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PubMed1991

Classical conditioning selectively increases AMPA receptor binding in rabbit hippocampus.

The NMDA and AMPA receptors have been shown to play critical roles in various forms of synaptic plasticity (learning and memory, long-term potentiation). The present study investigated the involvement of these two receptors in a well-characterized classical conditioning paradigm. Following classical conditioning of the rabbit nictitating membrane the binding properties of these two subclasses of excitatory amino acid transmitter receptors were analyzed in dorsal hippocampi by quantitative autoradiography. [3H] TCP and [3H] AMPA were used to identify the NMDA and AMPA receptors, respectively. The binding of [3H]TCP to the NMDA receptor remained unchanged in all the experimental groups tested. Paired presentations of the conditioned and unconditioned stimuli resulted in increased [3H] AMPA binding to the AMPA receptor in several subfields of the hippocampus, while unpaired presentations had no significant effects. The increase in binding was due to an increased affinity of the low-affinity component of the AMPA receptor. The results support the hypothesis that changes in glutamate receptors participate in the synaptic plasticity involved in certain forms of learning.

Animals↗
PubMed1991

Selective increase of AMPA binding to the AMPA/quisqualate receptor in the hippocampus in response to acute stress.

The binding properties of ligands specific for two subclasses of glutamate receptors were studied by quantitative autoradiography after one hour of acute immobilization/shock stress. [3H]N-(1-(2-thienyl)cyclohexyl)-3,4-piperidine (TCP) and [3H]alpha-amino-3-methylisoxazole-4-propionic acid (AMPA) were used to visualize the N-methyl-D-aspartate receptor and the AMPA/quisqualate receptor types, respectively. While no change was observed in the binding properties of the [3H]TCP, [3H]AMPA binding was significantly increased in several areas of the hippocampus of acutely stressed rats relative to naive controls.

Animals↗
PubMed1992

Long-term potentiation is associated with increased [3H]AMPA binding in rat hippocampus.

The location and nature of the changes underlying long-term potentiation (LTP) remain controversial issues. In this study, we tested the possibility that changes in binding properties of the alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA/quisqualate and N-methyl-D-aspartate (NMDA) subtype of glutamate receptors are associated with LTP. LTP was elicited in vivo by stimulation of the perforant pathway in anesthetized rats. One hour following stimulation the animals were sacrificed. We performed quantitative ligand binding autoradiography on frozen brain sections using [3H]AMPA and [3H]N-(1-(2-thienyl)cyclohexyl)-3,4-piperidine ([3H]TCP) to label the AMPA/quisqualate and the NMDA receptors, respectively. No changes in [3H]TCP binding were detected in any of the treatment groups. However, increases in [3H]AMPA binding were observed only in animals that exhibited LTP. These increases were bilateral and present in several subfields of the hippocampus and cortical areas. Administration of the NMDA receptor antagonist, ketamine, prior to tetanic stimulation prevented both the increase in binding and the induction of LTP. These results suggest that changes in the characteristics of AMPA/quisqualate receptors are a biochemical correlate of LTP.

Analysis of Variance↗
PubMed1995

Cryopreserved neuronal cells in long-term cultures of dissociated rat cerebral cortex: survival and morphometric characteristics as revealed by immunocytochemistry.

Blocks of fresh tissue from embryonic rat cerebral cortex, dissociated either prior to or after freezing, were stored for up to 10 months in liquid nitrogen at -196 degrees C with 7% dimethylsulfoxide (DMSO) as cryoprotectant. Slow freezing and rapid thawing, a reduced medium volume and moderate elevation of both extracellular K+ (20 mM) and sera (20%) promoted survival of neurons (up to 7 weeks) on polylysine-coated glass coverslips. Although there was cell loss associated with freezing, the surviving cells developed morphological and immunocytochemical properties similar to those expressed by unfrozen cells when using anti-GFAP (glial fibrillary acidic protein), anti-NSE (neuron specific enolase) and anti-GABA (gamma-aminobutyric acid) antibodies. A comparative computer-aided analysis of the morphometric patterns of GABA-IR neurons allowed the individualization of two similar populations in both fresh and frozen controls. NSE- and GABA-immunoreactive (IR) cells were counted in frozen controls and thienyl-phencyclidine (TCP)-treated cultures. The latter yielded fewer cells whereas it was the opposite in fresh TCP-treated cultures. In view of these findings, a detailed analysis of the effects of both neuroprotective and neurotoxic agents on frozen cells is undertaken before considering that cryopreservation might be a suitable storage method for clinical trials of neuron grafting.

