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PubMed1993

PAF molecular heterogeneity: pathobiological implications.

The existence and potential (patho)physiologic significance of PAF molecular heterogeneity can no longer be summarily dismissed or ignored. While significant advances in the chemistry of PAF have been made, the (patho)physiologic behaviors of most of the PAF molecular species of biologic origin await further study. This is because to date, investigators have studied the biologic activities of what was previously thought to be PAF, i.e., only 16:0- and 18:0-AGEPC. In view of the evidence presented in this review, a comprehensive investigation of the possible biologic relevance and significance of PAF molecular heterogeneity is warranted. Hopefully, such studies will be designed to elucidate the extent to which the various molecular species of PAF differ in their intrinsic in vitro and in vivo (patho)physiologic behaviors (agonistic, synergistic, and possibly antagonistic) and modes of action. Once this additional information has been derived, the pathobiologic relevance of this class of phospholipid autacoid may be better understood.

Animals↗
PubMed1993

Identification of partial agonists with low intrinsic activity at the inositol-1,4,5-trisphosphate receptor.

The interactions of synthetic L-chiro-inositol-2,3,5-trisphosphorothioate [L-ch-Ins(2,3,5)PS3] and D-6-deoxy-myo-inositol-1,4,5-trisphosphorothioate [D-6-deoxy-Ins(1,4,5)PS3] with D-myo-inositol-1,4,5-trisphosphate [Ins(1,4,5)P3] receptors have been examined using radioligand binding assays and Ca2+ mobilization from permeabilized SH-SY5Y cells. The ability of these analogues to compete with [3H]Ins(1,4,5)P3 for specific sites on adrenal cortical membranes indicated that, although weaker than Ins(1,4,5)P3, both ligands competed fully for these sites [L-ch-Ins(2,3,5)PS3,Ki = 0.5 microM; D-6-deoxy-Ins(1,4,5)PS3,Ki = 5.3 microM]. However, in assays examining the amount of Ca2+ mobilized from the stores of permeabilized SH-SY5Y cells, both of these synthetic analogues displayed low intrinsic activity [L-ch-Ins(2,3,5)PS3, 34%; D-6-deoxy-Ins(1,4,5)PS3, 42% of that of Ins(1,4,5)P3]. Moreover, L-ch-Ins(2,3,5)PS3 and D-6-deoxy-Ins(1,4,5)PS3 were able to inhibit the response to Ins(1,4,5)P3 with Ki values (6 microM and 33 microM, respectively) virtually identical to their EC50 values for Ca2+ release. This is consistent with partial agonist behavior, because these compounds exhibit low maximal responses when the extent of Ca2+ release is examined. These compounds represent the first examples of inositol-based analogues with low intrinsic activity and may point the way towards the design of selective antagonists at Ins(1,4,5)P3 receptors. It also seems probable that these may represent the first true affinity values of inositol phosphates at the active receptor.

Adrenal Cortex↗
PubMed1989

Effect of continuous exposure to selective D1 and D2 dopaminergic agonists on rotational behavior in supersensitive mice.

The effects of continuous exposure to selective dopaminergic agonists were examined in mice with unilateral 6-hydroxydopamine-induced lesions of the corpus striatum. Continuously infusing the D1 agonists, SKF 38393, SKF 75670 and Cy 208-243 with the use of implanted Alzet minipumps initially produced rotational behavior, but this effect decreased during the first 2 days and then stopped completely during days 3 to 7 of drug infusion. Infusion of the D2 agonists quinpirole and N-0437 also produced rotational behavior but, in contrast to the results seen with the D1 agonists, the rotational response remained present throughout the 7 days of drug exposure. The desensitization produced by continuous exposure to SKF 38393 was selective for the D1 system, as animals exposed continuously to SKF 38393 failed to rotate to an acute challenge dose of SKF 38393 but had a normal rotational response to quinpirole. SKF 75670 and CY 208-243 were less selective than SKF 38393; continuous exposure to SKF 75670 and CY 208-243 decreased the response to an acute injection of D1-agonists by 98 and 95%, respectively, and to that of D2-agonists by 64 and 38%, respectively. Infusing the peripherally acting D1 agonist, fenoldopam, or the inactive isomer (-)-SKF 38393 failed to produce desensitization, suggesting that SKF 38393-induced desensitization is produced by an action at D1 receptors within the central nervous system. These results demonstrate that the D1 system can be desensitized independently from the D2 system and that there are different mechanisms for the long term regulation of D1 and D2 dopaminergic systems.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1997

Intranigral transplants of fetal ventral mesencephalic tissue attenuate D1-agonist-induced rotational behavior.

