The electrophysiology of dopamine (D2) receptors: A study of the actions of dopamine on corticostriatal transmission

Brown, John R.; Arbuthnott, G.W.

doi:10.1016/0306-4522(83)90138-0

Cited by 133 publications

(45 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

Section: Da Regulation Of Cortical-evoked Epsps In Nac Spiny Neurons supporting

confidence: 91%

“…Given numerous studies investigate the D2 presynaptic action, identification of the potential presynaptic mechanism was not the purpose of present study that was examining the DA modulation occurred via DARPP-32 cascades. Nevertheless, our data are consistent with a D2 presynaptic action on PFC afferent terminals in the rat NAC/striatal spiny neurons (Brown and Arbuthnott, 1983;O'Donnell and Grace, 1994;Cepeda et al 2001; Bamford et al., 2004).KO spiny neurons had resting membrane potentials and input resistance (−78.1 ± 1.5 mV; 72 ± 7.6 MΩ; n = 24) similar to those in WT spiny neurons (p = 0.45; p = 0.22, respectively). Cortical stimulation-evoked EPSPs in KO spiny neurons (n = 24, 25 ± 1.8 mV; Figure 2B ) were similar in amplitude to those observed in the WT (n = 30, 22 ± 2.8 mV; p < 0.2, Figure 2A ).…”

supporting

confidence: 90%

“…Author manuscript; available in PMC 2011 March 8. Sesack et al, 1994;Delle Donne et al, 1997;Filoux et al, 1988;Jansson et al, 1998) plays an important role in regulating cortico-striatal/accumbal glutamate transmission in spiny projection neurons (Brown and Arbuthnott, 1983;O'Donnell and Grace, 1994;Flores-Hernandez et al, 1997;Cepeda et al, 2001; Bamford et al, 2004). One molecule involved in dopamine (DA) transmission, DA and cyclic-AMP Regulated Phosphoprotein-32 (DARPP-32), exerts complex actions on DA-dependent modulation in limbic prefrontal corticoaccumbens circuits and is decreased in brains of schizophrenia patients (Albert et al, 2002).…”

mentioning

confidence: 99%

See 2 more Smart Citations

Dopamine and cyclic-AMP regulated phosphoprotein-32–dependent modulation of prefrontal cortical input and intercellular coupling in mouse accumbens spiny and aspiny neurons

et al. 2008

View full text Add to dashboard Cite

The roles of DARPP-32 in mediating dopamine (DA)-dependent modulation of corticoaccumbens transmission and intercellular coupling were examined in mouse accumbens (NAC) neurons by both intracellular sharp electrode and whole cell recordings. In wildtype (WT) mice bath application of the D2-like agonist quinpirole resulted in 73% coupling incidence in NAC spiny neurons, compared to baseline (9%), whereas quinpirole failed to affect the basal coupling (24%) in slices from DARPP-32 knockout (KO) mice. Thus, D2 stimulation attenuated DARPP-32-mediated suppression of coupling in WT spiny neurons, but this modulation was absent in KO mice. Further, whole cell recordings revealed that quinpirole reversibly decreased the amplitude of cortical-evoked EPSPs in spiny neurons of WT mice, but this reduction was markedly attenuated in KO mice. Bath application of the D1/D5 agonist SKF 38393 did not alter evoked EPSP amplitude in WT or KO spiny neurons. Therefore, DA D2 receptor regulation of both cortical synaptic (chemical) and local non-synaptic (dye coupling) communications in NAC spiny neurons is critically dependent on intracellular DARPP-32 cascades. Conversely, in fast-spiking interneurons, blockade of D1/D5 receptors produced a substantial decrease in EPSP amplitude in WT, but not in KO mice. Lastly, in putative cholinergic interneurons, cortical-evoked disynaptic IPSPs were attenuated by D2-like receptor stimulation in WT but not KO slices. These data indicate that DARPP-32 plays a central role in 1) modulating intercellular coupling, 2) cortical excitatory drive of spiny and aspiny GABAergic neurons, and 3) local feedforward inhibitory drive of cholinergic-like interneurons within accumbens circuits KeywordsExcitatory and inhibitory synaptic transmission; non-synaptic gap junction-mediated morphological coupling; DA D1 & D2 receptor; mouse accumbens neurons; whole cell recording; sharp-electrode recording Altered glutamate transmission from the prefrontal cortex (PFC) to the ventral striatum is often implicated in schizophrenia and drug addiction; disorders that involve dopamine (DA) dysfunctional states (Grace, 1991;2000;2001;Albert et al., 2002;Saal et al., 2003). DA acting on D2-like receptors present on prefrontal cortical terminals (Levey et Correspondence: Shao-Pii Onn, PhD, Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA 15260, Onn@bns.pitt.edu. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2011 March 8. Sesack et al., 1994;Delle Donne et al., 1997;Filoux et al., 1988;Jansson et al., 1998) plays an important role in regulating cortico-striatal/accumbal glutamate transmission in spiny projection neurons (Brown and Arbuthnott, 1983;O'Donnell and Grace, 1994;Flores-Hernandez et al., 1997;Cepeda et al., 2001; Bamford et al., 2004). One molecule involved in dopamine (DA) transmission, DA and cyclic-AMP Regulated Phosphoprotein-32 (DARPP-32), exerts complex actions on DA-dependent modulation in limbic prefrontal corticoaccumbens circuits and i...