Animals↗
PubMed1994

Dendritic orientation of thalamocortical projection neurons in the ventrobasal complex of macaques.

This study describes the orientation of dendritic arbors from intracellularly labeled thalamocortical projection (TCP) neurons of Macaca fascicularis or Macaca mulatta. All neurons were located in the ventrobasal complex and responded to non-noxious stimuli. Each neuron was composed of dendrites that varied considerably in size and each dendrite tended to occupy a particular region of the perisomatic space with minimal overlap with other dendrites. Quantitative and qualitative analysis of the dendritic arbors of the labeled neurons showed they had an asymmetric distribution so that some regions of the perisomatic space contained more of the dendritic tree than others. Eleven of the thirteen reconstructed neurons had a larger percentage of the dendritic tree projecting into the medial portion of the perisomatic space. These results show that the dendritic arbors of macaque TCP neurons are not organized in a radially symmetric pattern as previously described and the asymmetric distribution of dendrites may be related to synaptic input.

Animals↗
PubMed1989

The in vitro metabolites of 2,4,6-trichlorophenol and their DNA strand breaking properties.

The carcinogenic compound 2,4,6-trichlorophenol (2,4,6-TCP) was incubated with rat liver S-9 fraction. Three metabolites were identified: 2,6-dichloro-1,4-hydroquinone (DHQ), and two isomers of hydroxypentachlorodiphenyl ether (OH-Cl5-DPE). The latter are probably products of microsomal .OH radical attack on the trichlorophenol molecule forming phenoxy free radicals. These would undergo dimerizations with other molecules present in solution. The 2,6-dichloro-1,4-semiquinone free radical was identified by ESR spectroscopy. It is formed at physiological conditions in phosphate buffer at pH 7.2 and 7.8, with a more intensive signal at the more alkaline pH. The formation is probably due to the autoxidation of the corresponding hydroquinone. Incubation of a mixture of metabolites with PM2 DNA at pH 7.2 resulted in single strand breaks. Addition of catalase and dimethylsulfoxide (DMSO) inhibited the DNA strand scission. It was concluded that reactive oxygen species (ROS), produced during the formation of the semiquinone radical, were responsible for the observed DNA damage. The significance of the ROS and the semiquinone free radical is discussed in view of the reported tumorgenicity of 2,4,6-TCP in rats and mice.

Animals↗
PubMed1985

Serotonergic involvement in pharmacological action of the anxiolytic-sedatives thalidomide and supidimide.

The anxiolytic-sedative drugs thalidomide and supidimide inhibited spontaneous motor activity in rats. Both compounds inhibited the serotonin (5-HT) behavioural syndrome induced by tranylcypromine (TCP) plus L-tryptophan (TRP) or clorgyline plus the selective 5-HT uptake blocker, LM 5008 (4-[2-(3-indolyl)ethyl]piperidine) and delayed the behavioural effects of p-chloro-amphetamine, a releaser of 5-HT. The behavioural syndrome induced by the 5-HT agonist, 5-methoxy-N,N'-dimethyltryptamine (5-MeODMT) was unaffected by supidimide pretreatment. Thus supidimide does not possess 5-HT receptor antagonistic properties. This was further substantiated by the unaltered 5-HT-induced platelet aggregation in the presence of supidimide (10(-7)-10(-4) M). A decrease of 5-HT release into the synaptic cleft will lead to a diminished behavioural response to drugs that act presynaptically. Supidimide induced a greater increase in accumulation of brain 5-HT in TCP (5 mg/kg) plus TRP (100 mg/kg)-treated animals as compared to that in the corresponding controls. These data indicate that the behavioural and pharmacological actions of supidimide may be related to its inhibition of 5-HT release.