Rats were given unilateral 6-hydroxydopamine lesions and tested 4 weeks later for rotational behavior elicited by either systemic or intranigral injections of dopamine agonists. Subsequently, transplants of fetal (E14) ventral mesencephalic (VM) or cortical tissue were implanted into the lesioned substantia nigra and allowed to develop and integrate within the parenchyma of the host midbrain for a 4-week period before rotational behavior was retested. In animals receiving transplants of fetal VM tissue, systemic injections of amphetamine (5.0 mg/kg,i.p.) or the D2-agonist, quinpirole (0.2 mg/kg, s.c.), elicited rotational behavior that was quantitatively similar to rotational behavior observed (1) before animals received transplants of fetal VM tissue or (2) in animals with midbrain transplants of fetal cortical tissue. Intranigral administration of quinpirole (10.0 microg) immobilized most animals and did not elicit rotational behavior in any animals regardless of treatment. Rotational behavior elicited by systemic administration of the D1-agonist, SKF 82958 (0.01 mg/kg, s.c.), was slightly attenuated by VM transplants placed into the midbrain. Rotational behavior elicited by intranigral injections of SKF 82958 (7.5 microg) was markedly reduced in animals with VM transplants. These data support the hypothesis that midbrain D1-receptors modulate the expression of dopamine agonist-induced rotational behavior.

Animals↗
PubMed1995

Intrastriatal injection of cannabinoid receptor agonists induced turning behavior in mice.

When injected unilaterally into the mouse striatum, cannabinoid agonists such as Win 55212-2 (1-100 ng/mouse), CP 55940 (0.1-50 ng/mouse), and anandamide (0.5-50 ng/mouse), the putative endogenous ligand of CB1 receptor, dose-dependently induced turning behavior. SR 141716A [N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-me thyl-1H- pyrazole-3-carboxamide hydrochloride], the selective antagonist of CB1 receptor, antagonized the three cannabinoid receptor agonists-induced turning with similar ED50s (0.13-0.15 mg/kg, IP). Spiroperidol (a D2 receptor blocker), (+)-SCH 23390 (a D1 receptor blocker), or prior 6-OHDA lesions of the striatum blocked Win 55212-2- and CP 55940-induced turning, thus suggesting the involvement of DA transmission in cannabinoid-induced turning. Taken together, these findings reinforce the notion of a cannabinoid receptor-mediated control of nigrostriatal function.

Analgesics↗
PubMed1988

Selective protection from the inhibition by EEDQ of D1 and D2 dopamine agonist-induced rotational behavior in mice.

Mice with unilateral lesions of dopamine nigrostriatal neurons produced by injecting 6-hydroxydopamine into the striatum exhibited contralateral rotational behavior to the non-selective dopamine agonist apomorphine, the D1 dopamine agonist SKF 38393, and the D2 agonist quinpirole. The non-specific dopamine antagonist EEDQ blocked the circling responses to the three agonists. Pretreatment with specific, reversible dopamine antagonists before the EEDQ injection selectively prevented this blockade. Thus, if mice were pretreated with the D1 receptor antagonist SCH 23390 before EEDQ and the animals challenged with the D1 and D2 agonists 24 hours later, the rotational response to quinpirole was still inhibited, but the response to SKF 38393 was now evident. Similarly, in mice pretreated with the D2 receptor antagonist sulpiride before EEDQ and again challenged with the D1 and D2 agonists 24 hours later, the rotational response to SKF 38393 was still inhibited but the response to quinpirole was no longer inhibited. These results indicate that in vivo blockade of either D1 or D2 subpopulations of dopamine receptors may be achieved by selective protection with a reversible dopamine antagonist given prior to the administration of an irreversibly acting dopamine antagonist such as EEDQ.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1991

Effects of type of cage front and feed trough partitions on productivity and ingestive, agonistic, and fearful behaviors of egg-type hens.