show abstract

Section: Da Regulation Of Cortical-evoked Epsps In Nac Spiny Neurons supporting

confidence: 91%

supporting

confidence: 90%

mentioning

confidence: 99%

See 1 more Smart Citation

Dopamine and cyclic-AMP regulated phosphoprotein-32–dependent modulation of prefrontal cortical input and intercellular coupling in mouse accumbens spiny and aspiny neurons

et al. 2008

View full text Add to dashboard Cite

show abstract

“…8): (1) a loss of the inhibition exerted by DA on excitatory corticostriatal afferents. This may occur by a direct effect on D2 receptors located on corticostriatal neurons (Brown et al, 1983;Mercuri et al, 1985;Filloux et al, 1988). Alternatively, DA afferents synapse onto the shafts of dendritic spines, thereby inhibiting the glutamatergic input which arrives onto spine heads (Freund et al, 1984).…”

Section: Discussionmentioning

confidence: 99%

Effects of dopamine depletion on striatal neurotensin: biochemical and immunohistochemical studies

et al. 1989

View full text Add to dashboard Cite

Interactions between striatal dopamine (DA) and neurotensin (NT) have been suggested by anatomical, behavioral, and biochemical studies. Nigrostriatal DA neurons, in contrast to mesocotticolimbic DA neurons, do not appear to contain NT. Thus, distinct neuronal elements subserve interactions between DA and NT within the striatum. We have previously demonstrated that reserpine-induced depletion of striatal DA is accompanied by a dose-and time-dependent increase in striatal NT concentrations. In order to further characterize the effects of reserpine and to define the mechanism by which reserpine acts to increase striatal NT concentrations, we have used immunohistochemical and biochemical approaches. lmmunohistochemical examination of rats pretreated with reserpine revealed marked increases in the density of NT-like immunoreactive (NT-Ii) perikarya and fibers, and the development of NT-Ii patches. Pretreatment with reserpine had no apparent effect on NT synthesis, as assessed by examination of cycloheximide-induced inhibition of protein synthesis. However, reserpine administration resulted in a significant decrease in the release of both DA and NT into the striatal extracellular fluid, as measured by in viva microdialysis. These data suggest that the increase in striatal NT concentrations observed after reserpine treatment results from decreased release, rather than increased synthesis of the peptide.Neurotensin (NT) is a tridecapeptide originally isolated from bovine hypothalamus Leeman, 1973,1976) which is heterogeneously distributed through the CNS (Carraway and Leeman, 1976;Uhl et al., 1977;Jennes et al., 1982;Uhl, 1982). The demonstration that NT perikarya, fibers, and receptors exist within the striatum (Young and Kuhar, 198 1;Jennes et al., 1982;Uhl et al., 1982), a brain region known to contain high concentrations of dopamine (DA), has led to studies aimed at elucidating the possible interactions between these transmitters/ modulators in this brain region. Nigrostriatal DA system function is influenced by NT. For example, NT enhances both basal Received Feb. 10, 1989; revised Apr. 27, 1989; accepted June 1, 1989. This and stimulated DA release from striatal slices; these effects may be mediated by NT receptors localized to the terminals of dopaminergic axons (De Quidt and Emson, 1983;Quirion et al., 1985;Hetier et al., 1988). Striatal NT levels have been shown to be influenced by DA; dopamine receptor antagonists have been reported to alter striatal NT levels and distribution (Govoni et al., 1980;Goedert et al., 1985;Frey et al., 1986;Nemeroff, 1986;Letter et al., 1987; Eggerman and Zahm, 1988). We have recently demonstrated that reserpine, which depletes monoamines by disrupting their vesicular storage, produces a dose-and time-related increase in striatal NT concentrations (Bean et al., 1989). The influence of reserpine on striatal NT levels might be anticipated on the basis of a postulated tonic inhibitory influence of DA on striatal NT levels (Merchant et al., 1988a). The increase in striatal NT tiss...

