Modifications in glutamatergic transmission after dopamine depletion of the nucleus accumbens. A combinedin vivo/in vitro electrophysiological study in the rat

Mulder, A. H.; Manshanden, Ilonka; Vos, Pieter E.; Wolterink, Gerrit; Ree, Jan M. van; Silva, F.H. Lopes Da

doi:10.1016/0306-4522(96)00035-8

Cited by 16 publications

(17 citation statements)

References 43 publications

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“…But a persistent depolarization alone may not always be sufficient or necessary for the observed effects. For example, Mulder et al (1996) saw profound changes in responses of nucleus accumbens neurons to iontophoretically applied glutamate in vivo despite finding no changes in intrinsic membrane properties (determined in vitro). It also is possible that alterations in the ability of VP neurons to process intracellular Ca 2ϩ may be relevant to the enhanced effects seen with EAA in the lesioned state.…”

Section: Da Depletion Enhances Effects Of Nmda In Vp 379mentioning

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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Section: Da Depletion Enhances Effects Of Nmda In Vp 379mentioning

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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“…Although dopamine is typically found to depolarize accumbens neurons (Uchimura et al, 1986;Yim and Mogenson, 1988;Grace, 1994, 1996;Goto and O'Donnell, 2001), these apparently excitatory effects are often accompanied by reduced excitability (O'Donnell and Grace, 1996) or a decrease in action potential firing Goto and O'Donnell, 2001). There is also some evidence that dopamine may exert a tonic inhibition on accumbens neurons (Mulder et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Dopaminergic Modulation of Prefrontal Cortical Input to Nucleus Accumbens NeuronsIn Vivo

Brady¹,

O’Donnell²

2004

J. Neurosci.

128

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Dopaminergic transmission in the nucleus accumbens has been proposed to modulate the effects of converging excitatory inputs from the cortex, hippocampus, and amygdala. Here, we used in vivo intracellular recording in anesthetized rats to examine the response of nucleus accumbens neurons to stimulation of the prefrontal cortex (PFC) and the ventral tegmental area (VTA). The EPSP elicited in accumbens neurons by PFC stimulation was attenuated by VTA train stimulation in a pattern mimicking dopamine cell burst firing. PFC-elicited EPSPs were smaller in amplitude and faster to decay after VTA stimulation. These changes could not be explained by membrane depolarization alone, because EPSPs evoked during the sustained depolarization after VTA stimulation were significantly smaller than EPSPs evoked during spontaneously occurring up states. Furthermore, no attenuation of PFC-elicited responses was observed during depolarization produced by positive current injection through the recording electrode. Administration of a D 1 antagonist (SCH 23390; 0.5 mg/kg, i.p.) had no effect on the VTA reduction of PFC-elicited responses, whereas administration of a D 2 antagonist (eticlopride; 0.5 mg/kg, i.p.) reversed the reduction of PFC inputs when the analysis was limited to comparisons with spontaneous up states. These results suggest that the ability of PFC inputs to drive accumbens neurons is dampened by dopamine acting primarily at D 2 receptors. Along with previous reports of dopaminergic attenuation of limbic afferents to the accumbens, these findings support the hypothesis that dopamine mediates the selection and integration of excitatory inputs and thus shapes information processing in accumbens output neurons.

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“…Stimulation of the fimbria, which is know to primarily contain efferents from the subiculum of the hippocampus, produces a characteristic field potential in the NAc, which has been electrophysiologically characterized (Boeijinga et al, , 1993Mulder et al, 1996;Hugues et al, 2003). The early (p10) component of the field potential represents monosynaptic activation (Boeijinga et al, 1993).…”

Section: Introductionmentioning

confidence: 99%

“…The NAc also receives a dense dopamine (DA) projection arising from the ventral tegmental area (VTA) (Oades and Halliday, 1987). By a complex mechanism, almost certainly involving DA, an important modulator of glutamatergic synapses, information from excitatory pathways is believed to be integrated at the level of the NAc (DeFrance et al, 1980;Yim and Mogenson, 1982;Mulder et al, 1996;Floresco et al, 2001;Brady and O'Donnell, 2004). It has been suggested that reduced excitatory neurotransmission of NAc afferents may modify the tonic level of DA release in the NAc producing a DA-hypersensitive state (Grace, 1991(Grace, , 2000.…”

Section: Introductionmentioning

confidence: 99%

Ketamine Induces Dopamine-Dependent Depression of Evoked Hippocampal Activity in the Nucleus Accumbens in Freely Moving Rats

Hunt¹,

Kessal²,

García³

2005

J. Neurosci.

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Modifications in glutamatergic transmission after dopamine depletion of the nucleus accumbens. A combinedin vivo/in vitro electrophysiological study in the rat

Cited by 16 publications

References 43 publications

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

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

Dopaminergic Modulation of Prefrontal Cortical Input to Nucleus Accumbens NeuronsIn Vivo

Ketamine Induces Dopamine-Dependent Depression of Evoked Hippocampal Activity in the Nucleus Accumbens in Freely Moving Rats

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