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R B Mailman

Publications and source records attributed to R B Mailman.

At least 73 records · Page 4Linked to original sources

Long-term effects of early social isolation in Macaca mulatta: changes in dopamine receptor function following apomorphine challenge.

The hypothesis that early social isolation results in long-term alterations in dopamine receptor sensitivity was tested using older adult rhesus monkeys. Isolated and control monkeys were challenged with apomorphine (0.1 and 0.3 mg/kg), and the drug effects on spontaneous blink rate, stereotyped behavior, and self-injurious behavior were quantified using observational measures. Monoamine metabolites were quantified from cisternal CSF by HPLC-EC, prior to pharmacological challenge. Isolated and control monkeys did not differ in CSF concentrations of HVA, 5-HIAA, or MHPG. At the higher dose, apomorphine significantly increased the rate of blinking, the occurrence of whole-body stereotypies, and the intensity of stereotyped behavior (as measured by observer ratings) in isolated monkeys. The frequency of occurrence of self-injurious behavior was too low to allow for meaningful comparisons. These significant differences in response to apomorphine challenge support the hypothesis that long-term or permanent alterations in dopamine receptor sensitivity, as assessed by drug challenge, are a consequence of early social deprivation.

Animals↗

Triadimefon, a triazole fungicide, induces stereotyped behavior and alters monoamine metabolism in rats.

Triadimefon, a triazole fungicide, has been observed to increase locomotion and induce stereotyped behavior in rodents. The present experiments designed to characterize the stereotyped behavior induced by triadimefon used a computer-supported observational method, and tested the hypothesis that these observed effects involved central dopaminergic systems. Adult male and female Sprague-Dawley rats were injected with triadimefon (0, 50, 100, and 200 mg/kg) in corn oil (2 ml/kg ip) 4 hr prior to behavioral assessment. The two lowest doses of triadimefon increased the frequency of locomotion and rearing, while the highest dose induced highly stereotyped behaviors, including backward locomotion, circling, and head weaving. Immediately after behavioral testing, the rats were sacrificed, and the striata and olfactory tubercles, terminal fields of the nigrostriatal and mesolimbic dopamine systems, respectively, were removed. Steady-state concentrations of the monoamines dopamine and serotonin and their metabolites were determined by HPLC-EC. In independent experiments, the direct effects of triadimefon on dopamine (D1 and D2) receptor binding and dopamine-sensitive adenylate cyclase activity were assessed in vitro using rat striata. Dopamine concentrations were increased in olfactory tubercles, but decreased in striatum. Concentrations of 5-hydroxyindoleacetic acid (the major metabolite of serotonin) were increased only in striatum, and only in animals treated with 200 mg/kg triadimefon. In vitro, triadimefon neither competed with D1 or D2 dopaminergic radioligands nor affected dopamine-stimulated adenylate cyclase activity. Together these behavioral and biochemical data lend support to the hypothesis that triadimefon may have actions similar to those produced by indirect-acting dopamine agonists.

Adenylyl Cyclases↗

trans-10,11-dihydroxy-5,6,6a,7,8,12b-hexahydrobenzo[a]phenanthridine: a highly potent selective dopamine D1 full agonist.

trans-10,11-Dihydroxy-5,6,6a,7,8,12b-hexahydrobenzo[a]phenan thridine (4a, dihydrexidine) has been found to be a highly potent and selective agonist of the dopamine D1 receptor in rat brain. Dihydrexidine had an EC50 of approximately 70 nM in activating dopamine-sensitive rat striatal adenylate cyclase and a maximal stimulation equal to or slightly greater than that produced by dopamine. Dihydrexidine had an IC50 of 12 nM in competing for [3H]SCH23390 (1a) binding sites in rat striatal homogenate, and of 120 nM versus [3H]spiperone. These data demonstrate that dihydroxidine has about ten-fold selectivity for D1/D2 receptors. More importantly, however, is the fact that dihydrexidine is a full agonist. Previously available agents, such as SKF38393 (1b), while being somewhat more selective for the D1 receptor, are only partial agonists. The isomeric cis-dihydroxybenzo[a]-phenanthridine neither stimulated cAMP synthesis nor inhibited the cAMP synthesis induced by dopamine. The cis isomer also lacked appreciable affinity for [3H]-1a binding sites. N-Methylation of the title compound decreased affinity for D1 sites about 7-8-fold and markedly decreased ability to stimulate adenylate cyclase. Addition of an N-n-propyl group reduced affinity for D1 sites by about 50-fold and essentially abolished the ability to stimulate adenylate cyclase. However, this latter derivative had twice the affinity of the D2-selective agonist quinpirole for the D2 receptor. The results are discussed in the context of a conceptual model for the agonist state of the D1 receptor.

