D<sub>1</sub>-Like Dopamine Receptor Activation Modulates GABAergic Inhibition But Not Electrical Coupling between Neocortical Fast-Spiking Interneurons

Towers, Stephen K.; Hestrin, Shaul

doi:10.1523/jneurosci.5079-07.2008

Cited by 48 publications

(25 citation statements)

References 71 publications

(96 reference statements)

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“…D1-like receptor stimulation decreases release of glutamate onto L5 pyramidal cells in PFC (Gao et al, 2001; Gao and Goldman-Rakic, 2003; Gonzalez-Islas and Hablitz, 2003; Seamans et al, 2001a) and SPNs in ventral striatum (Harvey and Lacey, 1997; Nicola and Malenka, 1997; Pennartz et al, 1992; Wang et al, 2012) but not dorsal striatum (Nicola and Malenka, 1998). Moreover, DA-mediated activation of D1-like receptors reduces GABA release onto cortical FS interneurons (Towers and Hestrin, 2008), L2–5 PFC pyramidal neurons (Gao et al, 2003; Gonzalez-Islas and Hablitz, 2001), and SPNs in ventral striatum only (Nicola and Malenka, 1997, 1998; Pennartz et al, 1992; Taverna et al, 2005). Thus, at synapses responsive to DA modulation, DA typically acts to decrease P release .…”

Section: Da Modulation Of Neurotransmitter Releasementioning

confidence: 99%

“…In striatum, D1 and D5 receptors respectively decrease and enhance GABA A receptor currents evoked by local application of GABA on the somata of acutely-dissociated SPNs (Flores-Hernandez et al, 2000) and cholinergic interneurons (Yan and Surmeier, 1997). Aside from these, most studies investigating DA modulation of synaptic GABAergic transmission either failed to detect changes in postsynaptic inhibitory currents or potentials, or assigned them to presynaptic modifications in GABA release or postsynaptic membrane properties in PFC (Gao et al, 2003; Gonzalez-Islas and Hablitz, 2001; Gulledge and Jaffe, 2001; Kroner et al, 2007; Towers and Hestrin, 2008; Zhou and Hablitz, 1999) and striatum (Bracci et al, 2002; Centonze et al, 2003; Delgado et al, 2000; Kohnomi et al, 2011; Nicola and Malenka, 1997, 1998; Pisani et al, 2000; Taverna et al, 2005; Tecuapetla et al, 2009). …”

Section: Da Modulation Of Postsynaptic Neurotransmitter Receptorsmentioning

confidence: 99%

“…This effect is largely attributed to PV-expressing FS basket and chandelier cells. Indeed, in vitro studies in PFC slices have repeatedly demonstrated that DA acting on D1-like receptors induces a direct membrane depolarization and increases the input resistance and excitability of the majority of FS interneurons (Gao and Goldman-Rakic, 2003; Gao et al, 2003; Gorelova et al, 2002; Kroner et al, 2007; Towers and Hestrin, 2008; Trantham-Davidson et al, 2008; Zhou and Hablitz, 1999), but exerts variable facilitatory effect on the excitability of other non-FS interneurons (Gao et al, 2003; Gorelova et al, 2002; Kroner et al, 2007). D2 receptor agonists have occasionally been reported to further promote interneuron excitability (Tseng and O’Donnell, 2004; Wu and Hablitz, 2005).…”

Section: Da Modulation Of Postsynaptic Excitability and Synaptic Intementioning

confidence: 99%

“…Indeed, bath application of GABA A receptor antagonists reverses the polarity of DA’s influence on pyramidal neuron excitability, from inhibition to facilitation (Gulledge and Jaffe, 2001; Zhou and Hablitz, 1999), stressing the importance of excluding synaptic contributions to investigate modulation of intrinsic excitability. In addition to these changes, DA alters the release of glutamate and GABA onto pyramidal and non-pyramidal neurons differentially based pre- and postsynaptic cell identity through D1- and D2-like receptors (Chiu et al, 2010; Gao et al, 2001; Gao and Goldman-Rakic, 2003; Gao et al, 2003; Gonzalez-Islas and Hablitz, 2001; Penit-Soria et al, 1987; Seamans et al, 2001b; Towers and Hestrin, 2008; Trantham-Davidson et al, 2004), revealing a rich and complex array of modulatory influences that collectively contribute to DA’s important role in PFC function.…”

Section: Da Modulation Of Postsynaptic Excitability and Synaptic Intementioning

confidence: 99%

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Dopaminergic Modulation of Synaptic Transmission in Cortex and Striatum

Tritsch

Sabatini

2012

Neuron

627

570

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Among the many neuromodulators used by the mammalian brain to regulate circuit function and plasticity, dopamine (DA) stands out as one of the most behaviorally powerful. For example, release of DA within nucleus accumbens signals reward and rapidly modifies brain function to drive repetition of motor action in search of further reward. The control that DA exerts over behavior is also clear in humans, as mimicry of dopaminergic reward signals underlies addiction to drugs of abuse, whereas death of midbrain dopaminergic neurons causes Parkinson’s disease (PD). In addition, perturbations of DA are implicated in the pathogenesis, or exploited in the treatment of many neuropsychiatric diseases including schizophrenia, obsessive compulsive disorder, and Tourette’s syndrome. Although the precise mechanisms employed by DA to exert its control over behavior are not fully understood, DA is known to regulate many electrical and biochemical aspects of neuronal function including excitability, synaptic transmission, integration and plasticity, protein trafficking and gene transcription. In this review, we discuss the actions of DA on ionic and synaptic signaling in neurons of the prefrontal cortex and striatum, brain areas in which dopaminergic dysfunction is thought to be central to the above-mentioned diseases. We focus on actions of DA on the pre- and postsynaptic terminals and restrict our discussion to studies in which the site of action or the molecular target of DA is clearly identified.

