Author
Gaylord Ellison
Other affiliations: University of New Mexico, University of Wisconsin–Platteville
Bio: Gaylord Ellison is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: Amphetamine & Dopamine. The author has an hindex of 40, co-authored 98 publications receiving 4299 citations. Previous affiliations of Gaylord Ellison include University of New Mexico & University of Wisconsin–Platteville.
Topics: Amphetamine, Dopamine, Haloperidol, Dopamine receptor, Phencyclidine
Papers published on a yearly basis
Papers
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TL;DR: Silicone pellets containing d-amphetamine base were implanted subcutaneously in rats and swollen dopamine axons concomitant with large decreases in tyrosine hydroxylase activity were observed in the caudate nucleus, implying that continuous amphetamine administration has a selective neurotoxic effect on dopamine terminals in the Caudate.
Abstract: Silicone pellets containing d-amphetamine base were implanted subcutaneously in rats. These pellets release amphetamine continuously for at least 10 days. Several days after implantation, swollen dopamine axons concomitant with large decreases in tyrosine hydroxylase activity were observed in the caudate nucleus. Decreased tyrosine hydroxylase activity was still present 110 days after pellet removal in the caudate but not in several other brain regions, nor in the caudate of rats injected with an equivalent amount of amphetamine in daily injections. This implies that continuous amphetamine administration has a selective neurotoxic effect on dopamine terminals in the caudate.
316 citations
TL;DR: Behavioral observations and drug-discrimination studies in animals indicate that PCP and dizocilpine are similar in their effects and they both have a neurotoxic effect on neurons in posterior cingulate cortex, which suggests these non-competitive NMDA antagonists may provide a more complete model of psychoses and memory disturbances than previously recognized.
300 citations
TL;DR: It is argued that alterations in these pathways are ideal candidates for producing the behaviors which occur during psychosis and that future considerations of the circuitry underlying psychoses need to include this highly important but relatively neglected system.
189 citations
TL;DR: D1 and D2 dopamine receptors appear to have opposite effects on oral movements, for there was an inhibition of all categories of behavior measured, as well as of all amplitudes of computer-scored movements and slow, sluggish movements.
132 citations
TL;DR: Notably, the significant facilitation of the nicotine-treated rats relative to controls continued for 2 weeks after the end of nicotine administration, and no effects of nicotine were seen on choice latency or the strategy to make adjacent arm entries.
127 citations
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TL;DR: A major unifying thread of the review is a consideration of how the changes occurring during and after ischemia conspire to produce damaging levels of free radicals and peroxynitrite to activate calpain and other Ca(2+)-driven processes that are damaging, and to initiate the apoptotic process.
Abstract: This review is directed at understanding how neuronal death occurs in two distinct insults, global ischemia and focal ischemia. These are the two principal rodent models for human disease. Cell dea...
2,960 citations
TL;DR: There is not convincing evidence for an increase in postsynaptic DA receptors or in DA synthesis in animals sensitized to AMPH, but there is strong evidence to support the notion that behavioral sensitization is due to enhanced mesotelencephalic DA release, especially upon re-exposure to the drug.
2,208 citations
TL;DR: It is suggested that dysregulation of locus coeruleus-noradrenergic neurotransmission may contribute to cognitive and/or arousal dysfunction associated with a variety of psychiatric disorders, including attention-deficit hyperactivity disorder, sleep and arousal disorders, as well as certain affective Disorders, including post-traumatic stress disorder.
2,207 citations
TL;DR: It is found that the dopamine neurons of sensitized animals have become increasingly sensitive to excitatory pharmacological and environmental stimuli or desensitized to inhibitory regulation, and changes in cellular activity or protein synthesis may result in a change in the presynaptic regulation of axon terminal dopamine release.
2,042 citations
TL;DR: It is proposed that since N-methyl-D-aspartate receptor hypofunction can cause psychosis in humans and corticolimbic neurodegenerative changes in the rat brain, and since these changes are prevented by certain antipsychotic drugs, including atypical neuroleptic agents, a better understanding of this mechanism may lead to improved pharmacotherapy in schizophrenia.
Abstract: In this article, we advance a unified hypothesis pertaining to combined dysfunction of dopamine andN-methyl-D-aspartate glutamate receptors that highlights N-methyl-D-aspartate receptor hypofunction as a key mechanism that can help explain major clinical and pathophysiological aspects of schizophrenia. The following fundamental features of schizophrenia are accommodated by this hypothesis: (1) the occurrence of structural brain changes during early development that have the potential for producing subsequent clinical manifestations of schizophrenia, (2) a quiescent period in infancy and adolescence before clinical manifestations are expressed, (3) onset in early adulthood of psychotic symptoms, (4) involvement of dopamine (D2) receptors in some cases but not others that would explain why some but not all patients are responsive to typical neuroleptic therapy, and (5) ongoing neurodegenerative changes and cognitive deterioration in some patients. We propose that since N-methyl-D-aspartate receptor hypofunction can cause psychosis in humans and corticolimbic neurodegenerative changes in the rat brain, and since these changes are prevented by certain antipsychotic drugs, including atypical neuroleptic agents (clozapine, olanzapine, fluperlapine), a better understanding of the N-methyl-D-aspartate receptor hypofunction mechanism and ways of preventing its neurodegenerative consequences in the rat brain may lead to improved pharmacotherapy in schizophrenia.
1,663 citations