min increased mean arterial pressure from 77.3 +/- 3.0 to 94.3 +/- 4.1 mm Hg (P less than 0.001) without changing HR [212.1 +/- 7.2 to 218.0 +/- 9.8 beats/min (bpm)] and shifted (reset) the baroreflex curve with phenylephrine to a higher pressure level (P less than 0.001) without changing its slope (-1.40 +/- 0.40 to -1.65 +/- 0.46 bpm/mm Hg; P = 0.4). Background infusion of an equipressor dose of phenylephrine did not shift the baroreflex curve or change its slope. Ang II also shifted the baroreflex curve with nitroprusside to a higher pressure level (P less than 0.01), but again the slope was not significantly changed (-2.30 +/- 1.25 to -1.51 +/- 0.52 bpm/mm Hg; P = 0.2). Background intraventricular infusion of Ang II at 1 ng/kg.min had the same effects as iv infusion of Ang II at 10 ng/kg.min; the curve was shifted to a higher pressure level (P less than 0.001), but the slope was not changed (-0.76 +/- 0.47 to -1.143 +/- 0.48 bpm/mm Hg). Intravenous infusion of Ang II at 1 ng/kg.min had no effect on the baroreflex. The resetting of the baroreflex with phenylephrine by iv Ang II (10 ng/kg.min) was not blocked by propranolol: atropine markedly reduced the baroreflex response to phenylephrine in both the absence and presence of Ang II. These results indicate that in conscious rabbits, Ang II resets the baroreflex control of HR, but does not change its sensitivity. This effect apparently results from an action of Ang II on the brain that is mediated by withdrawal of vagal tone to the heart. The resetting of the baroreflex by Ang II can explain the ability of the peptide to increase arterial pressure without decreasing HR.

Angiotensin II↗

PubMed1984

Involvement of hypothalamic vasoactive intestinal polypeptide (VIP) in prolactin secretion induced by serotonin in rats.

To study the possible involvement of hypothalamic vasoactive intestinal polypeptide (VIP) in regulating the secretion of prolactin (PRL), the effect of anti-VIP rabbit serum on serotonin (5-HT)-induced PRL release was examined in urethane-anesthetized male rats. Anti-VIP serum (AVS) or normal rabbit serum (NRS) was infused into a single hypophysial portal vessel of the rat for 40 min at a rate of 2 microliters/min with the aid of a fine glass cannula and 5-HT was injected into a lateral ventricle 10 min after the start of the infusion. Intraventricular injection of 5-HT (10 micrograms/rat) caused an increase in plasma PRL levels in control animals infused with NRS and 5-HT-induced PRL release was blunted in animals infused with AVS (mean +/- SE peak plasma PRL: 118.9 +/- 19.8 ng/ml vs 54.7 +/- 16.2 ng/ml, p less than 0.05). These findings suggest that the secretion of PRL induced by 5-HT is mediated, at least in part, by hypothalamic VIP release into the hypophysial portal blood in the rat.

Animals↗

PubMed1993

Effects of a muscarinic antagonist on various components of female sexual behavior in the rat.

The effects of the muscarinic antagonist scopolamine on lordosis, solicitation, pacing, approach, attractivity, and activity were evaluated in ovariectomized rats brought into sexual receptivity with estrogen and progesterone. Systemic (1 mg/rat) or intraventricular (10 micrograms bilaterally) administration of scopolamine significantly reduced the incidence of lordosis and solicitation behaviors and disrupted typical pacing of sexual contacts with a stimulus male. In addition, females avoided contact with a stimulus male, but not a stimulus female, following intraventricular infusion of scopolamine. The levels of general activity and frequencies of sexual contacts were similar in females treated intraventricularly with scopolamine and vehicle solutions. Consequently, scopolamine disrupted various components of sexual behavior, including lordosis, solicitation, pacing, and approach, without altering female attractivity or general activity.

Animals↗

PubMed2001

Locus coeruleus noradrenergic lesions attenuate intraoral intake.

I.p. injections of DSP-4 in male rats decreased norepinephrine (NE) levels to varying degrees throughout the brain with 66.7% reductions in the hypothalamic paraventricular nucleus. Intake of intraorally infused sucrose was reduced for 14 days but daily pellet intake recovered within 5 days post-injection. Intraventricular NE restored intraoral sucrose intake in DSP-4-lesioned rats without affecting controls. Intraventricular infusion of neuropeptide Y (NPY) reduced intraoral intake in controls but had no effect in DSP-4-lesioned rats. NPY markedly inhibited intraoral intake in DSP-4-treated rats that also received NE. These data confirm studies showing that NPY decreases consummatory ingestive behavior and suggest that this inhibition involves ascending noradrenergic projections from locus coeruleus.

