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G Ellison

Publications and source records attributed to G Ellison.

At least 37 records · Page 2Linked to original sources
PubMed1992

Continuous amphetamine and cocaine have similar neurotoxic effects in lateral habenular nucleus and fasciculus retroflexus.

Both amphetamine and cocaine lead to an intake pattern in chronic addicts in which the drug is taken repeatedly over prolonged periods. While continuously administered amphetamines, designed to mimic this intake pattern, have a neurotoxic effect on caudate dopamine terminals, several studies have failed to find similar effects following continuous cocaine. In this study, these findings in striatum were replicated in rats using silver staining for degenerating neurons. But it was further found that either amphetamine or cocaine given continuously over a 3- to 5-day period induce a highly specific pattern of axonal degeneration extending from the lateral habenular nucleus along the fasciculus retroflexus towards the ventral tegmentum. This finding supports a rich literature on the involvement of these same pathways in the actions of dopamine agonists, reward mechanisms, and the integration of limbic, extrapyramidal, and midbrain centers.

Amphetamine↗
PubMed1991

Hyperthyroidism associated with a thyroid adenoma in a dog.

Hyperthyroidism associated with thyroid adenoma was diagnosed in a dog. Typical clinical signs of hyperthyroidism were resolved with surgical excision of the adenoma. Hyperthyroidism in dogs usually is associated with thyroid carcinoma, which has a poor prognosis. This case emphasizes the importance of obtaining a histologic diagnosis of thyroid tumors in hyperthyroid dogs before giving a prognosis.

Adenoma↗
PubMed1991

Continuous cocaine administration produces persisting changes in brain neurochemistry and behavior.

Rats were administered either continuous cocaine, daily injections of cocaine, continuous amphetamine, or no drug for 5 days and then given a 30 day drug-free recovery period. When subsequently tested in open field, the daily cocaine injection animals were the most hyperactive whereas the cocaine pellet animals were the most fearful. In vitro autoradiography was then utilized to examine persisting changes in receptor binding for D2 ([3H]spiperone), D1 ([3H]SCH23390), benzodiazepine ([3H]flunitrazepam), 5-HT1 ([3H]5-HT), 5-HT2 ([3H]ketanserin), and muscarinic acetylcholine (ACh) receptors ([3H]QNB; quinuclidinyl benzilate). In the amphetamine pellet animals, there were large increases in [3H]spiperone binding in several dopamine (DA)-rich regions; these were accompanied by conversely decreased [3H]SCH23390 binding. Cocaine pellet animals showed a completely different pattern, with appreciable increases in [3H]flunitrazepam binding in DA-rich areas, cortex, and amygdala but decreased [3H]QNB binding in DA-rich areas, hippocampus, and amygdala. While cocaine injection animals showed elevated [3H]spiperone binding in caudate and substantia nigra, they had generally smaller changes in most brain regions than the other drug groups. These findings replicate and extend previous reports that continuous drug administration induces long-lasting alterations in brain chemistry, but indicate that continuous cocaine has enduring effects on different neurochemical systems from continuous amphetamine.

Amphetamine↗
PubMed1991

A silicone pellet for continuous cocaine: comparison with continuous amphetamine.

An inexpensive silicone pellet is described for the continuous administration of cocaine for up to 5 days. Rats implanted with this pellet show minimal skin irritation and go through distinct behavioral stages, with an initial period of hyperactivity followed by motor stereotypies. Then, at 3-4 days after implantation, a variety of hallucinogen-like ("late-stage") behaviors appear, including limb flicks, sudden startle responses, and repetitive mid-air grasping movements. Compared to continuous d-amphetamine, continuous cocaine induces decreased motor stereotypies but heightened "late-stage" behaviors.

Animals↗
PubMed1990

Comparison of chronic administration of haloperidol and the atypical neuroleptics, clozapine and raclopride, in an animal model of tardive dyskinesia.

Rats were administered haloperidol, clozapine, raclopride, or no drug for either 28 days or 8 months and then withdrawn from drug treatment for 3 weeks. Oral movements were repeatedly recorded, both by a human observer and by a computerized video analysis system which determined mouth openings and closings, or computer-scored movelets (CSMs). Four weeks of neuroleptic administration produced no changes in CSMs in any drug-treated group. Long-term administration induced distinctively different patterns of oral activity in the three drug groups, both in number of CSMs and the form of these movements. The oral movements which developed in the haloperidol-treated rats fit a previously described syndrome of late-onset oral dyskinesias which increased upon drug withdrawal. The clozapine- and raclopride-treated rats did not show the increased oral movements seen in the haloperidol animals, but each exhibited uniquely different CSM characteristics compared to controls. The results from this rodent model imply that haloperidol, but not clozapine or raclopride, produces late-onset oral dyskinesias in rats that fit the pattern expected for tardive dyskinesia.

