Dopamine in the rat ventral pallidum/substantia innominata: Biochemical and electrophysiological studies

Napier, T. Celeste; Potter, Pamela E.

doi:10.1016/0028-3908(89)90163-9

Cited by 61 publications

(33 citation statements)

References 11 publications

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“…Dopamine is a moderately abundant neurotransmitter in the VP (Napier and Potter, 1989;Zaborszky et al, 1993), and it has widespread influence on VP function (Maslowski and Napier, 1991;Napier et al, 1991b). VP opioids regulate local dopamine transmission (for review, see Napier and Mitrovic, 1999), and dopamine receptors in the VP are obligatory for acute motor function mediated by intra-VP m-opioid receptors (Napier, 1992).…”

Section: Discussionmentioning

confidence: 99%

The Ventral Pallidum is Critically Involved in the Development and Expression of Morphine-Induced Sensitization

Mickiewicz

Dallimore

Napier

2008

Neuropsychopharmacol

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Repeated, intermittent exposure to drugs of abuse results in response enhancements to subsequent drug treatments, a phenomenon referred to as sensitization. As persistent neuronal sensitization may contribute to the long-lasting consequences of drug abuse, characterizing the neuroanatomical substrates of sensitization is providing insights into addiction. It is known that the ventral tegmental area (VTA) is necessary for induction, and expression involves the nucleus accumbens (NAc). We reveal here that the ventral pallidum (VP), a brain region reciprocally innervated by the VTA and the NAc, is a critical mediator of opiate-induced behavioral sensitization. Blockade of VP m-opioid receptors (via intra-VP CTOP injections) negated the ability of systemic administration of the opiate, morphine to induce motor sensitization, and for sensitized rats to subsequently express enhanced responding to a morphine challenge. Intra-VP morphine was sufficient to induce motor sensitization, and this sensitization was expressed following 17 days of withdrawal. Rats with a treatment history of intra-VP morphine demonstrated cross-sensitization to a challenge injection of systemically administered morphine. Conversely, repeated systemic treatments of morphine cross-sensitized to an intra-VP morphine challenge. These results indicate that activation of VP m-opioid receptors is sufficient to evoke behavioral sensitization and that these receptors are necessary for sensitized responding to systemic morphine. The study pioneers the concept that both development and expression of drug-induced sensitization are regulated by the VP. Thus, the VP is likely an important contributor to neuronal adaptations that underlie addiction.

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Section: Discussionmentioning

confidence: 99%

The Ventral Pallidum is Critically Involved in the Development and Expression of Morphine-Induced Sensitization

Mickiewicz

Dallimore

Napier

2008

Neuropsychopharmacol

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“…To do so, at the conclusion of the electrophysiological experiments, the striatum and olfactory tubercles were dissected. The tissue was assayed for monoamine content by HPLC-EC, as used previously (Napier and Potter, 1989). The HPLC-EC data, presented as nanograms per milligram of wet tissue Ϯ S.E.M., were compared using ANOVA with post hoc Newman-Keuls (if significant) with P Ͻ 0.05 set for significance.…”

Section: Methodsmentioning

confidence: 99%

“…possible mechanism for this finding may involve interactions among local (VP) neurotransmitters. The VP is directly innervated by DA-containing terminals (Voorn et al, 1986), and local applications of DA induce robust changes in VP neuronal firing rate (Napier and Potter, 1989;Napier et al, 1991;Maslowski-Cobuzzi and Napier, 1994). DA also normally regulates the effects of several VP transmitters, including inhibiting glutamate-induced excitations (Johnson and Napier, 1997a).…”

Section: Discussionmentioning

confidence: 99%

Alterations in Responses of Ventral Pallidal Neurons to Excitatory Amino Acids after Long-Term Dopamine Depletion

