PubMed Health⌕ Search

Biomedical subjects

R F Lane

Publications and source records attributed to R F Lane.

At least 19 recordsLinked to original sources
PubMed1988

Selective inhibition of mesolimbic dopamine release following chronic administration of clozapine: involvement of alpha 1-noradrenergic receptors demonstrated by in vivo voltammetry.

The release of dopamine (DA) in vivo was compared in the striatum and nucleus accumbens following chronic (21 day) administration of clozapine (CLOZ) and repeated coadministration of haloperidol (HAL) and the alpha 1-noradrenergic (NE) receptor antagonist prazosin. Treatment with HAL reduced basal DA release in both brain regions, whereas treatment with CLOZ decreased basal DA release only in the accumbens. Chronic coadministration of HAL and prazosin resulted in decreased DA release in accumbens but not striatum. These results suggest that the alpha 1-NE receptor blocking properties of CLOZ may, in part, mediate its differential actions on nigrostriatal and mesolimbic DA release, an effect which may in addition contribute to its paucity of extrapyramidal side effects.

Animals↗
PubMed1987

Chronic treatment with classical and atypical antipsychotic drugs differentially decreases dopamine release in striatum and nucleus accumbens in vivo.

In vivo electrochemical techniques were employed to demonstrate that repeated treatment with classical antipsychotic drugs reduced basal dopamine (DA) release in the striatum and nucleus accumbens, whereas repeated treatment with atypical antipsychotics decreased DA release only in accumbens. Administration of apomorphine temporarily reversed these decreases to values comparable to those measured in vehicle-treated controls. These results suggest that the delayed onset of antipsychotic efficacy and extrapyramidal side effects involve a decrease in DA release in mesolimbic and nigrostriatal DA terminal fields, respectively. The results further suggest that induction of depolarization block in DA neurons may be the mechanism underlying these effects.

Animals↗
PubMed1987

Acute thioridazine stimulates mesolimbic but not nigrostriatal dopamine release: demonstration by in vivo electrochemistry.

In vivo electrochemical techniques were employed to demonstrate that haloperidol and (+)-butaclamol increased the release of dopamine (DA) in the striatum and nucleus accumbens, whereas thioridazine stimulated DA release only in the accumbens. The stimulatory effect of thioridazine was reversed by gamma-butyrolactone. Given that gamma-butyrolactone inhibits DA neuronal activity, these data indicate that the regional selectivity of thioridazine on DA release is due to its ability to preferentially stimulate DA cell firing in the ventral tegmental (A10) area and suggest that its antipsychotic properties depend on its actions in the mesolimbic DA system.

4-Butyrolactone↗
PubMed1987

A functional separation of behavioral stereotypy based on naloxone-reversible effects of seryl enkephalinamide: comparison with morphine.

Amphetamine's stereotypic behavioral actions, produced by the stimulant at a moderate dose, were inhibited by the systemic administration of seryl enkephalinamide, D-Ser2-D-Ser5-enkephalinamide, (Wy 42,896). The classical sequelae of stimulatory behavioral events: sniffing, head bobbing, rearing and locomotor activity, were significantly inhibited by the seryl enkephalinamide. Subsequently, pretreatment with the opiate receptor antagonist, naloxone, significantly blocked the inhibitory effects of the seryl enkephalinamide on the stereotypic and locomotor components. Concomitantly, the behavioral stereotypic component, licking, a behavior usually produced by opiates and only high doses of amphetamine, was significantly induced by the seryl enkephalinamide. Pretreatment with naloxone on the stimulatory behavioral effect of licking, produced a significant inhibitory effect. The combination treatment, consisting of both the seryl enkephalinamide and the stimulant amphetamine, caused a naloxone-reversible synergistic effect. These data show that the seryl enkephalinamide, produced concomitant, naloxone-reversible, inhibitory and stimulatory behavioral stereotypic effects. These data are discussed within the context of current neuronal theories which might underly the observed dose-related continuum of behavioral stereotypies produced by morphine and amphetamine.

Amphetamine↗
PubMed1987

Reversal by cholecystokinin of apomorphine-induced inhibition of dopamine release in the nucleus accumbens of the rat.