Adenylyl Cyclases↗

Blockade of only spinal alpha 1 adrenoceptors is insufficient to attenuate DDT-induced alterations in motor function.

Male Fischer 344N rats were chronically implanted with an intrathecal cannula and gavaged with p,p'-DDT (1,1,1-trichloro-2,2-bis[p-chlorophenyl]ethane; 30 or 45 mg/kg) or corn oil. Seven hours later, subjects were intrathecally infused with vehicle, 15, 30, 60, or 120 micrograms of prazosin (an alpha 1-adrenergic antagonist). Spectral analysis of bodily movements was performed 7.5, 8, and 10 hr after DDT administration. In control rats, 15 micrograms of prazosin reduced the spectral profiles of spontaneous movements. A 30-micrograms dose produced motor impairments, without significantly changing the spectral profiles. Tremulous movements induced by DDT were unaffected by 15 or 30 micrograms, whereas 60 or 120 micrograms of intrathecal prazosin significantly reduced the spectral profiles of rats pretreated with 45 mg/kg of DDT. Other subjects were administered vehicle or DDT (45 mg/kg), intrathecally infused with 15 or 60 micrograms of prazosin (7 hr), and sacrificed (7.5 hr). Noncannulated rats were gavaged with 60 mg/kg of DDT, injected subcutaneously (sc) with 0.5 mg/kg of prazosin (5.5 hr), and sacrificed (8 hr). Cortical and spinal tissues were used in ex vivo binding assay utilizing [3H]prazosin. Fifteen or sixty micrograms of intrathecal prazosin occupied similar percentages of spinal [3H]prazosin binding sites, but produced a dose-related increase in cortical prazosin equivalents. Sixty micrograms of intrathecal or 0.5 mg/kg of sc prazosin resulted in similar concentrations of cortical prazosin equivalents. Together, these data indicate that while intrathecal prazosin will attenuate DDT-induced motor dysfunction, this effect requires blockade of alpha 1 adrenoceptors in regions other than solely the spinal cord.

Analysis of Variance↗

Buffer effects on high affinity [3H]-prazosin binding in brain and spinal cord.

[3H]-Prazosin binding was characterized in cortical and spinal membranes from Fischer 344N and Sprague-Dawley rats. Estimates of Bmax and Kd values were comparable with earlier studies of these regions in the central nervous system (CNS). However, the Kd obtained using Tris buffer system was greater than when HEPES or phosphate buffer was used. These data indicate that high affinity [3H]-prazosin binding in the homogenates of tissue from the CNS is affected critically by buffer selection.

Animals↗

The effect of 2-(o-cresyl)-4H-1:3:2-benzodioxaphosphorin-2-oxide on tissue cholinesterase and carboxylesterase activities of the rat.

The dose-response (0.1 to 1000 mg/kg sc) effects of 2-(o-cresyl)-4H-1:3:2-benzodioxaphosphorin-2-oxide (CBDP; a metabolite of the organophosphorus compound tri-o-cresylphosphate) on total cholinesterase (ChE) and carboxylesterase (CaE) activities in tissues from the rat were examined. Doses of CBDP greater than 1.0 mg/kg inhibited CaE activity maximally (greater than 99%) in plasma and lung, two important sites for detoxification of organophosphorus toxicants. A biphasic dose-dependent inhibition of ChE activity was seen in all tissues; the ED50 values showed a difference of two orders of magnitude between the first and the second phases of the dose-response curves. CBDP inhibited the blood esterases in the order plasma CaE much greater than plasma ChE much greater than red blood cell (RBC) ChE. The biphasic dose-response curve and preferential inhibition of the blood esterases may reflect the inhibition of butyrylcholinesterase in preference to acetylcholinesterase in these tissues. At doses of CBDP below 1.0 mg/kg, plasma, RBC, and brain regional ChE activities were inhibited by less than 10%, whereas at doses above 2.0 mg/kg, ChE activities were inhibited substantially (up to 80% in plasma, up to 60% in RBC, and greater than 90% in brain regions). On the basis of these results, a dose of CBDP between 1.0 and 2.0 mg/kg should prove useful as a pretreatment for studies of OP toxicity in the rat.