Two groups of White Leghorn pullets reared in floor pens were used to study the effects on performance and behavior in cages of horizontal wire cage fronts with and without feed trough partitions (HP and H, respectively) and vertical wire cage fronts with and without feed trough partitions (VP and V, respectively). In Experiment 1, hens in HP and VP cages consumed more (P less than .05) feed than hens in either H or V cages. This greater feed consumption combined with similar egg production resulted in significantly poorer feed conversion (P less than .05) for hens in VP cages. Hens in HP cages had fewer drinking bouts (P less than .05) and an intermediate amount of feeding time. Hens in H, V, and VP cages did not differ significantly in number of drinking bouts and feeding times. There were differences in feeding location preferences among treatments (P less than .05) but not within treatments. In Experiment 2, effects of horizontal (H) and vertical (V) wire cage fronts were examined to determine their effects on productivity and fearful behavior. Hens in H cages had better feather scores (P less than .05) than hens in V cages. Type of cage front had no significant effects on age at sexual maturity, egg production, mortality rate, average egg weight, and body weight.

Agonistic Behavior↗
PubMed1992

Differential antagonism of the effects of dopamine D1-receptor agonists on feeding behavior in the rat.

A series of experiments was conducted to examine the effects of dopamine D1 receptor agonists on food intake in rats. In the first experiment, the D1 agonist SKF 38393 (3.0-30.0 mg/kg) dose-dependently suppressed feeding during a 40 min food-access period, both in food-deprived rats and in non-deprived rats fed a highly palatable diet. Non-deprived rats were more sensitive to these effects of SKF 38393. Using the limited-access, food-deprivation procedure, a comparison was made between the anorectic effects of three D1 agonists with differing intrinsic efficacies and receptor selectivities. Rank order of potencies for reducing food intake was SKF 82958 > SKF 77434 > SKF 38393 (ED50 values: 0.7, 3.6 and 15.7 mg/kg, respectively). Dose-related, surmountable antagonism by the D1 antagonist SCH 23390 (0.01 and 0.03 mg/kg) was only obtained with SKF 82958 (0.1-10.0 mg/kg). In contrast to the other compounds, the effects of SKF 38393 were not appreciably altered by the D1 antagonist. The effects of SKF 82958 were also antagonized by the D2 receptor antagonist spiperone (0.05 and 0.1 mg/kg), although not in a dose-dependent manner. The present results support a role for D1 receptors in central feeding mechanisms. They also suggest that the effects of SKF 38393 on feeding may not be mediated exclusively by the D1 receptor and, further, that SKF 38393 may not serve well in behavioral studies as a prototypical D1 agonist. The results also demonstrate the need for comparisons among several compounds in studies of D1 mediated behavioral effects.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1999

Differences in anxiolytic-like profile of two novel nonbenzodiazepine BZ (omega) receptor agonists on defensive behaviors of mice.