Animals↗
PubMed1990

Autoradiographic analysis of regional alterations in brain receptors following chronic administration and withdrawal of typical and atypical neuroleptics in rats.

Rats were administered haloperidol, clozapine, raclopride, or no drug for 28 days or 8 months. Following a 3 week withdrawal period, in vitro autoradiography was utilized to examine receptor binding for dopamine D2 ([3H]spiperone and [3H]raclopride), dopamine D 1 ([3H]SCH23390), GABA(A) ([3H]muscimol), benzodiazepine ([3H]RO15-1788), and muscarinic ACh receptors ([3H]QNB). [3H]spiperone was elevated in striatal subregions only in haloperidol-treated rats, with the largest increases seen in the 8 month duration animals. Striatal [3H]raclopride binding was increased after both short- and long-term treatment in both haloperidol and raclopride, but not clozapine-treated animals. Clozapine-treated rats showed significant increases in [3H]SCH23390 in the nucleus accumbens after 28-day administration; otherwise no changes were seen for this ligand in any other groups. Increases in [3H]muscimol binding in the substantia nigra reticulata were seen in haloperidol-treated rats after 8 month treatment. Binding of [3H]QNB and [3H]RO151788 were not significantly different from control for any of the drug-treated groups. These data suggest that persisting alterations in receptor binding are primarily seen in dopamine D2 and GABA receptors after withdrawal from chronic administration of haloperidol but not the atypical neuroleptics, clozapine and raclopride.

Animals↗
PubMed1990

Intermittent and continuous haloperidol regimens produce different types of oral dyskinesias in rats.

Rats were administered equivalent doses of haloperidol for either 28 days or 8 months using one of two different drug regimens: intermittent (i.e., weekly injections) or continuously (via drinking water and osmotic mini-pumps). Oral movements were determined by human observers and by a computerized video analysis system, which determined number and amplitude of jaw openings and closings (computer-scored movelets "CSMs") as well as the slope (amplitude/duration) and frequency spectrum (fourier transform) of oral activity. The two drug groups developed distinctively different changes over time. Continuous administration resulted in late-onset oral activity changes at 1-3 Hz and withdrawal increases in CSMs, a pattern expected of tardive dyskinesia. Intermittent treatment produced a primed dystonia-like pattern: large amplitude CSMs which had steep onset slopes and a peak energy at 4-7 Hz. These results demonstrate the importance of drug regimen in determining the type of neuroleptic-induced dyskinesias which develop with prolonged neuroleptic treatment in rodents.

Animals↗
PubMed1990

Chronic administration of typical, but not atypical neuroleptics induce persisting alterations in rest-activity cycles in rats.

The behavior of rats administered chronic neuroleptics was observed using an extremely sensitive, computerized device which detected any cage movements, thereby continuously monitoring even very small levels of activity. In the first experiment, it was found that normal rats have a strong rest-activity rhythm with a cycle length of 60-70 min, whereas rats which have been chronically administered either haloperidol (HAL) or fluphenazine (FLU) decanoate for 20 months show a distinct lengthening of this cycle and that this effect persists long after cessation of drug injections. In a second experiment, it was further observed that these lengthened rest-activity cycles also occur when HAL is administered chronically either via osmotic minipumps or in the drinking water, but not following the chronic administration of two atypical neuroleptics (clozapine and raclopride). These findings suggest a useful new technique for the study of side-effects of neuroleptics in rats.

Animals↗
PubMed1990

Chronic nicotine induces a specific appetite for sucrose in rats.

Thirty female albino rats were implanted with subcutaneous pellets releasing nicotine or amphetamine in order to study the effects of chronic pharmacological treatment on food intake and body weight. The pellets were removed after tolerance (a decrease in anorectic properties of the drugs) had developed. Nicotine administration produced a specific appetite for sucrose both during and following treatment (p less than 0.05).

Amphetamine↗
PubMed1990

Chronic nicotine and withdrawal effects on radial-arm maze performance in rats.