Adrenergic Agents↗

PubMed1977

Inhibition of prostaglandin-enhanced release of LH by antiserum to luteinizing hormone releasing hormone.

Prostaglandin E2 (PGE2), PGF2alpha, PGF2beta was infused into a lateral ventricle of the brain of adult male rats, after pretreatment with normal rabbit serum (NRS) or anti-LH-RH serum, and the concentration of LH in arterial plasma was determined. I.v. administration of anti-LH-RH serum 2.5 min prior to the infusion of 2 microgram or 20 microgram of PGE2 significantly inhibited the PGE2-induced rise of plasma LH. Intraventricular infusion of 20 microgram of PGF2alpha or PGF2beta into NRS-pretreated animals caused a marked increase in the plasma LH concentration; whereas, prior i.v. administration of anti-LH-RH serum blocked the PG-induced rise in plasma LH levels. It is concluded that PGE2, PGF2alpha, and PGF2beta stimulate the release of LH primarily by enhancing the release of LH-RH.

Animals↗

PubMed1976

Intraventricular self-administration of morphine in naive laboratory rats.

Male Wistar rats implanted with cannulae aimed at the left lateral cerebral ventricle were individually maintained in Skinner boxes for 11 consecutive days. Animals were neither predependent on morphine nor shaped to press the operant lever. Experimental animals (n = 7) obtained intraventricular infusions of a 1% morphine HCl solution (2 mul per 5-s infusion) for each lever press while control animals (n = 7) received only the vehicle. Four animals were yoked to experimental animals and received equivalent but non-contingent morphine HCl infusions. The mean number of lever presses per day for the experimental group was significantly higher than for the vehicle control or yoked control groups suggesting that naive rats will work for the positive reinforcing properties of morphine when it is infused centrally.

Animals↗

PubMed1977

Ingestive behavior after intracerebral and intracerebroventricular infusions of glucose and 2-deoxy-D-glucose.

Direct infusions of 2-DG into the lateral hypothalamic area (LHA), the ventromedial hypothalamus (VMH), the dorsal hippocampus, the amygdaloid complex or the caudate nucleus were all ineffective in eliciting drinking or feeding in satiated rats. However, 2-DG (but not D-glucose) infused into the lateral ventricles of satiated rats elicited feeding preceded by an initial burst of drinking, which could be blocked by prior intraventricular infusion of the alpha-adrenergic antagonist, phentolamine, by the serotonergic blocker, methysergide, but only slightly by the dopaminergic receptor blocker, spiroperidol. The feeding response was totally blocked by phentolamine but not by methysergide or spiroperidol. These results show that 1) intraventricular administration of 2-DG can induce feeding, as well as drinking, supporting the hypothesis of cerebral glucoreceptors for the initiation of feeding behavior; and 2) local cytoglucopenia in the LHA, the VMH, or other limbic structures is not sufficient to initiate feeding. It is hypothesized that a specific pattern of cerebral glucoprivation rather than local glucoprivation, or an action of 2-DG on the presynaptic membrane of noradrenergic "feeding neurons" could be the mechanisms of 2-DG-induced feeding.

Animals↗

PubMed1985

[Inhibition of insulin secretion by intracerebroventricular infusion of pancreatic polypeptide in conscious dogs].