Animals↗
PubMed1987

Phencyclidine analogues inhibit NMDA-stimulated [3H]GABA release from cultured cortex neurons.

The inhibition of [3H]TCP binding to rat cortical membranes by substances of the PCP/sigma-opiate type was compared with effects of the same compounds on N-methyl-D-aspartate (NMDA) responses in cultured mouse cortex neurons. A new technique of excitatory amino acid-induced [3H]GABA (gamma-amino-butyric acid) release in a continuous superfusion model was used for the purpose. A similar rank order of potencies was found for the substances whether as inhibitors of [3H]TCP binding (MK 801 greater than PCP greater than ketamine-cyclazocine) or as antagonists of NMDA (20 microM)-stimulated [3H]GABA release in the cultured neurons (phencyclidine = MK 801 greater than ketamine greater than cyclazocine).

Animals↗
PubMed1988

Hippocampal NMDA/phencyclidine receptor binding sites are reduced following forebrain ischaemia in the gerbil.

The binding of [3H]N-(1-[2-thienyl]cyclohexyl)piperidine (TCP) to N-methyl-D-aspartate (NMDA) receptor sites in synaptic membranes prepared from the dorsal hippocampus of the ischaemic gerbil, has been studied. Forebrain ischaemia was induced by 10 min bilateral carotid occlusion and receptor binding determined in the dorsal hippocampus 1 week later. [3H]TCP binding capacity was significantly reduced by 28% in ischaemic tissue with no change in affinity. This result is consistent with the involvement of NMDA receptors in ischaemic brain damage.

Animals↗
PubMed1989

NMDA antagonists block restraint-induced increase in extracellular DOPAC in rat nucleus accumbens.

The effects of the N-methyl-D-aspartate (NMDA) receptor antagonists CPP, TCP, PK 26124 and ifenprodil, and of the minor tranquillizer diazepam on stress-induced changes of dopamine metabolism in the nucleus accumbens were investigated in the rat. Dopamine metabolism was assessed by measuring the extracellular levels of 3,4-dihydroxyphenylacetic acid (DOPAC) by means of in vivo differential pulse voltammetry with electrochemically pretreated carbon fiber electrodes. Physical immobilization of the rats for 4 min caused a marked and long-lasting increase in extracellular DOPAC levels in the nucleus accumbens. A similar, though shorter-lasting, augmentation of extracellular DOPAC was observed in the nucleus accumbens after systemic administration of the anxiogenic agent methyl-beta-carboline-3-carboxylate (beta-CCM) (10 mg/kg s.c.). Pretreatment with CPP (1 mg/kg i.p.), TCP (3 mg/kg i.p.), PK 26124 (3 mg/kg i.p.), ifenprodil (3 mg/kg i.p.) or diazepam (2 mg/kg i.p.) totally antagonized the immobilization-induced increase in extracellular DOPAC in the nucleus accumbens. Diazepam and the benzodiazepine (omega 1-2) receptor antagonist flumazenil (30 mg/kg i.p.), but not ifenprodil, also antagonized the beta-CCM-induced activation of dopamine metabolism in the nucleus accumbens. Finally, systemic administration of haloperidol (25 micrograms/kg i.p.) increased the extracellular concentrations of DOPAC in the nucleus accumbens, but pretreatment with ifenprodil (3 mg/kg i.p.) did not modify this response. These data indicate that NMDA receptor antagonists prevent the activation of dopamine metabolism in the nucleus accumbens caused by immobilization stress but not by beta-CCM-induced anxiogenic stimulation. These results suggest that NMDA receptor antagonists may possess an anxiolytic-like action in the rodent, which is exerted via neuroanatomical circuits distinct from those acted upon by diazepam.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

The behavioural effects of MK-801: a comparison with antagonists acting non-competitively and competitively at the NMDA receptor.

