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      Dopamine-deficient mice are severely hypoactive, adipsic, and aphagic.

      Cell
      Adrenergic Fibers, metabolism, Animals, Animals, Newborn, Behavior, Animal, physiology, Dopamine, analysis, deficiency, Dopamine beta-Hydroxylase, Drinking Behavior, Dynorphins, biosynthesis, Embryo, Mammalian, Feeding Behavior, Immunohistochemistry, In Situ Hybridization, Levodopa, pharmacology, Mesencephalon, enzymology, Mice, Mice, Transgenic, Mutation, Neostriatum, cytology, Neurons, chemistry, Norepinephrine, Substance P, Transgenes, Tyrosine 3-Monooxygenase, genetics

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          Abstract

          Mice unable to synthesize dopamine (DA) specifically in dopaminergic neurons were created by inactivating the tyrosine hydroxylase (TH) gene then by restoring TH function in noradrenergic cells. These DA-deficient (DA-/-) mice were born at expected frequency but became hypoactive and stopped feeding a few weeks after birth. Midbrain dopaminergic neurons, their projections, and most characteristics of their target neurons in the striatum appeared normal. Within a few minutes of being injected with L-dihdroxyphenylalanine (L-DOPA), the product of TH, the DA-/- mice became more active and consumed more food than control mice. With continued administration of L-DOPA, nearly normal growth was achieved. These studies indicate that DA is essential for movement and feeding, but is not required for the development of neural circuits that control these behaviors.

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          Most cited references53

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          Drugs of abuse: anatomy, pharmacology and function of reward pathways.

          Drugs of abuse are very powerful reinforcers, and even in conditions of limited access (where the organism is not dependent) these drugs will motivate high rates of operant responding. This presumed hedonic property and the drugs' neuropharmacological specificity provide a means of studying the neuropharmacology and neuroanatomy of brain reward. Three major brain systems appear to be involved in drug reward--dopamine, opioid and GABA. Evidence suggests a midbrain-forebrain-extrapyramidal circuit with its focus in the nucleus accumbens. Data implicating dopamine and opioid systems in indirect sympathomimetic and opiate reward include critical elements in both the nucleus accumbens and ventral tegmental areas. Ethanol reward appears to depend on an interaction with the GABAA receptor complex but may also involve common elements such as dopamine and opioid peptides in this midbrain-forebrain-extrapyramidal circuit. These results suggest that brain reward systems have a multidetermined neuropharmacological basis that may involve some common neuroanatomical elements.
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            Neurotransmitters and neuromodulators in the basal ganglia.

            The basal ganglia have become a focus for work on neurotransmitter interactions in the brain. These structures contain a remarkable diversity of neuroactive substances, organized into functional subsystems that have unique developmental histories and vulnerabilities in neurodegenerative diseases. A new view of the basal ganglia is emerging on the basis of this neurochemical heterogeneity, suggesting that dynamic regulation of transmitter expression may be a key to extrapyramidal function.
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              Neurotransmitter transporters: recent progress.

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