The present experiments compared the behavioral effects of two novel BZ (omega) receptor agonists, the pyridazinone Y-23684 (1-30 mg/kg) and the pyrido[1,2-a]benzimidazole RWJ-46771 (0.01-0.3 mg/kg) with the BZs diazepam (0.5-3 mg/kg) and clobazam (1-30 mg/kg) in the mouse defense test battery (MDTB), a model for the screening of anxiolytic drugs. In the MDTB, Swiss mice were confronted with a natural threat (a rat) and situations associated with this threat. Primary measures taken during and after rat confrontation were flight, risk assessment, defensive threat/attack, and escape attempts. Results showed that clobazam and Y-23684 significantly modified all defense responses in the presence of the rat at doses that did not decrease spontaneous locomotor activity. These drugs decreased avoidance reactions after the rat was introduced into the runway, reduced flight speed and risk assessment activities of mice chased by the rat, increased risk assessment displayed when subjects were constrained in a straight alley, and reduced defensive threat and attack behaviors upon forced contact. Diazepam significantly decreased all but one (number of avoidances when the rat was first introduced into the runway) defensive behaviors. RWJ-46771 reduced risk assessment in the chase test, avoidance responses, flight speed, and defensive threat and attack reactions, but these effects occurred in the great part at motor-impairing doses, suggesting that the decrease in defensiveness may have been contaminated by behavioral suppression. Finally, following the removal of the rat from the runway, only Y-23684 reduced escape behavior at doses that did not decrease spontaneous behavior. Taken together, these findings demonstrate that Y-23684 displayed anxiolytic-like activity comparable to that of BZs in the MDTB. Although RWJ-46771 significantly modified most defensive behaviors, the effects may have been confounded by decreases in locomotor activity.

Aggression↗
PubMed1993

Metabotropic and ionotropic excitatory amino acid receptor agonists induce different behavioral effects in mice.

Intracerebroventricular (i.c.v.) infusion in mice of the selective metabotropic excitatory amino acid receptor agonist 1S,3R-1- aminocyclopentane-1,3-dicarboxylate (1S,3R-ACPD) (0.6-575 nmol/min) dose dependently induced face washing and scratching. In contrast, the subtype-specific ionotropic excitatory amino acid receptor agonists N-methyl-D-aspartate (NMDA), kainate and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) (0.3-3.0 nmol/min) dose dependently induced clonic convulsions. I.c.v. infusion of the non-selective metabotropic receptor agonists ibotenate (6 nmol/min) or quisqualate (30 nmol/min) induced clonic convulsions. However, when ionotropic receptors were blocked with (+)-5-methyl-10,11-dihydro-5H-dibenzo-(a,d)cyclohepten-5,10-imine maleate (MK-801, dizoclipine) (3 nmol/min) or 2,3-dihydroxy-6-nitro-7- sulfamoyl-benzo(f)-quinoxaline (NBQX) (9 nmol/min), respectively, face washing and scratching behavior emerged. Neither MK-801 or NBQX (ED50 value > 100 nmol/min), nor the putative metabotropic receptor antagonist L-amino-3-phosphoro-propionic acid (L-AP3) (> 176 nmol/min); nor the dopamine receptor antagonists SCH 23390 (> 74 nmol/min), metoclopramide (> 89 nmol/min) and haloperidol (> 27 nmol/min) antagonized 1S,3R-ACPD-induced scratching (144 nmol/min). These results suggest that the behavioral consequences of i.c.v. infusion of 1S,3R-ACPD in mice reflect a selective activation of metabotropic receptors that differs from the behavioral changes observed with i.c.v. infusion of ionotropic receptor agonists.

Animals↗
PubMed2006

Effects of dopamine D1-like receptor agonists on food-maintained operant behavior in rats.

The effects on learned operant behavior of agonist actions at dopamine D1-like receptors have not been fully characterized. We compared three D1-like receptor agonists (SKF 38393, SKF 77434 and SKF 82958), both alone and in combination with the D1-like receptor antagonist, SCH 23390. Binding affinities for the agonists at dopamine D1 receptors from rat striatum membranes were determined and compared with effects on behavior. Lever pressing was maintained by food reinforcement under a fixed-ratio 30-response schedule (each 30th response produced reinforcement), and the effects of the three agonists were assessed by cumulative dosing. Each drug produced dose-related reductions in response rates, with an order of potency (SKF 82958>SKF 77434>SKF 38393) that agreed with rank order of binding affinities. Antagonism of these behavioral effects by SCH 23390 was only significant for SKF 82958; surprisingly, SCH 23390 enhanced the effects of SKF 38393. For SKF 82958, the antagonism was receptor subtype-specific, as the D2-like receptor antagonist spiperone was ineffective. The nonselective serotonergic antagonist metergoline produced a significant rightward shift of the SKF 38393 dose-response function, indicating effective antagonism, although the degree of antagonism was not dose-related. These results support the view that the behavioral effects of D1-like receptor agonists differ in their susceptibility to antagonism by D1-like receptor antagonists, and that some effects of SKF 38393 may be mediated by serotonergic activity rather than by activity at D1-like receptors.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1996

Dopamine D3 agonists disrupt social behavior in rats.

