Synergism between D1 and D2 dopamine receptors in the inhibition of the evoked release of [3H]GABA in the rat prefrontal cortex

Rétaux, Sylvie; Besson, Marie‐Jo; Penit-Soria, J.

doi:10.1016/0306-4522(91)90296-z

Cited by 59 publications

(25 citation statements)

References 35 publications

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“…The role of GABA interneurons in affecting the DA (via D4 receptor) inhibitory effect or in affecting the D4 receptor blockadeinduced repetitive spike discharge is supported by the following observations: (1) the absence of D4 antagonistinduced increase in response to afferent stimulation in slices superfused with buffer containing bicuculline or picrotoxin ( Figure 10a) and (2) activation of D2/D4 receptors by the D2/D4 receptor agonist (quinpirole) or upon washout of the D4 receptor antagonist consistently uncovered afferent-evoked IPSPs in identified pyramidal neurons (Figures 9 and 10b). Furthermore, the potentiation of previously subthreshold IPSPs by D2/D4 receptor activation (see Figures 9 and 10d) is consistent with a DA enhancement of GABA release (Retaux et al, 1991;Grobin and Deutch, 1998), although activation of D2/D4 receptors was recently reported to briefly decrease GABA release probability (Seamans et al, 2001b). However, the presence of a tonic inhibitory role of D2/D4 receptors in the prefrontal cortex reported here is consistent with the observed hyperexcitability present in pyramidal neurons of D4-deficient mice (Rubinstein et al, 2001).…”

Section: Discussionsupporting

confidence: 68%

“…(e) Bar graph summarizing the group data of normalized EPSP amplitude (ie early EPSP component) indicating no significant changes by quinpirole or D4 selective agonists (in the absence of bicuculline, BIC) or by D4 antagonist in the presence of BIC. Thus, quinpirole acting like the D4 agonist did not significantly affect monosynaptic unitary EPSPs (ie early EPSP component), but attenuating late polysynaptic EPSPs and spike discharge, probably via activation of GABA interneurons (Retaux et al, 1991;Grobin and Deutch, 1998), as IPSPs were frequently evoked in the pyramidal neuron recorded during bath application of D4 agonists or quinpirole.…”

Section: Discussionmentioning

confidence: 92%

“…Whole-cell recording studies have further revealed that DA activates D1 receptors to enhance NMDAmediated responses in both PFC and striatum (Cepeda et al, 1993;Cepeda and Levine, 1998;Zheng et al, 1999;Seamans et al, 2001a;Chen et al, 2003;Tseng and O'Donnell, 2004). On the other hand, the observed inhibitory action of DA (Gulledge and Jaffe, 1998) has been attributed to activation of GABA interneurons via D1 (Gorelova et al, 2002) or D2 receptor activation (Retaux et al, 1991;Grobin and Deutch, 1998). Evidence for an inhibitory action of D2-D4 receptors in the frontal cortex is derived from studies in which D4-deficient mice exhibit spontaneous hyperexcitability in PFC pyramidal neurons (Rubinstein et al, 2001); however, this could be due to enhanced expression of NMDA and D1 receptors in D4 knockout mice (Gan et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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Dopamine D1 and D4 Receptor Subtypes Differentially Modulate Recurrent Excitatory Synapses in Prefrontal Cortical Pyramidal Neurons