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Section: Da Modulation Of Neurotransmitter Releasementioning

confidence: 99%

Section: Da Modulation Of Postsynaptic Neurotransmitter Receptorsmentioning

confidence: 99%

Section: Da Modulation Of Postsynaptic Excitability and Synaptic Intementioning

confidence: 99%

Section: Da Modulation Of Postsynaptic Excitability and Synaptic Intementioning

confidence: 99%

See 2 more Smart Citations

Dopaminergic Modulation of Synaptic Transmission in Cortex and Striatum

Tritsch

Sabatini

2012

Neuron

627

570

View full text Add to dashboard Cite

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“…FS basket and chandelier cells seem to be the predominant target for DA regulation of prefrontal cortical GABAergic interneurons (Gao and Goldman-Rakic, 2003; Gao et al, 2003; Gorelova et al, 2002; Towers and Hestrin, 2008; Zhou and Hablitz, 1999). Transgenic mice expressing the Cre recombinase in specific interneuron populations have allowed researchers to begin to identify cortical circuit elements that modulate complex PFC-dependent behaviors (Perova et al, 2015).…”

Section: Ne and Da Modulation Of Synaptic Transmission In The Pfc mentioning

confidence: 99%

Norepinephrine versus dopamine and their interaction in modulating synaptic function in the prefrontal cortex

2016

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Among the neuromodulators that regulate prefrontal cortical circuit function, the catecholamine transmitters norepinephrine (NE) and dopamine (DA) stand out as powerful players in working memory and attention. Perturbation of either NE or DA signaling is implicated in the pathogenesis of several neuropsychiatric disorders, including attention deficit hyperactivity disorder (ADHD), post-traumatic stress disorder (PTSD), schizophrenia, and drug addiction. Although the precise mechanisms employed by NE and DA to cooperatively control prefrontal functions are not fully understood, emerging research indicates that both transmitters regulate electrical and biochemical aspects of neuronal function by modulating convergent ionic and synaptic signaling in the prefrontal cortex (PFC). This review summarizes previous studies that investigated the effects of both NE and DA on excitatory and inhibitory transmissions in the prefrontal cortical circuitry. Specifically, we focus on the functional interaction between NE and DA in prefrontal cortical local circuitry, synaptic integration, signaling pathways, and receptor properties. Although it is clear that both NE and DA innervate the PFC extensively and modulate synaptic function by activating distinctly different receptor subtypes and signaling pathways, it remains unclear how these two systems coordinate their actions to optimize PFC function for appropriate behavior. Throughout this review, we provide perspectives and highlight several critical topics for future studies.

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Orofacial movements in phospholipase C‐related catalytically inactive protein‐1/2 double knockout mice: Effect of the GABAergic agent diazepam and the D₁ dopamine receptor agonist SKF 83959

Tomiyama

Song

Kobayashi

et al. 2010

Synapse

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Orofacial movements are regulated by D(1)-like dopamine receptors interacting with additional mechanisms. Phospholipase C-related catalytically inactive protein (PRIP) regulates cell surface expression of GABA(A) receptors containing a gamma2 subunit. Mutant mice with double knockout of PRIP-1 and PRIP-2 were used to investigate aspects of GABAergic regulation of orofacial movements and interactions with D(1) mechanisms. Vertical jaw movements, tongue protrusions and movements of the head and vibrissae were reduced in PRIP-1/2 double knockouts. The GABA(A)ergic agent diazepam reduced movements of the head and vibrissae; these effects were unaltered in PRIP-1/2 double knockouts. The D(1)-like agonist SKF 83959 induced vertical jaw movements, incisor chattering, and movements of the head and vibrissae that were unaltered in PRIP-1/2 double knockouts. However, SKF 83959-induced tongue protrusions were reduced in PRIP-1/2 double knockouts. PRIP-mediated regulation of GABA(A)ergic receptor mechanisms influences topographically distinct aspects of orofacial movement and interacts with D(1) receptor systems.

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D₁-Like Dopamine Receptor Activation Modulates GABAergic Inhibition But Not Electrical Coupling between Neocortical Fast-Spiking Interneurons

Cited by 48 publications

References 71 publications

Dopaminergic Modulation of Synaptic Transmission in Cortex and Striatum

Dopaminergic Modulation of Synaptic Transmission in Cortex and Striatum

Norepinephrine versus dopamine and their interaction in modulating synaptic function in the prefrontal cortex

Orofacial movements in phospholipase C‐related catalytically inactive protein‐1/2 double knockout mice: Effect of the GABAergic agent diazepam and the D₁ dopamine receptor agonist SKF 83959

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D1-Like Dopamine Receptor Activation Modulates GABAergic Inhibition But Not Electrical Coupling between Neocortical Fast-Spiking Interneurons

Cited by 48 publications

References 71 publications

Dopaminergic Modulation of Synaptic Transmission in Cortex and Striatum

Dopaminergic Modulation of Synaptic Transmission in Cortex and Striatum

Norepinephrine versus dopamine and their interaction in modulating synaptic function in the prefrontal cortex

Orofacial movements in phospholipase C‐related catalytically inactive protein‐1/2 double knockout mice: Effect of the GABAergic agent diazepam and the D1 dopamine receptor agonist SKF 83959

Contact Info

Product

Resources

About

D₁-Like Dopamine Receptor Activation Modulates GABAergic Inhibition But Not Electrical Coupling between Neocortical Fast-Spiking Interneurons

Orofacial movements in phospholipase C‐related catalytically inactive protein‐1/2 double knockout mice: Effect of the GABAergic agent diazepam and the D₁ dopamine receptor agonist SKF 83959