Animals↗

Variability in soman toxicity in the rat: correlation with biochemical and behavioral measures.

The inhibition of cholinesterase (ChE) activity in the central nervous system of the rat by the potent organophosphorus compound soman was examined. At soman doses greater than 55 micrograms/kg s.c. (0.5 LD50), there were: (1) dose-related inhibition of ChE activity in brain regions; (2) variability in the degree of ChE inhibition at each soman dose in each brain region; and (3) variability in the severity of signs of intoxication at each dose. These data suggest that measurements of ChE should be made directly or predicted individually in each animal for which the effects of soman are assessed. At the estimated ED50 soman dose for signs of intoxication (66 micrograms/kg s.c.), the remaining ChE activity in brain correlated poorly with ChE activity in plasma and red blood cells (R = 0.14-0.20), moderately with behavioral scores based on overt signs of intoxication (R = 0.63-0.94), and well with spinal cord ChE activity (R = 0.93-0.98). Finally, ChE activity in the thoracic and lumbosacral regions of spinal cord were not affected by headfocused microwave inactivation of brain enzymes, demonstrating that ChE activity in these regions of the cord can be used to predict the level of ChE inhibition in brain when direct measurement in brain is unfeasible.

Animals↗

Cresylbenzodioxaphosphorin oxide pretreatment alters soman-induced toxicity and inhibition of tissue cholinesterase activity of the rat.

The toxicity of soman was investigated in the rat with and without pretreatment with cresylbenzodioxaphosphorin oxide (CBDP). Without pretreatment, the 24-h LD50 for soman was 118.2 micrograms/kg s.c., and soman inhibited carboxylesterase (CaE) activity in plasma (ED50 of 55 micrograms/kg) and cholinesterase (ChE) activity in brain regions (ED50 values of 65-105 micrograms/kg) in a dose-related manner. With pretreatment, the 24-h LD50 for soman was reduced by approximately 6-fold and 8-fold (by 1.0 mg/kg and 16.0 mg/kg of CBDP, respectively), and the ED50 values for soman-induced inhibition of ChE activity in brain regions were reduced by approximately 10-fold (by 1.0 mg/kg of CBDP). The dose-dependent severity of soman intoxication varied widely in rats treated with soman alone but not in CBDP-pretreated rats, and the ED50 for the occurrence of signs of soman intoxication was reduced approximately 7-fold following CBDP (1.0 mg/kg) pretreatment. These data support the hypothesis that CBDP pretreatment effectively blocks tissue CaE sites which serve to detoxify soman, thus potentiating both the soman-induced inhibition of ChE in the CNS and the lethality of soman.

Animals↗

Conformational analysis and molecular modeling of 1-phenyl-, 4-phenyl-, and 1-benzyl-1,2,3,4-tetrahydroisoquinolines as D1 dopamine receptor ligands.