Onn

Wang

Lin

et al. 2005

Neuropsychopharmacol

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Although dopamine (DA) effects in the prefrontal cortex (PFC) have been studied extensively, the function of steady-state ambient levels of DA in the regulation of afferent excitatory transmission in PFC pyramidal neurons remains relatively unexplored. Using intracellular sharp-electrode and whole-cell recordings combined with intracellular labeling in brain slices, we found that D1/D5 receptor blockade did not alter synaptic responses in the PFC, but D1/D5 receptor activation consistently enhanced recurrent synaptic excitation in the majority of pyramidal neurons tested. In contrast, D4 receptor blockade resulted in an evoked complex multiple spike discharge pattern that contained both early and late (presumably multisynaptic) components of the evoked response that is contingent upon the preservation of axon collaterals of the neuron under study. Moreover, GABAergic interneurons were found to play a role in both responses; blockade of GABA a -mediated inhibition caused bath application of DA to convert monosynaptic excitatory postsynaptic potentials (EPSPs) to complex spike bursts riding on the late component of the EPSP. On the other hand, during the blockade of GABA amediated conductances, administration of a D4 receptor antagonist failed to facilitate evoked multiple spike discharge. Morphological analysis of axon collaterals of labeled neurons revealed that neurons in which the D4 receptor blockade induced the putative polysynaptic response had axon collaterals that were largely preserved. These data suggest that DA exerts a bidirectional modulation of PFC pyramidal neurons in brain slices provided that local network connections with interneurons are preserved, with D4 receptors under tonic stimulation by ambient low levels of DA, whereas D1/D5 receptors activated upon phasic DA input.

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Section: Discussionsupporting

confidence: 68%

Section: Discussionmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

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Dopamine D1 and D4 Receptor Subtypes Differentially Modulate Recurrent Excitatory Synapses in Prefrontal Cortical Pyramidal Neurons

Onn

Wang

Lin

et al. 2005

Neuropsychopharmacol

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“…If these findings were correct, they would suggest that dopaminergic afferents might be providing a non-adaptive hyperinnervation of a subpopulation of GABAergic interneurons, perhaps ones that are intrinsically impaired in schizophrenia. Since dopamine appears to exert an inhibitory effect on cortical GABA cells (Retaux et al 1991), these findings would predict that an excessive release of dopamine under conditions of stress (Thierry et al 1976;Roth et al 1988) could lead to an impairment of GABAergic function and ultimately to a decompensation of the intrinsic circuitry in layer II of anterior cingulate cortex (Benes 1997).…”

Section: Postmortem Evidence For a Gaba Defect In Schizophreniamentioning

confidence: 99%

GABAergic Interneurons Implications for Understanding Schizophrenia and Bipolar Disorder

Beneš

Berretta

2001

Neuropsychopharmacology

996

643

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Neurons that express the compound, ␥ -aminobutyric acid (GABA), are broadly present throughout the central nervous system, although telencephalic structures, such as the cerebral cortex, show the most abundant quantities of this neurotransmitter (Jones 1987). In the discussion that follows, the anatomy and physiology of various types of GABAergic interneurons in the cortex and hippocampus will be discussed and related to recent postmortem studies implicating this transmitter system in the pathophysiology of schizophrenia and bi- 25 , NO . 1 polar disorder and their treatment with neuroleptic drugs (for more comprehensive reviews on cortical and hippocampal neurons see: Hof et al. 1993;Freund and Buzsaki 1996;Somogyi et al. 1998). NEUROBIOLOGY OF GABAERGIC INTERNEURONSBased on Golgi-impregnation studies, Ramon y Cajal provided the first descriptions of several different morphological subtypes of interneurons in the cerebral cortex and hippocampus (Ramon y Cajal 1893, 1911. In more recent years, it has been shown that, with some overlap, different morphological subtypes also have distinct distributions, connectivity, neurochemistry, and electrophysiological properties (for reviews see Hof et al. 1993;Freund and Buzsaki 1996). It is interesting to note that every segment of a pyramidal neuron, such as the soma, dendritic branches and spines, and the initial axonal segment, receives dense GABAergic synaptic innervation (O'Kusky and Colonnier 1982;Hendry et al. 1983;Houser et al. 1983; Beaulieu et al. 1992; for reviews see Jones 1993;Freund and Buzsaki 1996). Even more interestingly, each of these segments appears to be innervated by distinct GABAergic neuronal subtypes (see below).These differences strongly suggest that each of these subtypes plays a fundamentally different role in physiological and pathological mechanisms. In the discussion that follows, cortical interneurons will be described first, since our most basic understanding of GABAergic cells is derived from these populations. In more recent years, however, similar characterizations of interneurons in hippocampus have emerged. Although these cells show some striking similarities to their cortical counterparts, there are also some unique features that distinguish them. For this reason, interneurons in the hippocampus are discussed separately. Cortex Neuroanatomical Studies of Cortical Interneurons.Various types of GABAergic neurons can be categorized according to the type of synaptic profiles they are associated with, as this has direct implications for understanding the physiological role of these cells in cortical circuits. These categories are discussed below.A XO -S OMATIC I NHIBITORY S YNAPSES (B ASKET C ELLS ). The most commonly encountered interneurons ( Figure 1A) are multipolar in shape, i.e., they may have three or more primary dendritic branches emanating from their cell bodies, some having somata that are as large as those of pyramidal neurons (Jones and Hendry 1984). Using immunocytochemistry to localize the enzyme ). These cells also ...