The selective non-competitive NMDA receptor antagonist, MK-801, potently blocked convulsions induced in the mouse by N-methyl-DL-aspartic acid (NMDLA) with an i.v. ED50 dose of 0.2 mg/kg. Similar doses of MK-801 were also effective in blocking seizures induced by pentylenetetrazol (PTZ), electroshock and by sound in audiogenic seizure-prone animals. Other less selective non-competitive NMDA receptor antagonists including phencyclidine (PCP), thienylcyclohexylpiperidine (TCP), (+)-N-allylnormetazocine [+)-NANM, (+)-SKF 10,047) and ketamine also blocked NMDLA-induced seizures with a rank order of potency of MK-801 greater than PCP greater than TCP = (+)-NANM greater than ketamine. The competitive NMDA receptor antagonist, 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP) blocked NMDLA-induced seizures with an ED50 of 4.5 mg/kg, 22- and 560-fold more potently than the competitive antagonists, 2-DL-amino-7-phosphonoheptanoic acid (2-APH) and 2-DL-amino-5-phosphonovaleric acid (2-APV), respectively. MK-801 was the most potent of the non-competitive antagonists to induce a motor syndrome including head weaving, body rolling, increased locomotion and ataxia, characteristic of the behavioural response to PCP in the mouse. The syndrome was also present following injection of the competitive NMDA receptor antagonists, although they were generally less potent (probably a reflection of poor brain penetration) and less efficacious than the non-competitive antagonists. For all compounds except CPP, the anticonvulsant ED50 dose was close to the minimum effective dose to induce motor stimulation: CPP was 5- to 10-fold more potent as an anticonvulsant.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Thiokynurenates: a new group of antagonists of the glycine modulatory site of the NMDA receptor.

Several substituted derivatives of kynurenic acid were tested on the N-methyl-D-aspartate (NMDA) receptor/ion channel complex present in the guinea pig myenteric plexus, on the binding of [3H]glycine and of [3H]N-[1-(2-thienyl)cyclohexyl]piperidine [( 3H]TCP) to rat cortical membranes and on the depolarization of mice cortical wedges induced by NMDA or quisqualic acid (QA). Kynurenic acid derivatives, having a chlorine (CI) or a fluorine atom in position 5 or 7 but not in position 6 or 8 had significantly lower IC50s than the parent compound when tested on the antagonism of glutamate-induced ileal contraction and in the glycine binding assay. A further significant increase in potency was obtained by substituting a thio group for the hydroxy group in position 4 of kynurenic acid: the IC50 was 160 +/- 20 microM of kynurenic acid and 70 +/- 15 microM of thiokynurenic acid in the myenteric plexus whereas these IC50s for glycine binding were 25 +/- 3 and 9 +/- 2 microM respectively. Several thiokynurenic acid derivatives were synthetized and showed an increased affinity for the glycine recognition site over the corresponding kynurenic acid derivatives. Glycine competitively antagonized the actions of the thiokynurenates in the ileum, in cortical wedges and on [3H]TCP binding. In this preparation, 7-Cl-thiokynurenic acid had an IC50 of 8 microM for antagonizing 10 microM NMDA-induced depolarization while 50% of the 10 microM QA depolarization was antagonized at 300 microM. Thus thiokynurenic acid derivatives seem to be a new group of potent and selective antagonists of strychnine-insensitive glycine receptors.

Animals↗
PubMed1992

Thiokynurenates prevent excitotoxic neuronal death in vitro and in vivo by acting as glycine antagonists and as inhibitors of lipid peroxidation.

Several derivatives of kynurenic and thiokynurenic acids were synthesized and tested for their ability to protect primary cultures of cerebellar granule cells against excitotoxic damage, and to affect the binding of [3H]glycine ([3H]Gly), [3H]alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid ([3H]AMPA), [3H]3-(2-carboxypiperazine-4-yl-)propyl-1-phosphonic acid ([3H]CPP), [3H]kainic acid and [3H]N-[1-(2-thienyl)cyclohexyl]-3,4-piperidine ([3H]TCP) to rat cortical membranes. Kynurenic and thiokynurenic acid derivatives with one or two halogens in position 5 or 7 were selective glycine antagonists, failing to affect N-methyl-D-aspartate (NMDA), kainate or AMPA sites at micromolar concentrations. 7-Cl-kynurenic, 7-Cl-thiokynurenic, 5,7-diCl-kynurenic and 5,7-diCl-thiokynurenic acids had similar IC50s for displacing [3H]Gly from its strychnine-insensitive site and for reducing the stimulated (0.5 microM NMDA and 1 microM glycine) [3H]TCP binding to cortical membranes. However, 7-Cl-thiokynurenic acid was particularly potent to prevent excitotoxic neuronal death in cultured cerebellar granule cells. This action may be ascribed to inhibition of lipid peroxidation, a property which was demonstrated for the 5- or 7-Cl derivatives of thiokynurenic acid. Furthermore, 7-Cl-thiokynurenic acid reduced excitotoxic damage caused by the injection of quinolinic acid in the rat striatum. Thus, 7-Cl-thiokynurenic acid appears to be a new compound with interesting antiexcitotoxic properties both in vitro and in vivo.