Conformational studies on a series of 1-phenyl-, 4-phenyl-, and 1-benzyl-1,2,3,4-tetrahydroisoquinolines that possess an identical substituent pattern to the prototypical D1 dopamine receptor antagonist SCH23390 [(R)-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5- tetrahydro-1H-3-benzazepine (1)] were performed with use of molecular mechanics calculations [MM2(85), with newly developed aromatic halide bending and torsional parameters that are now incorporated into MM2(87)], single-crystal X-ray analysis, and high-field NMR spectroscopy. The synthesis and biological testing of compounds 2-7 has been previously reported. The test compounds were compared both quantitatively and graphically to compound 1. Calculations on both the free-base and protonated forms of each compound were carried out. To insure that conformation space was adequately sampled, the test compounds were energy minimized from different starting geometries; ring inversion of the heterocycle was employed, as were dihedral driver calculations on the phenyl or benzyl rings. For N-methyl-6-chloro-7-hydroxy-1-phenyl-1,2,3,4-tetrahydroisoquinoline (2), it was determined that the torsion angle tau(C8a-C1-C12-C17) had energy minima at approximately 60 degrees and 240 degrees. This finding was corroborated by NMR studies that indicated a dramatic upfield chemical shift of ArH8 after ring cyclization. The nitrogen lone pair or hydrogen vector was approximately orthogonal to the plane of the substituted aromatic ring in the tetrahydroisoquinolines; this explained the upfield chemical shift of the vicinal chiral proton (H1). In all instances, the 6-membered heterocyclic ring in the energy-minimized structures preferred the half-chair conformation with the phenyl rings pseudo-equatorial. Distance comparisons of the proposed pharmacophoric atoms (Cl, N, O, centroid of the phenyl or benzyl ring) showed that the phenyl or benzyl centroid to ammonium H distance, Cl to N distance, and distance of the nitrogen above or below the plane of the isoquinoline aromatic ring are the distances most highly correlated with biological activity (r = 0.82, 0.75, 0.81, respectively). Resolution and single-crystal X-ray analysis of compound 2 showed the most active enantiomer to possess the S absolute configuration, in contrast to the benzazepine (R)-1. Least-squares fitting of the energy-minimized structures with SYBYL molecular modeling software showed (S)-(+)-2, rather than (R)-(-)-2, gave a better fit to (R)-1. Volume determinations derived from SYBYL multifit analyses aided in receptor mapping to qualitatively describe areas of "active" pharmacophore space as well as areas of "inactive" substituent space.(ABSTRACT TRUNCATED AT 400 WORDS)

Benzazepines↗

Comparative antidopaminergic properties of thioridazine, mesoridazine and sulforidazine on the corpus striatum.

The functional antidopaminergic potencies of the atypical antipsychotic drug thioridazine (THD), as well as its active metabolites mesoridazine (MES) and sulforidazine (SUL), were assessed by testing their blockade of the inhibitory effects of endogenous dopamine (DA) or apomorphine on the electrically evoked release of radiolabeled DA and acetylcholine (ACh) from perfused rabbit striatal slices. These functional comparisons (reflecting presynaptic and postsynaptic DA receptors, respectively) were correlated with potency estimations of these drugs in competing for D2 DA receptors (i.e., [3H]spiperone binding sites) in rabbit striatal homogenates. Similar orders of potency (SUL greater than MES much greater than THD) were found for blockade of pre- and postsynaptic DA receptors modulating DA and ACh release, respectively, as well as in competing for [3H]spiperone binding sites in the striatum. MES, SUL and haloperidol were 2 to 3 times more potent at DA release modulatory receptors than postsynaptic DA receptors. In contrast, THD was 8 times more potent at antagonizing the apomorphine-induced inhibition of DA release than against apomorphine's effect on ACh release. THD was virtually inactive in antagonizing the inhibition of ACh release induced when nomifensine was used to increase endogenous synaptic DA, despite significantly antagonizing these effects on DA release in the same slices. Together, these data indicate that: 1) MES and SUL are responsible for a significant part of the antidopaminergic effects attributed to THD; 2) THD should produce less cholinergic activation than other neuroleptics; and 3) that nonreceptor-mediated effects at high THD concentrations may mask effects due to receptor blockade.

Acetylcholine↗

Comparative anticholinergic properties of thioridazine, mesoridazine and sulforidazine.