In vivo electrochemical techniques were used to study the effects of the sulfated (CCK8-S) and unsulfated (CCK8-US) forms of cholecystokinin octapeptide on apomorphine-induced inhibition of dopamine (DA) release in the nucleus accumbens of the anesthetized rat. A dose-dependent inhibition of DA release was observed with intravenous (i.v.) injections of apomorphine. CCK8-S administered i.v. at the nadir of the apomorphine-induced inhibition of DA release produced a transient and dose-dependent increase followed by a prolonged decrease in DA release CCK8-US was ineffective in altering apomorphine's inhibitory effects on DA release. The CCK receptor antagonist proglumide injected i.v. 10 min after apomorphine administration had no effect on apomorphine-induced inhibition of DA release, but blocked the effects of CCK8-S on this inhibition. Given that apomorphine may inhibit DA release by a direct hyperpolarizing action on DA neurons, the observation that CCK8-S temporarily reverses apomorphine-induced effects and further inhibits DA release suggests that CCK8-S exerts its inhibitory effects via a process of depolarization block in DA neurons. These findings indicate that apomorphine and CCK8-S may inhibit DA release in vivo by opposite effects on DA cell membrane potentials and suggest that endogenously released CCK may serve to modulate mesolimbic DA neurotransmission.

Animals↗
PubMed1987

Cholecystokinin-induced inhibition of dopamine neurotransmission: comparison with chronic haloperidol treatment.

A dose-dependent inhibition of DA release was observed by in vivo electrochemical techniques after acute i.v. injections of CCK8-S (1.0-8.0 micrograms/kg). The threshold dose was 1.0 microgram/kg, and maximum inhibition of release (90%) was obtained with doses of 4 and 8 micrograms/kg. Injections of CCK8-US (4-20 micrograms/kg) had no effect on DA release. Repeated treatment with haloperidol (0.5 mg/kg s.c.) for 21 days produced a 47% inhibition of DA release in the nucleus accumbens. Apomorphine (50 micrograms/kg) reversed the inhibitory effects of both acute injections of CCK8-S and prolonged haloperidol treatment on DA release. In contrast, apomorphine (50 micrograms/kg) administered alone inhibited DA release, presumably via hyperpolarization of DA neurons. The attenuation of DA release by either an acute injection of CCK8-S or repeated treatment with haloperidol is attributed to the induction of depolarization block in mesolimbic DA neurons. These data may be indicative of antipsychotic properties of CCK8-S.

Animals↗
PubMed1987

Chronic haloperidol decreases dopamine release in striatum and nucleus accumbens in vivo: depolarization block as a possible mechanism of action.

The effects of chronic haloperidol administration on the basal release of endogenous dopamine (DA) in the intact rat striatum and nucleus accumbens were investigated using in vivo electrochemical techniques. Repeated (21 day) treatment with haloperidol produced marked decreases in the release of DA in both brain regions. Administration of apomorphine to vehicle-treated control animals rapidly reduced DA release, in accord with its inhibitory, hyperpolarizing actions on DA neurons. In contrast, apomorphine reversed the haloperidol-induced reductions in DA release to values that were not significantly different from those measured in control animals. The present study is the first report to demonstrate decreased DA release in response to chronic neuroleptic treatment and to present evidence for induction of depolarization block of DA cell firing as a possible mechanism underlying this effect.

Animals↗
PubMed1987

Electrochemistry in vivo: monitoring dopamine release in the brain of the conscious, freely moving rat.

Changes in electrochemical responses at stearate-modified and unmodified graphite paste electrodes were compared simultaneously by intrastriatal chronoamperometry in freely moving rats. Responses at the modified electrodes were unaffected by ascorbate administration, decreased by pergolide and increased by pargyline and haloperidol. The effects of haloperidol were reversed by gamma-butyrolactone but not by pargyline. In contrast, responses at the unmodified electrodes were increased by ascorbate or pergolide and decreased by pargyline. Haloperidol-induced increases at these electrodes were rapidly reversed by pargyline. Responses of the two electrodes differed significantly in both magnitude and temporal characteristics after amphetamine administration. The results demonstrate that the modified electrodes can selectively monitor released dopamine in the freely moving animal, even when there are simultaneous, large changes in ascorbate and 3,4-dihydroxyphenylacetic acid.

Animals↗
PubMed1987

Release of cortical catecholamines by visual stimulation requires activity in thalamocortical afferents of monkey and cat.