Animals↗
PubMed1996

Autoradiographic study on the pharmacological characteristics of [3H]3-OH-PCP binding sites in rat brain.

The pharmacological characteristics and the regional distribution of [3H]3-OH-PCP (1-[1(3-hydroxyphenyl)-cyclohexyl]piperidine) binding were investigated in rat brain by quantitative autoradiography. Kinetic analysis of [3H]3-OH-PCP binding revealed fast and slow components, in the association and dissociation studies. The regional distribution of binding closely corresponded to those of binding sites labeled by [3H]N-[l-(2-thienyl)-cyclohexyl]3,4-piperidine (TCP) and [3H](+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imi ne maleate (MK 801). High densities of [3H]3-OH-PCP binding sites were found in the stratum radiatum and orients of field CA1 in the hippocampus and in the outer layers of cerebral cortices. In contrast, low levels of binding were seen in the brain stem and the granular cell layer of the cerebellum. [3H]3-OH-PCP binding was strongly inhibited by MK 801 and 3-OH-PCP, while the potency of (+)-SKF 10047 in inhibiting [3H]3-OH-PCP binding was less in the cerebral cortex and hippocampus. The antagonists for the glutamate, glycine and polyamine recognition sites at the NMDA/PCP receptor complex displaced [3H]3-OH-PCP binding sites with a potency similar to that of [3H]MK 801. These findings suggest that the [3H]3-OH-PCP binding site is similar or identical to the PCP binding site labeled by [3H]TCP and [3H]MK 801.

Animals↗
PubMed1992

Electrical fields in the vicinity of epithelial wounds in the isolated bovine eye.

A lateral potential drop along the outer surface of the cornea could be measured at the edge of wounds made in the corneal epithelium of the isolated bovine eye when the cornea was covered by simulated tear film of modified Hanks' solution. These lateral fields (LFs) had an average magnitude of 42 +/- 1.4 mV mm-1 in the first 0.25 mm from the wound edge. The polarity of these surface LFs is more positive at the wound than in regions away from the wound. Very little if any lateral field could be measured at the edge of wounds along the inner surface of the corneal epithelium. The surface LFs depend on the cornea's transepithelial potential (TEP), which in this isolated bovine eye preparation we determined (with conventional microelectrode techniques) to have an average value of 24.7 +/- 2.2 mV, stroma-side positive. We found that this TEP drives a current from wounds in the epithelium with an average current density of 55 +/- 12 microA cm-2. We also have found that the average transcorneal potential (TCP) was 3.2 +/- 0.5 mV greater than the average TEP, confirming that the major contribution to the TCP comes from the corneal epithelium.

Animals↗
PubMed1989

Differentiation of phencyclidine and sigma receptor types affecting the central inspiratory termination mechanism in cat.

The effects of 1) the phencyclidine receptor ligand TCP, 2) sigma receptor ligands (+)3-PPP and DTG, and 3) N-methyl-D-aspartate receptor blockers MK-801 and dextrorphan were determined on a brainstem mechanism which controls the termination of the inspiratory phase of the breathing cycle. Inspiratory bursts were recorded from the phrenic nerve in decerebrate paralyzed cats ventilated by means of a phrenic driven servoventilator. The central mechanism which terminates inspiration was tested by withholding lung inflation, thus suppressing the contribution of the vagal feedback from the lungs to inspiratory termination. TCP increased the duration of test inspiration (tTi) by 17% at 0.03 mg/kg and by 14-fold (from 1.6 to 23 s) at 1 mg/kg. With dextrorphan, tTi was significantly increased at 3 mg/kg. In contrast, (+)3-PPP and DTG did not increase tTi at doses up to 10 mg/kg, although MK-801 (0.03 mg/kg), given after the sigma ligands, increased tTi by 59-90%. It is concluded that phencyclidine but not sigma receptor ligands block the central mechanism which terminates inspiration and that the likely site of action is the NMDA receptor complex.