Previously, we demonstrated that peripheral infusion of pancreatic polypeptide (PP) inhibits insulin response to several stimuli through vagal innervation. Since PP is found not only in pancreas but also in brain or cerebrospinal fluid, we studied the effect of intracerebroventricular infusion of PP on insulin secretion before and after vagotomy in dogs. Mongrel dogs were settled with a chronic cannula allowing intraventricular infusions into the third (n = 4) or lateral (n = 4) cerebral ventricle. All the experiments were performed one week after the operation in a fully conscious, relaxed state. Porcine PP (pPP, 50 ng or 5 micrograms/dog in 100 microliter saline), which has the same primary structure with that of canine PP, or saline alone was infused into the cerebral ventricles for 5 minutes at the rate of 20 microliter/minutes. As stimuli of insulin secretion, modified sham feeding (MSF; sight and smell of food for 5 minutes), glucose injection (IV-Glucose; 0.5 g/kg/30 seconds, intravenously) and CCK-octapeptide infusion (IV-CCK-8; 0.07 micrograms/kg/5 minutes, intravenously) were applied immediately after (and in some experiments various intervals after) the end of pPP or saline infusion into the ventricles. Immunoreactive PP or insulin was measured by a specific radioimmunoassay. Administration of PP caused significant inhibition of insulin secretion by MSF, IV-Glucose and IV-CCK-8 without affecting basal insulin secretion. The observed effect of the peptide was most potent when infused into the third cerebral ventricle at a dose of 50 ng/dog and not in a dose-related fashion. The integrated insulin responses to MSF, IV-Glucose and IV-CCK-8 were 28, 58 and 30%, respectively, as those of controls. This effect was likely to be of central origin because an overflow of PP to the periphery could not be observed by PP radioimmunoassay. Prior transthoracic bilateral truncal vagotomy abolished the suppressive effect of PP on glucose- and CCK-8-induced insulin secretion. Furthermore, the time course study of CCK-8 suggested that PP could interact with the regions surrounding the third cerebral ventricle. These results suggest that PP affects the central nervous system to control pancreatic insulin secretion via the vagus nerve like other peptides/neuroregulators which modify physiological processes (e.g. insulin release, acid secretion, motility).

Animals↗

PubMed1986

The role of spinal cord cyclic AMP in the acoustic startle response in rats.

Drugs thought to increase intracellular levels of cAMP were infused intrathecally into the subarachnoid space of the lumbar spinal cord, and the effects on the acoustic startle response in rats were measured. Intrathecal infusions of the cAMP analogs dibutyryl cAMP or 8-bromo cAMP (12.5-100 micrograms) produced marked, dose-dependent increases in startle amplitude compared to the infusion of artificial cerebrospinal fluid (CSF). Local infusions of dibutyryl cAMP at more rostral levels of the spinal cord or brain failed to mimic the excitatory effect seen following lumbar intrathecal infusion. No excitation of startle was seen following intrathecal infusion of cAMP itself, ATP, 5'-AMP, or dibutyryl cGMP. A weak excitation of startle was seen following intrathecal, but not intraventricular, infusion of the water-soluble adenylate cyclase activator forskolin 7-deacetyl-7-O-hemisuccinic acid (forskolin-DHA; 5.0-100 micrograms, in artificial CSF), whereas forskolin itself [0.01-200 micrograms, in dimethyl sulfoxide (DMSO)] was without consistent effect. Finally, intrathecal infusion of the selective phosphodiesterase inhibitor Rolipram (12.5-200 micrograms) produced a marked excitation of startle similar in magnitude to the effects produced by cAMP analogs. The excitatory effects of intrathecally infused dibutyryl cAMP, 8-bromo cAMP, forskolin-DHA, or Rolipram support a functional link between spinal cord cAMP and the acoustic startle reflex. Possible sites of cAMP action on startle are discussed.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1976

Effects of intraventricular catecholamines on luteinizing hormone release in ovariectomized-steroid-primed rats.

The effects of intraventricular norepinephrine (NE) and dopamine (DA) were studied in the awake, freely behaving rat. In long-term ovariectomized, estrogen-progesterone-primed (OVE E2-P) animals, blood samples were taken via indwelling intra-atrial catheters before and after intraventricular infusion of either pH-adjusted saline, NE )5 mug, 15 mug, 20 mug), or DA (4 mug, 15 mug), and plasma LH was measured by radioimmunoassay. Under urethane anesthesia, records were made of the effects of intraventricular saline and NE on the electrical activity of the arcuate nucleus in the form of multi-unit spike activity. In unanesthetized animals, intraventricular NE caused marked changes in behavior. The typical response consisted of three phases: generalized activation (5-7 min), feeding (5-15 min), and sleep 1-2 h). DA exerted similar behavioral effects but without the marked sleep phase characteristic of the NE response. The effects of the catecholamines on LH output were significant increases in plasma LH levels for all NE doses tested (5 mug, p less than .025; 15 mug, p less than .05; 20 mug, p less than .005), while DA had no effect. The dynamics of the LH response to NEwere similar at all dosage levels, and the increase caused by 20 mug NE was found to be essentially equal to that induced by a quick intravenous infusion of 1.25 ng LHRH. Arcuate nucleus multi-unit spike activity (MUSA) showed a clear response to intraventricular NE at a dosage capable of stimulating the release of LH. In every case, the initial effect was a decrease in spike activity. These results, considered in relation to previous findings, suggest that NE may be stimulatory to neurons secreting LH-releasing hormone (LHRH). The decrease in arcuate nucleus MUSA in response to NE implies that certain elements of this nucleus are inhibited during LH release, perhaps the dopaminergic tuberoinfundibular neurons.

