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C D Blaha

Publications and source records attributed to C D Blaha.

50 records · Page 3Linked to original sources
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

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↗
PubMed1983

In vivo electrochemical evidence for an enkephalinergic modulation underlying stereotyped behavior: reversibility by naloxone.

The effect of the enkephalin pentapeptide analog (WY 42,896) on amphetamine-induced stereotypy was studied in male, albino rats. WY 42,896 significantly inhibited amphetamine-induced stereotypy. The inhibition of the head-bobbing and sniffing components was significantly reversed by naloxone. Disinhibition of the rearing components by naloxone reached borderline significance. In vivo electrochemical measurements in rat caudate showed that WY 42,896 inhibited both basal and amphetamine-induced dopamine release. This inhibition was prevented by naloxone. These data show an enkephalinergic-dopaminergic interaction in rat striatum, both behaviorally and biochemically, and suggest a presynaptic site of action of the enkephalin on dopamine neurons.

Animals↗
PubMed1983

Chemically modified electrode for in vivo monitoring of brain catecholamines.

A chemically modified graphite paste electrode was developed to allow catecholamines to be electrochemically distinguished from ascorbic acid and the dopamine metabolite 3,4-dihydroxyphenylacetic acid (DOPAC). Interference from 5-hydroxyindoles is eliminated through appropriate choice of electrode potential. The electrode gives linear current responses with increasing concentrations of catecholamines unaffected by the presence of ascorbic acid or DOPAC and exhibits long-term response stability in brain tissue. Examples are provided demonstrating the selectivity of the electrode to changes in extracellular dopamine in the rat striatum.

Animals↗
PubMedDate not supplied

Neurochemical correlates of brain-stimulation reward measured by ex vivo and in vivo analyses.

Evidence from ex vivo analyses of dopaminergic function following self-stimulation behavior is reviewed and compared to in vivo analyses of extracellular dopamine measured by chronoamperometry during self-stimulation. Both data bases provide strong support for a dopaminergic substrate for brain-stimulation reward obtained by electrical stimulation of the ventral tegmental area (VTA). Data obtained from in vivo measures of dopamine release are particularly compelling as a positive correlation was observed between the rate/intensity function for self-stimulation and increments in the oxidation current for dopamine. An examination of the effects of the dopamine uptake blockers, cocaine and GBR 12909 on self-stimulation and stimulated release of dopamine revealed a facilitation of both measures. In contrast, the noradrenaline uptake blocker desipramine had no effect on either self-stimulation or extracellular dopamine. These pharmacological experiments also are consistent with a dopaminergic substrate of brain-stimulation reward at electrode sites in the VTA.

Animals↗
PubMedDate not supplied

Increased extracellular dopamine in the nucleus accumbens of the rat elicited by a conditional stimulus for food: an electrochemical study.

Stearate-modified graphite paste electrodes were implanted chronically into dopamine terminal regions in the nucleus accumbens or caudate nucleus of the rat. Reverse dialysis was used to demonstrate a selective response of these electrodes to dopamine, but not 3,4-dihydroxyphenylacetic acid or ascorbic acid. In a separate behavioural experiment, a significant increase in the chronoamperometric response was observed during presentation of a conditional stimulus predictive of food, and the electrochemical response remained elevated during and following consumption of the meal. Similar trends were observed from electrodes in the caudate nucleus. These data confirm the activation of mesolimbic dopamine neurons by incentive stimuli predictive of food and possibly by consumption of food. Together with other recent data on sex- and thirst-related increases in dopamine levels in the nucleus accumbens, these findings are consistent with a role for the nucleus accumbens as an interface between motivation and activation of the motor system.

Animals↗