Catecholamine (CA) release was measured in vivo in the monkey and cat visual cortices electrochemically. Stereate-modified, graphite-paste electrodes were used to monitor changes in norepinephrine and dopamine release. Micromolar changes in CA concentration were obtained by stimulation of the eye with nonspecific (strobe) or specific (oriented bars, radial gratings) stimuli. CA release depended on which eye was illuminated. Electrodes passed tangentially through the striate area recorded release following visual stimulation of one eye or the other in succession, and the shift in eye dominance occurred at about 500 microns intervals. The magnitude of CA release was highly correlated with the ocular dominance of neuronal activity measured with tungsten microelectrodes. Light-stimulated release was not recorded in monkey area V2, V4, or somatosensory area 1, but was recorded in cat V2, suggesting that the presence of LGN afferents is associated with CA release. Results are discussed in terms of the role of geniculate activity and the specific role of CAs in cortical information processing.

Animals↗
PubMed1986

In vivo electrochemical analysis of cholecystokinin-induced inhibition of dopamine release in the nucleus accumbens.

In vivo electrochemical techniques were used to study the effects of the sulfated (CCK8-S) and unsulfated (CCK8-US) forms of the cholecystokinin octapeptide on dopamine (DA) release in the nucleus accumbens. A dose-dependent inhibition of DA release was observed only with CCK8-S. This inhibitory effect was blocked by the CCK receptor antagonist proglumide, and was reversed by systemic injections of apomorphine. Given that apomorphine can hyperpolarize DA neurons, these data indicate that CCK may inhibit the release of DA by a process of depolarization block and suggest a mechanism by which CCK may regulate overactive mesolimbic DA transmission.

Animals↗
PubMed1986

Dynamics of noradrenergic circadian input to the chicken pineal gland.

To analyze the dynamics of sympathetic input to the chicken pineal the concentrations of catecholamines, indoleamines and some of their metabolites were determined by high performance liquid chromatography with electrochemical detection (HPLC-EC) in the pineal glands of young chickens killed at different times of day. Rhythmic variations over 24 h were observed in tissue levels of dopamine (DA), 5-hydroxytryptamine (5-HT), N-acetylserotonin (NAS) and 5-hydroxyindoleacetic acid (5-HIAA), while norepinephrine (NE) concentrations exhibited no significant change. DA content peaked 2 h after onset of darkness and NAS was detectable only during the night. A bimodal pattern of 5-HT and 5-HIAA levels was observed with peak tissue levels occurring at dawn and dusk. To determine the possible differential effects of light on these biogenic amines, birds were sacrificed at midday, midnight and at midnight following a 1 h exposure to light, and their pineals processed for HPLC-EC. NE, DA and 5-HT levels were similar at midday and midnight, while 5-HIAA and NAS were elevated during the night. Midnight illumination decreased NE and NAS levels, increased 5-HT and 5-HIAA levels and had no effect on DA levels. Temporal variations in NE turnover were determined by pretreating young chickens with alpha-methyl-p-tyrosine, a tyrosine hydroxylase inhibitor, and measuring the rates of decline in NE content over 2 h at midday and midnight in birds held on light cycles and at mid-subjective day in birds held in constant darkness (DD).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Melatonin-induced increases in serotonin concentrations in specific regions of the chicken brain.

Day-night differences in the concentrations of melatonin and serotonin (5HT) were measured in several regions of the chicken brain, pineal gland and serum. Melatonin concentrations are higher at midnight than at midday in 8 of the 10 tissues studied although the amplitudes of these rhythms varied greatly. Day-night differences in the pineal, hypothalamus, thalamus, retina and pons-midbrain regions had the highest amplitudes. 5HT concentrations were rhythmic in only 3 of the tissues studied: the hypothalamus, thalamus and retina. These were also the areas of highest 5HT concentration. Exogenous melatonin, injected at midday, was taken up with similar patterns; the pineal, hypothalamus, thalamus and pons-midbrain contained more melatonin 20 min after injection than did other tissues. The rate of decline of melatonin concentration varied little among all tissues studied, suggesting that the differences among tissue concentrations were due to selective uptake mechanisms rather than specialized degradation pathways. The effects of exogenous melatonin on 5HT concentration were restricted to hypothalamus, thalamus, pons-midbrain, retina and pineal. No effect was seen in cerebellum, optic tectum, neostriatum, hippocampus and medulla oblongata. Together, these data strongly suggest that pineal (and exogenous) melatonin is selectively taken up primarily by three brain regions, hypothalamus, thalamus and pons-midbrain, in which it produces increases in 5HT concentrations. Regional selectivity of uptake may be the mechanism by means of which the effects of melatonin on 5HT-mediated function are restricted to specific brain areas.