Animals↗

PubMed1996

TrkA activation is sufficient to rescue axotomized cholinergic neurons.

To test the molecular nature of the NGF receptor responsible for the ability of NGF to rescue septal cholinergic neurons following axotomy, we infused polyclonal antibodies that act as specific agonists of trkA (RTA) into the lateral ventricle of fimbria-fornix lesioned animals. Rats receiving chronic intraventricular infusions of RTA showed significantly more low affinity NGF receptor immunoreactive (p75NGFR-IR) neurons on the lesioned side than did control animals 2 weeks following unilateral fimbria-fornix lesion. RTA also initiated cholinergic sprouting. Infusions of RTA in combination with an antibody that blocks p75NGFR (REX) did not reduce the cell savings effect observed with RTA alone. However, animals infused with RTA plus REX demonstrated significantly less sprouting. These findings suggest that antibody-induced trkA activation is sufficient to mediate NGF-promoted survival of axotomized cholinergic neurons in vivo.

Animals↗

PubMed2002

Activation of mu-opioid receptors inhibits lordosis behavior in estrogen and progesterone-primed female rats.

The present study investigated the effect of highly selective mu-opioid receptor (OR) agonists on lordosis behavior in ovariectomized rats treated with 3 microg of estradiol benzoate followed 48 h later by 200 microg of progesterone. Ventricular infusion of the endogenous mu-OR agonists endomorphin-1 and -2 suppressed receptive behavior in a time- and dose-dependent fashion. At 6 microg, both endomorphin-1 and -2 inhibited lordosis behavior within 30 min. However, while the effect of endomorphin-1 lasted 60 min, endomorphin-2 inhibition lasted up to 120 min after infusion. Pretreatment with naloxone (5 mg/kg sc) was able to block both endomorphin-1 and endomorphin-2 effects on lordosis. Site-specific infusions of endomorphin-1 or endomorphin-2 into the medial preoptic area (mPOA), the ventromedial nucleus of the hypothalamus (VMH), or into the mesencephalic central gray did not affect receptivity. In contrast, infusion of 1 mug of either compound into the medial septum/horizontal diagonal band of Broca inhibited lordosis in a pattern very similar to that seen after intraventricular infusions. Infusion of the potent synthetic mu-OR agonist [D-Ala(2),N-Me-Phe(4),Gly-ol(5)]-enkephalin (0.08 microg) into the VMH and mPOA inhibited lordosis behavior for at least 60 min after infusion. The nonspecific opioid receptor antagonist naloxone was able to facilitate lordosis in partially receptive female rats when infused into the mPOA but not when infused into the VMH. The behavioral effects of the agonists and antagonist used in this study suggest that the endogenous mu-opioid system modulates estrogen and progesterone-induced lordosis behavior.

Analgesics, Opioid↗

PubMed1993

Role of neuropeptide-Y in episodic luteinizing hormone release in ovariectomized rats: an excitatory component and opioid involvement.