show abstract

“…Corticostriatal, presumably glutamatergic, terminals contact the heads of spines that often receive DA synapses on their necks (Totterdell and Smith, 1989;Meredith and Wouterlood, 1990;Sesack and Pickel, 1990). Since the DA input appears to modulate the corticostriatal input (Brown and Arbuthnott, 1983;Pennartz et al, 1992a), its removal may produce excitotoxic conditions that result in spine loss. Certainly, small increases of glutamate underlie spine swelling and loss in hippocampal slices (Siman and Card, 1988).…”

Section: Potential Mechanisms Underlying Dendritic Remodelingmentioning

confidence: 99%

Effects of dopamine depletion on the morphology of medium spiny neurons in the shell and core of the rat nucleus accumbens

1995

View full text Add to dashboard Cite

Nucleus accumbens receives a dense dopaminergic innervation which is important in regulating motivated states of behavior such as goal- directed actions, stimulus-reward associations and reinforcement of addictive substances. The shell and core territories of this nucleus each receive functionally and morphologically distinct dopaminergic inputs and lesions of the ascending pathways totally deprive the core but not the shell of dopaminergic fibers. Medium spiny neurons are the principal targets of dopaminergic terminals. The present study explored whether the loss of dopamine inputs can affect these neurons and whether cells in the shell and core would be equally susceptible to such a loss. Intracellular injection in fixed slices and neuronal reconstruction were used to analyze the dendritic trees of 62 neurons in the shell and core of animals that received a unilateral, chronic 6- hydroxydopamine lesion of the medial forebrain bundle. In the dopamine- depleted core, dendrites are significantly shorter (16% decrease) than in the intact core and in both the dopamine-depleted core and lateral shell, dendrites are less spiny than in respective control regions. Dopamine loss in the medial shell is associated with significantly more tortuous dendrites that are lower in spine density. However, the number of spines is not reduced which may mean that the increase recorded for segment length, although insignificant in tests, could be responsible for the change in spine density. These data suggest that the loss of dopamine can affect accumbal neuronal morphology and, moreover, can affect neuronal structures differentially in the shell and core.

show abstract

The electrophysiology of dopamine (D2) receptors: A study of the actions of dopamine on corticostriatal transmission

Cited by 133 publications

References 31 publications

Dopamine and cyclic-AMP regulated phosphoprotein-32–dependent modulation of prefrontal cortical input and intercellular coupling in mouse accumbens spiny and aspiny neurons

Dopamine and cyclic-AMP regulated phosphoprotein-32–dependent modulation of prefrontal cortical input and intercellular coupling in mouse accumbens spiny and aspiny neurons

Effects of dopamine depletion on striatal neurotensin: biochemical and immunohistochemical studies

Effects of dopamine depletion on the morphology of medium spiny neurons in the shell and core of the rat nucleus accumbens

Contact Info

Product

Resources

About