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“…Dopamine D1 and D2 receptors are located on parvalbumin containing interneurons located primarily in the deep cortical layers (Le Moine and Gaspar, 1998). The dopamine D2 receptor mediates dopamine induced alterations in GABAergic neurons (Retaux et al, 1991) and parvalbumin expression . The preponderance of the dopamine receptors in the deep cortical layers may account for the selective effect of dopaminergic modulation on parvalbumin expression in neurons of the deep cortical layers.…”

Section: '-'_4mentioning

confidence: 99%

The Effects of Dopamine and Estrogen upon Cortical Parvalbumin Expression

Ross¹

2001

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Physiology and Genetics, and the Neuroscience ProgramEstrogen plays a protective role in several neurologic disorders known to involve alterations in both the dopamine system and (gamma amino butyric acid containing) GABAergic neurons that contain parvalbumin. Two studies were conducted to identify the effects of estrogen and dopamine upon cortical parvalbumin expression. In the first study, organotypic slice cultures of the frontal cortex were prepared from male rats (postnatal age 2/3) and maintained for 14 days in serum-enriched medium or media containing either: dopamine, estrogen, or a combination of the two. In control slices, parvalbumin immunoreactive neurons were primarily clustered near cortical layer V. All treatment conditions increased the distribution of parvalbumin labeled neurons in layer VI and enhanced the maturation of dendritic measures of labeled neurons in the deep layers (V-VI). Both estrogen and the combination treatment induced similar alterations in the superficial cortical layers, as well. In the second study, gonadectomy (male rats, postnatal age 2) induced long lasting decreased in the density of parvalbumin immunoreactive neurons throughout all cortical layers. Estrogen replacement restored parvalbumin expression to control levels in the superficial cortical layers, only. Gonadectomy also Report Documentation PageForm Public reporting burden for the collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing the collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden, to Washington Headquarters Services, Directorate for Information Operations and Reports, 1215 Jefferson Davis Highway, Suite 1204, Arlington VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to a penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. Estrogen plays a protective role in several neurologic disorders known to involve alterations in both the dopamine system and (gamma amino butyric acid containing) GABAergic neurons that contain parvalbumin. Two studies were conducted to identify the effects of estrogen and dopamine upon cortical parvalbumin expression. In the first study, organotypic slice cultures of the frontal cortex were prepared from male rats (postnatal age 2/3) and maintained for 14 days in serum-enriched medium or media containing either: dopamine, estrogen, or a combination of the two. In control slices, parvalbumin immunoreactive neurons were primarily clustered near cortical layer V. All treatment conditions increased the distribution of parvalbumin labeled neurons in layer VI and enhanced the maturation of dendritic measures of labeled neurons in the deep layers (V-VI). Both estrog...

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Synergism between D1 and D2 dopamine receptors in the inhibition of the evoked release of [3H]GABA in the rat prefrontal cortex

Cited by 59 publications

References 35 publications

Dopamine D1 and D4 Receptor Subtypes Differentially Modulate Recurrent Excitatory Synapses in Prefrontal Cortical Pyramidal Neurons

Dopamine D1 and D4 Receptor Subtypes Differentially Modulate Recurrent Excitatory Synapses in Prefrontal Cortical Pyramidal Neurons

GABAergic Interneurons Implications for Understanding Schizophrenia and Bipolar Disorder

The Effects of Dopamine and Estrogen upon Cortical Parvalbumin Expression

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