Behavioral studies were conducted in rats administered a selective D3 agonist, 7-hydroxy-N,N-di-n-propyl-2-aminotetralin (7-OH-DPAT) or 4aR, 10bR-(+)-trans-3,4,4a,10b-tetrahydro-4-propyl-2H,5H-[1] benzopyrano[4,3-b]-1,4-oxazin-9-ol (PD 128907). Both drugs induced disruption of huddling behavior in rats at doses that did not produce hyperlocomotion. The effects of the D3 agonists were dependent upon dosage and time after administration. These results suggest that D3 receptors are concerned with social interaction in rats.

Animals↗
PubMed1988

5-HT1A, 5-HT1B and 5-HT2 receptor agonists induce differential behavioral responses in neonatal rat pups.

Sprague-Dawley rat pups at 3-4 days prenatally were tested in both the absence and presence of milk following administration of various doses of either the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OHDPAT), the 5-HT1B agonist 1-(3-chlorophenyl)piperazine (mCPP), or the 5-HT2 agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI). Administration of 8-OHDPAT decreased mouthing, increased probing and increased behavioral activation. Conversely, the 5-HT2 agonist DOI and the 5-HT1B agonist mCPP increased mouthing and decreased probing. mCPP and DOI differed in their effects on behavioral activation, with mCPP decreasing and DOI increasing this composite behavioral score. mCPP increased grooming, whereas DOI elicited a characteristic unusual positioning of the limbs. Thus it appears that 5-HT1A, 5-HT1B and 5-HT2 receptor subtypes are present in the neonate and elicit differential behavioral responses upon stimulation with selective agonists. Ontogenetic variations in the balance among these receptor subtypes during development may be related to the ontogenetic reversal that has been previously reported in the impact of serotonin manipulations on mouthing and suckling behavior during the neonatal to weanling age period.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1986

Mu- and kappa-opiate agonists modulate ingestive behaviors in the slug, Limax maximus.

Administration of the prototypical mu opiate agonist, morphine sulphate, 1-10 mg/kg, produced over three hours a significant dose-dependent increase in the ingestive responses of free-feeding slugs, Limax maximus, although lower doses, 0.10 mg/kg, attenuated feeding. The mixed mu and kappa opiate agonist, ketocyclazocine hydrochloride, in the dose range 1.0-10 mg/kg, also induced significant increases in food consumption. With both of these opiates there was a latency of about 0.5 hr before initiation of feeding. The more specific kappa opioid agonist, U-50,488H, given over the dose range 0.10-1.0 mg/kg, produced a more potent increase in three hour food consumption by Limax, whereas a dose of 10 mg/kg produced a significant increase in ingestive responses for 3-4 hr after a 1-2 hr period of inactivity. The prototypic mu opiate antagonist, naloxone hydrochloride (1.0 mg/kg) blocked the feeding effects of morphine and ketocyclazocine and reduced the effects of U-50,488H. The delta antagonist, ICI 154,129, in a dose of 10 mg/kg, reduced the effects of morphine as well as decreasing food intake of free-feeding slugs. These results indicate that activation of differential opiate receptors in invertebrates has similar effects on feeding behavior as occur in mammals, suggesting early evolutionary development of opioid involvement in the control of feeding.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1984

Kappa opiate receptor agonists: effects on behavior and on brain function and structure in rhesus monkeys.