We tested the hypothesis that hypothalamic neuropeptide-Y (NPY) is an excitatory signal in the episodic secretion of LH in ovariectomized (ovx) rats and that the suppression of LH secretion that consistently follows intracerebroventricular administration of NPY is due to concurrent release of opioids or CRH, both previously shown to readily inhibit LH release. In the first experiment, ovx rats received continuous intraventricular infusion of either serum containing NPY antibodies (NPY-Ab) or normal rabbit serum (control) at dilutions of 1:5 or 1:1. NPY-Ab infusion at a 1:5 dilution significantly decreased mean plasma LH levels and LH pulse amplitude without affecting LH pulse frequency over a 3-h period of observation. However, infusion of relatively more concentrated NPY-Ab (1:1) markedly decreased not only mean plasma LH levels and LH pulse amplitude, but also the frequency of LH episodes. In the next experiment, we observed that intraventricular administration of NPY (0.2 nmol) suppressed LH release for 60 min. However, blockade of opiate receptors with iv infusion of naloxone (2 mg/h) before and after NPY injection completely counteracted the NPY-induced inhibition of LH release. On the other hand, prior blockade of the CRH receptors with alpha-helical CRH-(9-41) (25 or 100 micrograms/rat) was ineffective in reversing the inhibitory LH response of NPY (0.125 nmol). These results together with our previous demonstration of morphological communication between NPY and beta-endorphin neurons, show that suppression of LH by exogenous NPY in ovx rats may result from concurrent stimulation of opioids, primarily beta-endorphin. However, diminution of all parameters of episodic LH secretion by NPY-Ab affirms the notion that the NPY network is a physiologically important excitatory component of the hypothalamic pulse generator circuitry that regulates episodic LH secretion in rats.

Animals↗

PubMed1989

Nerve growth factor affects uninjured, adult rat septohippocampal cholinergic neurons.

The effect of nerve growth factor on the intact versus injured septohippocampal cholinergic system of adult rats was studied. Nerve growth factor was continuously infused into the lateral ventricle of adult uninjured rats or rats that had received unilateral partial transection of the fimbria. Controls (operated and unoperated) received intraventricular infusion of cytochrome c. After 2 weeks of nerve growth factor or cytochrome c treatments, choline acetyltransferase and acetylcholinesterase activities were measured in the septal area and in the hippocampus (divided into dorsal, medial and ventral parts). The continuous infusion of nerve growth factor resulted in a marked dose-dependent increase of choline acetyltransferase activity in both septum and hippocampus of adult unlesioned rats. In lesioned rats the nerve growth factor treatment was capable of inducing choline acetyltransferase activity in the hippocampus of not only the lesioned but also the unlesioned side, as well as in the septal area. In addition, nerve growth factor affected choline acetyltransferase activity differently in the hippocampus of the operated side with respect to the contralateral side or in unoperated animals. The chronic infusion of nerve growth factor did not affect acetylcholinesterase activity in the septum or in the hippocampus of either lesioned or unlesioned rats. The present findings indicate that nerve growth factor is capable of modulating the function of not only damaged but also normal adult forebrain cholinergic neurons. This suggests that nerve growth factor may modulate the function of these neurons in adulthood.

Acetylcholinesterase↗

PubMed1989

Forskolin infusion in vivo increases ouabain binding in brain.

In order to investigate the possible regulation of brain Na,K-ATPase by cyclic AMP, we measured Na,K-ATPase activity and ouabain binding in cerebral cortex after intraventricular infusion of forskolin for 7 days. There was a dose-related increase in high-affinity ouabain binding, with a 75% increase at 12.5 micrograms/h forskolin. The effect on total enzyme activity was smaller but enzyme activity with high affinity for ouabain was increased by 65%, suggesting a selective effect on enzyme with high affinity for ouabain. Forskolin appeared not to interact directly with Na,K-ATPase in vitro.

Animals↗

PubMed1981

Potentiation of prostaglandin E2-induced release of LH by the prostaglandin analogue, 7-oxa-13-prostynoic acid.

The prostaglandin (PG) analogue 7-oxa-13-prostynoic acid (7-OPA) was infused into a lateral ventricle of the brain of adult male rats and the effect of the analogue on the subsequent stimulation of LH release by intraventricular infusion of PG's was determined. Pretreatment of the animals with 44- 132 micrograms of 7-OPA potentiated the stimulatory effect of 2 micrograms PGE2 on the release of LH but the analogue alone had no effect on the hormone secretion. The minimal effective dose of PGE2 was determined to be within the range 0.01-0.05 micrograms and it was found that priming with 132 micrograms of 7-OPA caused a formerly sub-threshold dose (0.01 micrograms) of PGE2 to become an effective stimulus for the release of LH. In contrast to its potentiating effect on PGE2-induced LH release 7-OPA did not alter the stimulatory action of PGF2 alpha (2 micrograms) on the secretion of LH. 7-OPA had no effect on LRH-induced release of LH indicating that PG analogue acts at a suprapituitary site to enhance PGE2-induced LH release. The potentiating effect of 7-OPA may be exerted at a binding site for PGE2 in the brain and the results suggest the existence of a different binding site for PGF2 alpha. The possibility also exists that 7-OPA inhibit metabolic inactivation of PGE2.