The anticholinergic properties of thioridazine (THD) and its metabolites mesoridazine (MES) and sulforidazine (SUL) were compared to the antimuscarinics atropine and quinuclidinylbenzilate (QNB). THD, MES and SUL were virtually inactive in antagonizing the carbachol-induced inhibition of evoked ACh release from perfused rabbit striatal slices. This lack of effect was seen even when dopamine influences were abolished by treatment with reserpine and alpha-methyl-p-tyrosine. The lack of functional anticholinergic potency contrasted with the affinity of THD for muscarinic receptors measured as competition for [3H]QNB binding sites in striatal homogenates (Ki values: atropine, 2.7 nM; THD 14 nM; SUL, 66 nM; and MES, 90 nM). Both atropine and QNB blocked carbachol-induced inhibition of ACh release in a dose-dependent manner (IC50 values vs. 3 microM carbachol: 0.5 nM for QNB; 1.25 nM for atropine). THD, only 5 times less potent than atropine in competing for [3H]QNB binding sites, was inactive in antagonizing carbachol-induced ACh release. At very high concentrations (3-30 microM), THD, MES and SUL did enhance dopamine efflux and inhibit ACh release. In summary, the lack of effect of THD on release modulatory muscarinic receptors suggest that THD is selective for the M1 subtype. Because the M2 subtype is a small fraction of the total population in the striatum, it is not surprising that they would escape recognition in the QNB binding assays. These data suggest that inhibition of ACh release may contribute to the actions of THD only at very high doses, or when drug accumulation is abnormal.

Acetylcholine↗

Synthesis and pharmacological characterization of 1-phenyl-, 4-phenyl-, and 1-benzyl-1,2,3,4-tetrahydroisoquinolines as dopamine receptor ligands.

A series of 1-phenyl-, 4-phenyl-, and 1-benzyl-1,2,3,4-tetrahydroisoquinolines have been prepared as ring-contracted analogues of the prototypical D1 dopamine receptor antagonist SCH23390 [(R)-(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H- 3-benzazepine]. The affinity and selectivity of these isoquinolines for D1 receptors was determined by three biochemical endpoints in membrane homogenates prepared from rat corpus striatum: the potency to complete for [3H]SCH23390 binding sites; the potency to compete for [3H]spiperone (a D2 receptor ligand) binding sites; and effects on dopamine-stimulated adenylate cyclase. Competitive binding measurements at D1 sites showed SCH23390 to possess the highest affinity, followed by 1-phenyl greater than 1-benzyl greater than 4-phenyl for the isoquinolines. These results were highly correlated with the ability of the test compounds to antagonize dopamine-stimulated adenylate cyclase (r = 0.98). None of the compounds alone stimulated cAMP formation at concentrations of 10 nM to 100 microM. D2 competition binding showed the 1-benzyl derivative to possess the highest affinity, followed by 4-phenyl greater than SCH23390 greater than 1-phenyl. The tertiary 1-phenyl derivative was more potent than the secondary 1-phenyl analogue in all assays. Interestingly, resolution and single-crystal X-ray analysis of the tertiary N-methyl-1-phenyltetrahydroisoquinoline showed the most active enantiomer to possess the S absolute configuration, in contrast to the benzazepine (R)-SCH23390.

Adenylyl Cyclases↗

The biochemistry and pharmacology of mesoamygdaloid dopamine neurons.

Populations of DA neurons innervating the component nuclei of the amygdaloid complex differ in their inferred density of innervation, estimated rate of impulse activity, and adaptive response to the prolonged administration of antipsychotic drugs. Mesoamygdaloid DA neurons have in common the absence of tonically inhibitory, nerve terminal autoreceptors regulating DA synthesis, the nonassociation with a DA-stimulated adenylate cyclase, and the regulation of DA synthesis by receptor-mediated neuronal feedback mechanisms and end-product inhibition. The output of the amygdaloid complex appears to be organized into distinct functions subserved by component nuclei. The present findings suggest a differing role for DA afferents in modulating the functional output of discrete nuclei. The significance of this focal influence will be speculative pending a more complete understanding of the physiology of DA neurotransmission in the amygdaloid complex. Populations of DA neurons innervating discrete amygdaloid nuclei exhibit a composite of mechanisms of regulation and signal transduction and pharmacology that differ from that of other mesotelencephalic DA systems. These comparisons highlight the fact that the nucleus accumbens and olfactory tubercle do not represent or reflect DA neurotransmission in the limbic system. The study of the physiology, pharmacology, and pathology of mesolimbic DA neurons can and should extend beyond the nucleus accumbens and olfactory tubercle to the amygdala and other brain structures central to the organization of the limbic system. It is our opinion that the term "mesolimbic" DA system has purely anatomical connotations and that a more specific terminology (e.g., meso-central amygdaloid nuclear) would express the functional organization of this system more accurately.