In the present study several drugs that are predominantly agonists of kappa receptors were tested in rhesus monkeys prepared with deep and surface brain electrodes. The administration of two benzomorphan derivatives and of ethylketocyclazocine induced acute behavioral effects resembling catatonia concomitant with generalized spike and slow-wave electroencephalographic activity at widespread brain sites, that lasted for about 1 hr. After administration of one to three doses of these agonists (the benzomorphan derivatives to five monkeys and the ethylketocyclazocine to two monkeys), chronic recording changes developed, characterized by continuous high-amplitude spiking activity focal at the anterior septal region and periaqueductal gray of the mesencephalon. They increased in intensity with the passage of time, the monkeys having been followed as long as 5 months without further drug administration. Light microscopy and electron microscopy showed no structural abnormalities in the monkey brains at the sites of altered recordings, although occasional dendritic atrophy was noted at all cortical and subcortical brain sites examined. Chronic recording changes did not develop in a monkey that received U-50,488H on eight occasions. And none of the electrode-implanted monkeys that served as controls (having received no kappa agonists) developed recording changes. The sites affected by the active kappa agonists were those at which abnormal activity has been correlated with psychotic behavior. The ability of the kappa agonists to induce a lasting physiologic change without corresponding structural change at those focal sites implicated in schizophrenia may prove a useful probe in further investigations into the cause of schizophrenia and its ultimate treatment.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed2001

Role of striatal acetylcholine on dopamine D1 receptor agonist-induced turning behavior in 6-hydroxydopamine lesioned rats: a microdialysis-behavioral study.

The effects of MK-801, a non-competitive N-methyl D-aspartate (NMDA) receptor antagonist, of quinpirole, a dopamine (DA) D2 receptor agonist, and of SCH 58261, an A2A adenosine antagonist, were studied on acetylcholine (ACh) release in the striatum of 6-hydroxydopamine (60HDA) lesioned rats and on turning behavior induced by the administration of the DA D1 agonist CY 208-243. Administration of CY 208-243 to 6OHDA lesioned rats induced turning behavior and dose-dependently stimulated ACh release. At the dose of 50 microg/kg, MK-801 failed to affect basal ACh, while at 100 microg/kg MK-801 reduced it; however, MK-801 (50 and 100 microg/kg) potentiated the turning behavior elicited by CY 208-243, but failed to affect the CY 208-243-induced increase of striatal ACh release. The administration of quinpirole induced low-intensity turning behavior and decreased basal ACh release; on the other hand, quinpirole potentiated the turning behavior induced by CY 208-243, but failed to affect the CY 208-243-elicited increase of ACh release. Finally, intravenous administration of SCH 58261 stimulated basal ACh release but not turning behavior; SCH 58261, however, potentiated turning behavior induced by CY 208-243, while failing to affect the D1-elicited increase of ACh release. These results indicate that potentiation of D1-dependent turning behavior by MK-801, quinpirole and SCH 58261 is not mediated by a reduced ability of D1-agonists to stimulate ACh release from the denervated striatum.

Acetylcholine↗
PubMed1990

5-HT1A, 5-HT1B and 5-HT2 receptor agonists induce differential behavioral responses in preweanling rat pups.

Preweanling (postnatal day 17-18) Sprague-Dawley rat pups were tested in both the absence and presence of milk following administration of various doses of the 5-HT1A agonists 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) or ipsapirone, the 5-HT1B agonist 1-(3-chlorophenyl)piperazine (mCPP) or the 5-HT2 agonist 1-(2,5-dimethoxy-4-iodo-phenyl)-2-aminopropane (DOI). 8-OH-DPAT decreased mouthing while ipsapirone, mCPP and DOI had no effect upon this behavior. However, all four agonists significantly decreased grooming. Both 8-OH-DPAT and mCPP produced alterations in limb positioning, with 8-OH-DPAT administration resulting in a poor control of the hindlimbs and mCPP inducing a hindlimb straddle position. These functional responses to 5-HT1A, 5-HT1B and 5-HT2 agonists in preweanling pups vary from those observed previously in neonates. For instance, whereas inhibitory effects of 5-HT1A stimulation on mouthing are observed in both neonatal and preweanling pups, facilitory effects of 5-HT1B and 5-HT2 stimulation are only seen in neonates. These ontogenetic alterations may be related to the previously reported ontogenetic reversal in the effect of serotonergic activation upon mouthing and suckling that occurs during the neonatal to weanling age period.

8-Hydroxy-2-(di-n-propylamino)tetralin↗