Rats were tested for choice accuracy in an eight-arm radial maze during and after chronic administration of nicotine via subcutaneously implanted glass and Silastic capsules. Nicotine administration significantly improved choice accuracy relative to controls. The effect gradually became apparent over the first 2 weeks of exposure and persisted through the third week. Surprisingly, the significant facilitation of the nicotine-treated rats relative to controls continued for 2 weeks after the end of nicotine administration. No effects of nicotine were seen on choice latency or the strategy to make adjacent arm entries.

Animals↗
PubMed1989

Rats administered chronic neuroleptics develop oral movements which are similar in form to those in humans with tardive dyskinesia.

Oral movements (OMs) in rats chronically administered haloperidol (HAL), fluphenazine (FLU), or no drug were recorded using a computerized video analysis system which measured the distance between two fluorescent dots painted above and below the rat's mouth. The resulting data was analyzed using fast-fourier analysis. Following an initial period of sedation (decreased energy at all frequencies), the drugged animals (and especially the FLU animals) began to show increased oral movements of 1-2 Hz, an effect which increased substantially upon drug withdrawal. This is precisely the altered energy spectrum observed in humans with tardive dyskinesia.

Animals↗
PubMed1989

Delayed appearance of facial tics following chronic fluphenazine administration to guinea pigs.

Guinea pigs were administered chronic fluphenazine decanoate for 11 months and oral movements (OMs) were periodically observed using several different paradigms. Shortly after the initiation of neuroleptic treatment, increased OMs were seen in the drugged animals, but these did not persist and may have reflected a decreased fear (freezing) reaction in the tranquilized animals, being correlated with increased locomotion in open field. After 7 months of neuroleptics, twitch-like movements of the orofacial region were observed in the drugged animals; these dyskinetic movements were enhanced by administration of d-amphetamine. These twitch-like movements appear to be a better model of tardive dyskinesia in the guinea pig than the initially observed and normal-appearing OMs.

Animals↗
PubMed1989

Long-lasting alterations in behavior and brain neurochemistry following continuous low-level LSD administration.

Groups of rats were administered either 80 micrograms LSD-25 continuously over seven days using subcutaneous minipumps, or were given the same total amount of drug in seven daily injections, or were administered vehicle. When tested long after cessation of drug administration, persisting alterations in behavior and brain were found in the continuous LSD groups. In social open-field tests, this consisted of decreased social distance between animals; this effect increased upon repeated testing. In uptake of labeled ligands, this was reflected predominantly by decreased 3H-LSD binding in several limbic regions. LSD appears to have especially persisting neurotoxic effects when administered in a continuous, low-level fashion.

Animals↗
PubMed1988

Chronic neuroleptics alter the effects of the D1 agonist SK&F 38393 and the D2 agonist LY171555 on oral movements in rats.

Vacuous oral movements (OMs) in rats chronically administered haloperidol (HAL), fluphenazine (FLU), or no drug were studied following injections of one of three doses of either a D1 agonist (SK&F 38393) or a D2 agonist (LY171555). Oral movements were observed via closed-circuit television and simultaneously recorded using a computerized video analysis system which measured the distance between two fluorescent dots painted above and below the rat's mouth. SK&F 38393 induced a dose-dependent increase in tremorous oral movements and repetitive chewing movements in the controls; this effect was more pronounced in rats treated with chronic HAL or FLU, both during chronic neuroleptic treatment and even more so when they were tested after drug withdrawal following 5 or 14 months of chronic neuroleptic administration. Conversely, LY171555 produced an inhibition of oral activity at all dose levels in controls. This inhibition was attenuated during chronic administration of HAL or FLU, but returned to control levels (without any signs of supersensitivity) when the animals were retested shortly after discontinuation of neuroleptics. These results indicate that heightened oral movements in rodents following chronic neuroleptic administration can be more clearly induced by D1 than by D2 receptor activation.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1988

The long march of the cerebrospinal fluid profile indicative of clinical definite multiple sclerosis; and still marching.

Much progress has been made, especially in the last two decades, in laboratory aids to diagnosis and to follow the course of patients with multiple sclerosis (MS). The cerebrospinal fluid (CSF) profile indicative of MS, though not pathognomonic of MS, is present in almost every case of clinical definite MS in a chronic progressive phase (probably also true for early MS). The cardinal aspect of the profile is intra-blood-brain barrier (BBB) IgG synthesis which can be qualitatively detected by determining unique CSF oligoclonal IgG bands and quantitated by rate formula, mg/day. We believe that intra-BBB IgG synthesis is caused by a persistent antigen, most likely a virus, possibly measles. A number of issues about the profile are proposed and opportunities are presented to resolve them.

Antibodies↗