Animals↗

PubMed2002

Glial cell line-derived neurotrophic factor modulates kindling and activation-induced sprouting in hippocampus of adult rats.

Kindling, a phenomenon in which repeated electrical stimulation of certain forebrain structures leads to an increase in the evoked epileptogenic response, is widely used to investigate the mechanisms of epilepsy. Kindling also results in sprouting of the dentate gyrus mossy fiber pathway and triggers astrocyte hypertrophy and increased volume of the hilus of the dentate gyrus. Our previous studies showed that infusion of the neurotrophin nerve growth factor accelerated the behavioral progression of amygdala kindling and affected kindling-induced structural changes in the brain, whereas intrahilar infusion of another neurotrophin, brain-derived neurotrophic factor, delayed amygdala kindling-induced seizure development and reduced the growth in afterdischarge duration, but had little effect on kindling-induced structural changes. In this paper, we report the effects of infusion of glial cell line-derived neurotrophic factor, a neurotrophic factor of the TGF-beta superfamily having similar central nervous system neuronal targets as brain-derived neurotrophic factor. We show that continuous intraventricular infusion of glial cell line-derived neurotrophic factor inhibits the behavioral progression of perforant path kindling-induced seizures without affecting afterdischarge duration. In addition, we demonstrate that intraventricular administration of glial cell line-derived neurotrophic factor prevents kindling-induced increases in hilar area and blocks mossy fiber sprouting in the CA3 region of the hippocampus. Glial cell line-derived neurotrophic factor did not have a statistically significant effect on the mossy fiber density in the inner molecular layer. Our results raise the possibility that glial cell line-derived neurotrophic factor plays a role in kindling and activation-induced neural growth via mechanisms distinct from those of the neurotrophins.

Age Factors↗

PubMed1985

Effects of endogenous opioid peptides and opiates on luteinizing hormone and prolactin secretion in ovariectomized rats.

Adult female rats were implanted with permanent cannulae in the third ventricle of the brain and ovariectomized. 3 weeks later, blood samples were withdrawn every 5 min from intraatrial cannulae placed the previous day. After a control sampling period of 30 min, the rats received an intraventricular bolus injection of saline (2 microliter) or beta-endorphin (beta E; 10 micrograms); sampling was continued for an additional 2 h. Saline injection caused no effect on luteinizing hormone (LH) and prolactin (PRL) secretion. beta E stimulated PRL secretion within 5-10 min, the values peaked in the next 10 min. Thereafter, as PRL levels fell, a suppression of LH secretion became apparent. Inhibition of LH release started 20-35 min after beta E injection and lasted for 35-65 min. The antecendent PRL secretion was apparently not responsible for the observed delayed LH response, since blockade of PRL response with bromocriptine failed to affect the beta E-induced LH suppression. Further, continuous intraventricular infusion of beta E (5 or 10 micrograms/h) for 3 h markedly suppressed the amplitude and frequency of LH episodes in long-term ovariectomized rats. Bolus intraventricular injection of other endogenous opioid peptides and opiate receptor agonists produced different PRL and LH responses. Dynorphin (10 micrograms) similarly suppressed LH release but was only moderately effective in stimulating PRL. Leucine enkephalin (50 micrograms) stimulated LH and inhibited PRL release, while methionine-enkephalin (50 micrograms) selectively stimulated PRL release. The methionine-enkephalin analogs, FK-33824 (50 ng) and DALAMID (50 micrograms), evoked sequential PRL and LH responses similar to those seen after beta E injection. Interestingly, morphiceptin (a specific mu receptor agonist; 10 micrograms) markedly suppressed LH release, but only sparingly stimulated PRL release. Delta receptor peptide (a specific delta receptor agonist; 10 micrograms) selectively suppressed LH release. Bremazocine (a specific kappa receptor agonist; 0.5 mg/kg) administered intravenously suppressed LH release selectively. These studies show that of the four endogenous opioid peptides tested beta E was most effective in evoking sequential PRL and LH responses, and these effects may be mediated by either epsilon receptors or multiple opiate receptor subtypes; stimulation of kappa receptors by bynorphin or bremazocine suppressed LH release, and further studies would be needed to understand the mode of action of the two enkephalins and the delta opiate receptors in eliciting disparate PRL and LH responses.

Animals↗