Adenylyl Cyclases↗

Hemophilus influenzae meningitis in the rat: behavioral, electrophysiological, and biochemical consequences.

Hemophilus influenzae is the most common cause of bacterial meningitis in children, and a high percentage of survivors are at risk for long-term sequelae. To explore the mechanisms responsible for these sequelae, a neonatal rat model was used to define the behavioral, electrophysiological, and biochemical changes following meningitis. Three days after inoculation of 6-day-old rats with a minimum of 1 X 10(7) colony-forming units of a virulent Hemophilus influenzae, type b, cerebrospinal fluid and blood were cultured to confirm the presence of meningitis and bacteremia, respectively. At this time, forebrain norepinephrine and dopamine levels were significantly elevated in meningitic rats when standardized on a wet-weight basis. No changes in brain serotonin or heart norepinephrine levels could be found in the 9-day-old rats. No residual changes were found in steady-state concentrations of norepinephrine or dopamine in surviving adult rats. However, survivors that had had meningitis as neonates showed significant impairment in active and passive avoidance learning tasks and demonstrated a significantly higher level of activity during a habituation period in circular photocell activity cages. No change in the flinch-jump threshold was detected. Brainstem auditory evoked potentials showed delays of various waves in 3 of 10 Hemophilus influenzae type b-treated adult rats tested. These rats also exhibited markedly augmented locomotory responses to d-amphetamine (1 mg/kg), suggesting a long-lasting perturbation of central monoamine neuronal transmission.

Age Factors↗

Pyrethroid insecticides and radioligand displacement from the GABA receptor chloride ionophore complex.

Radioligand binding displacement studies were conducted to determine the effects of Type I and II pyrethroids on [3H]flunitrazepam (FLU), [3H]muscimol (MUS), and [35S]t-butylbicyclophosphorothionate (TBPS) binding. Competition experiments with [3H]FLU and [3H]MUS indicate a lack of competition for binding by the pyrethroids. Type I pyrethroids failed to compete for the binding of [35S]TBPS at concentrations as high as 50 microM. Type II pyrethroids inhibited [35S]TBPS binding to rat brain synaptosomes with Ki values ranging from 5-10 microM. The data presented here suggest that the interaction of Type II pyrethroids with the gamma-aminobutyric acid (GABA) receptor-ionophore complex is restricted to a site near the TBPS/picrotoxinin binding site.

Animals↗

A neurobiological alternative to the perceptual reinforcement hypothesis of stereotyped behavior: a commentary on "Self-stimulatory behavior and perceptual reinforcement".

A perceptual reinforcement theory of stereotyped movements is advanced by Lovaas, Newsom, and Hickman (1987) in an effort to integrate a number of diverse observations about the origins and maintenance of this behavior. We, in turn, argue that the theory, as presented, is logically flawed and fails to take into account important biological findings and theory concerning pathological stereotyped acts. An alternative theory, derived primarily from neurological concepts, is briefly described.

Autistic Disorder↗

Neurotoxicants and central catecholamine systems.

The ubiquitous functional roles of brain catecholamines have led to the notion that in vitro neurochemical changes in these systems may predict neurotoxicity. Conversely, others have argued that the appropriate use of neurochemical methods is for testing specific hypotheses that are developed based on observed phenomena. Three studies from this laboratory are presented in support of the latter hypothesis. The first example is with inorganic lead, a major environmental pollutant. The effects of small doses of lead on CNS development have been difficult to quantify or study mechanistically. However, the serendipitous finding that lead exposure during early postnatal development increased lithium-induced polydipsia (LIP) has provided clues that have permitted testing of specific neurochemical hypotheses related to dopamine systems. Conversely, the administration of either trimethyl- or triethyltin to rats during perinatal periods causes profound neurotoxicity. However, although some changes in the neurochemistry of catecholamine systems have been found, these data have provided little insight into either the cause or sequelae of toxicity. Finally, the food color erythrosin (FD & C Red #3) was hypothesized to be a neurotoxicant because it disrupted neurotransmitter uptake in vitro. Our data suggested this was an artifact of the methodology, a position supported by clinical and behavioral studies. These data provide examples of the strengths and weaknesses in neurochemical approaches to neurotoxicity.

Animals↗