Turner

Mignon²,

Napier³

2002

J Pharmacol Exp Ther

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The present study explored the possibility that excitatory amino acid (EAA) sensitivity within the ventral pallidum (VP) is altered by long-term removal of dopamine (DA). Electrophysiological experiments were conducted in chloral hydrate-anesthetized rats 21 to 28 days after they received unilateral substantia nigra injections of the dopaminergic toxin 6-hydroxydopamine (6-OHDA). VP neurons increased firing at low microiontophoretic ejection currents of the EAA agonists N-methyl-D-aspartate (NMDA) and ␣-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA); however, high currents decreased action potential amplitude and rapidly caused cessation of neuronal firing. These responses likely reflected the induction of depolarization block for they were reversed by coiontophoresis of the hyperpolarizing transmitter ␥-aminobutyric acid (GABA) at ejection current levels that normally suppressed firing. The ability of NMDA and AMPA to induce such inactivation was greater in the VP of 6-OHDA-lesioned hemispheres, but unchanged in reserpinized rats, verifying that the alterations in responding to NMDA were the result of chronic, rather than acute, DA removal. The adaptations do not appear to be the consequence of a diminished GABAergic tone for the ability of bicuculline to increase firing (due to blocking a tonic GABAergic input) was not changed. However, low ejection currents of GABA that were insufficient to alter firing rate greatly attenuated the ability of NMDA to induce an apparent depolarization inactivation when coiontophoresed with NMDA onto VP neurons of the lesioned, but not the unlesioned, hemisphere. These studies show that chronic DA removal altered the EAA-induced amplitude-decreasing (i.e., the apparent depolarization inactivation) effects in VP neurons in the absence of a decrease in GABAergic tone.EAAs provide the major excitatory drive within the basal ganglia and limbic systems of the brain. Popular circuitry models for basal ganglia adaptations that accompany chronic near-total lesions of the ascending dopaminergic system incorporate the wealth of evidence for an up-regulation of EAA transmission (for review, see Ossowska, 1994). Moreover, suppression of EAA transmission by EAA antagonists attenuates motor dysfunction and augments the beneficial effects of levodopa in animal models of PD (Ossowska, 1994). The neuroanatomical substrates engaged by the up-regulation of EAA transmission in the DA-deafferented brain include those influenced by the enhancement in activity of STN EAAcontaining projections, e.g., the GPi (Brotchie et al., 1991;Filion and Tremblay, 1991) and the substantia nigra zona reticulata (Rohlfs et al., 1997).The VP receives direct innervation of EAA-containing afferents from limbic regions (e.g., amygdala; Russchen and Price, 1984;Maslowski-Cobuzzi and Napier, 1994) and the basal ganglia (e.g., STN;Groenewegen and Berendse, 1990;Turner et al., 2001). These inputs act on two major subtypes of ionotropic EAA receptors in the VP, NMDA, and non-NMDA (Monaghan and Cotman, 1985;...

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“…The characterization of major dopamine systems in the forebrain has been and contin ues to be extensive [2][3][4], forming the neces sary basis of an eventual understanding of the diversity of function [5]. Since the introduc tion of the catecholamine neurotoxin, 6-hydroxydopamine (6-OHDA), as an effective pharmacological tool for the study of the functional roles of DA and noradrenaline (NA) [6,7], major efforts have been aimed at the elucidation of the functions of these neu rotransmitters.…”

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confidence: 99%

Functional Changes Implicating Dopaminergic Systems following Perinatal Treatments

Archer¹,

Fredriksson²

1992

Dev Pharmacol Ther

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A series of experiments, involving diverse perinatal treatments of either rats or mice, have been performed in order to investigate the effects of these treatments upon certain selected spontaneous and learned behaviors in the laboratory. Rat dams were administered either metallic mercury, organic tin or neuroleptic compounds, and the offspring of these dams was studied with behavioral tests at adult ages, prenatal studies. Newborn rat pups were administered either 6-hydroxydopamine (6-OHDA) (at various doses), or metallic mercury and then tested at adult ages. Newborn mice were administered either metaclopramide, an antiemetic compound, or haloperidol, a neuroleptic compound, and tested for spontaneous and d-amphetamine induced activity as adults. The behavioral battery the rats were tested with consisted of measures of spontaneous motor activity, including locomotion/ambulation, rearing, and head dipping behaviors, and a parameter under which diverse behaviors were collected, total activity. Alterations to instrumental maze learning performance were studied through application of the spatial learning tasks: the radial arm maze and the circular swim maze. Possible changes in dopaminergic pathways were assessed by measuring the effects of perinatal treatments upon d-amphctamine- induced activity. It was shown that prenatal metallic mercury, organic tin and the neuroleptic compounds, haloperidol and remoxipride altered various parameters of spontaneous motor activity, retarded maze learning in the radial arm maze and potentiated d-amphetamine-induced activity. Metallic mercury rats were not subjected to the amphetamine test and remoxipride rats were not retarded according to the learning task. Postnatal metallic mercury, 6-OHDA, haloperidol and the antiemetic compound, metaclopramide, also altered spontaneous and d-amphetamine- induced activity as well as radial arm maze performance, excluding in this case haloperidol and metaclopramide. None of these treatments altered performance in the circular swim maze, except for 6-OHDA where doses inflicting severe depletions (greater than 85 % depletion compared to control values) caused notable impairments. One tentative conclusion from the pattern of behavioral changes, generally in the absence of any measurable neurochemical changes, observed after these treatments is that the functional development of dopaminergic systems had, to a greater or lesser degree, been altered.

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Dopamine in the rat ventral pallidum/substantia innominata: Biochemical and electrophysiological studies

Cited by 61 publications

References 11 publications

The Ventral Pallidum is Critically Involved in the Development and Expression of Morphine-Induced Sensitization

The Ventral Pallidum is Critically Involved in the Development and Expression of Morphine-Induced Sensitization

Alterations in Responses of Ventral Pallidal Neurons to Excitatory Amino Acids after Long-Term Dopamine Depletion

Functional Changes Implicating Dopaminergic Systems following Perinatal Treatments

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