Animals↗
PubMed1987

The effects of low-protein diet and testosterone on sex hormone-binding globulin capacity in male rabbits.

The effects of a low-protein high-carbohydrate (LPHC) diet (8% protein 65% to 72% carbohydrate) were compared to those of regular rabbit chow (14% to 16% protein 57% to 64% carbohydrate) on sex hormone-binding globulin (SHBG) capacity in 12 male rabbits. The six rabbits who were fed the LPHC diet for 8 weeks showed a significant increase in their mean SHBG capacity (mean +/- SE: from 70 +/- 16 nmol/L to 332 +/- 45 nmol/L, P less than .01) whereas the six rabbits fed the standard diet showed a slight decrease (from 106 +/- 22 nmol/L to 76 +/- 20 nmol/L, NS). These changes in SHBG capacity were mirrored by a decrease in percent-free T (from 2.64 +/- 0.26% to 1.64 +/- 0.16%, P less than .01) in the LPHC diet group and no change in percent-free T in the regular diet group (from 2.36 +/- 0.21% to 2.19 +/- 0.10%). The changes in SHBG capacity and percent-free T were not associated with significant changes in testosterone (T), free T, estradiol (E2), thyroxine, triiodothyronine, thyroxine-binding globulin, or cortisol binding globulin levels. In a subsequent experiment, testosterone cyclopentyl propionate (TCP) was administered to six male rabbits while on regular rabbit chow and again after 6 weeks of the LPHC diet. TCP administration did not cause any significant change in the SHBG capacity, but the LPHC resulted again in a significant (P less than .05) increase in SHBG capacity from 80 +/- 18 nmol/L. to 198 +/- 22 nmol/L.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Wash-resistant inhibition of phencyclidine- and haloperidol-sensitive sigma receptor sites in guinea pig brain by putative affinity ligands: determination of selectivity.

Several putative affinity ligands, based on the structures of phencyclidine etoxadrol, 5-methyl-10,11-dihydro-5H-dibenzo[a,d] cycloheptene-5,10-imine (MK801) and 1,3-di-(2-methylphenyl)guanidine (DTG) were evaluated in vitro for their ability to produce a wash-resistant inhibition of phencyclidine and sigma receptor sites in homogenates of the brain of the guinea pig. All the phencyclidine-based ligands, including 1-[1-(3-isothiocyanatophenyl)cyclohexyl]piperidine (Metaphit) and (+/-)-N-(2-isothiocyanatoethyl) MK801 [(+/-)-MK801-NCS], produced a wash-resistant inhibition of binding sites for phencyclidine, labelled by [3H]-1-[1-(2-thienyl)cyclohexyl]piperidine ([3H]TCP) and sigma binding sites, labelled by [3H]DTG. The DTG-based ligands, 1-(4-isothiocyanato-2-methylphenyl)-3-(2-methylphenyl)guanidine (DIGIT) and 1-(4-[2-(2-isothiocyanatoethoxy)ethoxy]-2-methyl-phenyl)-3-(2- methylphenyl)guanidine (DIGIE), produced a wash-resistant inhibition of sigma sites, at concentrations as small as 1 microM and also inhibited binding sites for phencyclidine at larger concentrations (100 microM). Both 1-(3-isothiocyanatophenyl)-1-ethyl-4-(2-piperidyl)-1,3-dioxolane (ETOX-NCS) and 1-[1-(3-bromoacetyloxyphenyl)cyclohexyl]-1,2,3,6-tetrahydropyri din e (Bromoacetyl-PCP) were the most potent and selective inhibitors of the binding of [3H]TCP, while DIGIT was the most selective inhibitor of the binding of [3H]DTG. Future studies will examine the selectivity of these agents in vivo after intracerebroventricular administration.

Affinity Labels↗