Animals↗
PubMed1986

Doses of 6-hydroxydopamine sufficient to deplete norepinephrine are not sufficient to decrease plasticity in the visual cortex.

These experiments were designed to test Kasamatsu and Pettigrew's (1979, 1983, and see below) hypothesis that plasticity in the visual cortex requires cortical norepinephrine (NE). Kittens were treated with various doses of intraventricular 6-hydroxydopamine (6-OHDA) or vehicle solution. Cortical NE content was measured with high-performance liquid chromatography with electrochemical detection. We sutured the right eyes of some kittens approximately 6 weeks of age for 1 week and recorded from the left visual cortex of these kittens at the end of the week of suture. We measured the ability of the deprived eye to drive cortical cells in animals that received either 0.2 or 4.8 mg of 6-OHDA, and also in control animals that received only vehicle solution. We concluded that a particular dose of 6-OHDA decreased plasticity if it increased (relative to controls) the ability of the deprived eye to drive cortical cells. Doses of 6-OHDA as small as 0.2 mg were sufficient to produce approximately maximal depletion of NE but did not decrease cortical plasticity. Doses of 4.8 mg or more did decrease cortical plasticity, although not as much as was reported by Kasamatsu and Pettigrew. We conclude that 6-OHDA can alter cortical plasticity but the decrease in plasticity does not result from NE depletion.

Animals↗
PubMed1985

Differential effects of xylamine on extracellular concentrations of norepinephrine and dopamine in rat central nervous system: an in vivo electrochemical study.

The effects of xylamine (N-2-chloroethyl-N-ethyl-2-methylbenzylamine) on tissue content and extracellular concentration of catecholamines in the rat brain were examined after systemic administration using in vivo voltammetry and high-performance liquid chromatography-electrochemical detection. Xylamine at a dose of 12.5 mg/kg i.p. reduced the extracellular concentration of norepinephrine (NE) in the cortex, while having no effect on the extracellular concentration of dopamine in the striatum. The content of NE in the cortex was reduced by approximately 41% at a dose of 12.5 mg/kg and 62% at 25 mg/kg within a 4-hr period, whereas dopamine contents remained unaltered. Both the reduction in extracellular concentration and the depleting action of xylamine on NE content were blocked by pretreatment with desmethylimipramine. The data suggest that xylamine has a selective action on the NE system that is mediated through the neuronal uptake carrier; however, the depleting action of xylamine and its effect on extracellular NE concentration may be unrelated actions.

Animals↗
PubMed1984

Direct in vivo electrochemical monitoring of dopamine release in response to neuroleptic drugs.

The ability of stearate-modified graphite paste electrodes to monitor changes in dopamine (DA) release in response to haloperidol and chlorpromazine was examined in rat striatum. The increase in electrochemical signal produced by both neuroleptics was not reversed by pargyline and was abolished by 6-hydroxydopamine lesions of the substantia nigra. The electrodes did not respond to administration of ascorbic acid or promethazine. The results demonstrate that neuroleptic-induced release of DA can be directly monitored with these electrodes.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

A comparison of CNS stimulants with phencyclidine on dopamine release using in vivo voltammetry.

Phencyclidine (PCP) produces some neurochemical and behavioral effects in rats similar to those produced by the indirectly acting dopamine (DA) agonists amphetamine and amfonelic acid. In view of these findings, the effects of PCP, d-amphetamine and amfonelic acid on the release of DA in the rat striatum were examined by in vivo voltammetry. Drug effects on DA release were determined using newly developed electrodes selective for catecholamines. PCP (5 and 10 mg/kg IP) produced a dose-dependent decrease in the electrochemical signal that lasted for approximately 4 hr. In contrast, d-amphetamine (2.5 mg/kg, IP) and amfonelic acid (5.0 mg/kg, IP) both caused marked increases in electrochemical signals. The data provide evidence that PCP at the doses tested alters dopaminergic neurotransmission in a manner different from that of amphetamine and the non-amphetamine central nervous system stimulants by decreasing DA release from dopaminergic nerve terminals.

Animals↗