Excitation of rat prefrontal cortical neurons by dopamine: An in vitro electrophysiological study

Penit-Soria, J.; Audinat, Etienne; Crépel, F.

doi:10.1016/0006-8993(87)90509-9

Cited by 189 publications

(111 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Bath application of dopamine at high concentrations (0.4 mm) in the presence of a dopamine uptake blocker increases bicuculline-sensitive IPSPs in pyramidal neurons sampled in layers III, V, and VI of rat PFC slices (Penit-Soria et al 1987). This suggests that dopamine activates GABAergic interneurons synapsing onto PFC pyramidal neurons.…”

Section: Dopamine Interaction With Gabaergic Interneurons In Pfcmentioning

confidence: 99%

“…If these PFC neurons were depolarized by intracellular injection of depolarizing current pulses (which mimicked a selective postsynaptic depolarization) or long depolarizing current ramps, a brief period of bath applications (30-90 s) of dopamine D1/5 agonists lowered the firing threshold of the first spike and reduced the first spike latency evoked by the depolarizing pulses (Penit-Soria et al 1987;Yang and Seamans 1996; Gorelova and Yang, submitted) (Figure 2). These responses were similar, whether the recordings were made at room (whole cell patch-clamp recordings at 23 Њ C) or at a more phyisological temperature (intra-N EUROPSYCHOPHARMACOLOGY 1999 -VOL .…”

Section: Ionic Bases Of Direct Dopamine Actions On Pyramidal Neurons mentioning

confidence: 99%

“…In another PFC slice study, 1 to 5 minutes of application of dopamine in the presence of ascorbic acid (as antioxidant), induced a dosedependent small membrane depolarization (0.5 to 5 mV) that cannot be blocked by D1, D2, D4, alpha-, and beta-adrenergic antagonists . Therefore, dopamine does not exert a consistent action on inactive PFC neurons, which displayed little or no spontaneous activity in vitro (because of the removal of their excitatory afferents from the brain slice preparation procedures).If these PFC neurons were depolarized by intracellular injection of depolarizing current pulses (which mimicked a selective postsynaptic depolarization) or long depolarizing current ramps, a brief period of bath applications (30-90 s) of dopamine D1/5 agonists lowered the firing threshold of the first spike and reduced the first spike latency evoked by the depolarizing pulses (Penit-Soria et al 1987;Yang and Seamans 1996; Gorelova and Yang, submitted) (Figure 2). These responses were similar, whether the recordings were made at room (whole cell patch-clamp recordings at 23 Њ C) or at a more phyisological temperature (intra-N EUROPSYCHOPHARMACOLOGY 1999 -VOL .…”

mentioning

confidence: 99%

See 2 more Smart Citations

Developing a Neuronal Model for the Pathophysiology of Schizophrenia Based on the Nature of Electrophysiological Actions of Dopamine in the Prefrontal Cortex

Yang

Seamans

Gorelova

1999

Neuropsychopharmacology

164

View full text Add to dashboard Cite

This review covers some recent findings of the electrophysiological mechanisms through which mesocortical dopamine modulates prefrontal cortical neurons. Dopamine has been shown to modulate several ionic conductances located along the soma-dendritic axis of prefrontal cortical pyramidal neurons. These ionic currents include high-voltage-activated calcium currents and slowly inactivating NaReceived May 12, 1998; revised May 27, 1998; accepted May 29, 1998. 162 C.R. Yang et al. N EUROPSYCHOPHARMACOLOGY 1999 -VOL . 21 , NO Schizophrenia strikes one in one hundred people worldwide, regardless of cultural or racial origins. As the illness progresses and if it remains unattended, patients are frequently trapped in psychological, social, and economic devastation (Gottesman 1991;Jablensky 1995). Currently, our incomplete understanding of the neurobiological bases of schizophrenia suggests that defects in the genetic controls of brain development in such limbic regions (including temporal lobe structures such as hippocampus and the amygdala) as well as the prefrontal cortex (PFC) lead to cell loss or deformation, cytoarchitectural disorganization, and abnormal innervation in these brain regions (Roberts and Bruton 1990;Stevens 1992; Bogerts 1993;Shapiro 1993; Akbarian et al. 1993 Akbarian et al. , 1996Ross and Pearlson 1996;Weinberger 1996; Karayiorgou and Gogos 1997; Lewis 1997;Selemon et al. 1995Selemon et al. , 1998.Some results from recent imaging studies of brains from living schizophrenics have suggested that there are defective functional communications between the interconnected cortical (PFC and cingulate cortex) and limbic subcortical structures (thalamus, striatum, and temporal lobe limbic structures)(see reviews of Liddle 1996; Pfefferbaum and Marsh 1995; Andreasen 1997; Heckers et al. 1998). Findings from these studies suggest that in schizophrenics, abnormal recruitment of several interconnected cortical and subcortical structures may underlie such symptom clusters as psychomotor poverty, thought disorganization, and reality distortion (Liddle et al. 1992; Liddle 1996; Fletcher 1998; Heckers et al. 1998).As noted in Figure 1, the PFC receives converging limbic, association cortical, and mesocortical dopamine inputs. These inputs interact in the PFC and are involved functionally in high-level cognitive processes (Fuster 1995). Among the many brain regions that PFC output innervates, two important subcortical regions are emphasized in this review. These are the nucleus accumbens (where mesoaccumbens dopamine neurons terminate) and the ventral tegmental area (VTA, where the midbrain dopamine neurons reside) Groenewegen et al. 1990; Berendse et al. 1992a Berendse et al. , 1992bSesack and Pickel 1992;Gorelova and Yang 1997b). Several of the interconnected limbic, cortical, and subcortical structures known to be affected in schizophrenia are targets of the ascending midbrain dopamine systems that normally provide functional modulation of neurotransmission (Björklund and Lindvall 1984;Mogenson et ...

show abstract

Section: Dopamine Interaction With Gabaergic Interneurons In Pfcmentioning

confidence: 99%

Section: Ionic Bases Of Direct Dopamine Actions On Pyramidal Neurons mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Developing a Neuronal Model for the Pathophysiology of Schizophrenia Based on the Nature of Electrophysiological Actions of Dopamine in the Prefrontal Cortex

Yang

Seamans

Gorelova

1999

Neuropsychopharmacology

164

View full text Add to dashboard Cite

show abstract

“…Most in vitro studies have consistently demonstrated a facilitatory action of D1 receptor activation on membrane excitability (Penit-Soria et al, 1987;Yang and Seamans, 1996;Shi et al, 1997;Henze et al, 2000;Wang and O'Donnell, 2001). 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).…”

Section: Introductionmentioning

confidence: 99%

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

Onn

Wang

Lin

et al. 2005

Neuropsychopharmacol

View full text Add to dashboard Cite

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.

show abstract

“…Several studies have also indicated a close relationship between GABA and dopamine, involved in the precipitation of schizophrenia. Dopamine mediates the modulation of GABAergic neurotransmission in those brain regions, including nucleus accumbens and ventral tegmental area, involved in schizophrenia (Penit-Soria et al, 1987;Pennartz et al, 1992;Pirot et al, 1992;Pralong and Jones, 1993;Cameron and Williams, 1993;Law-Tho et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Role of Neuroactive Steroid Allopregnanolone in Antipsychotic-like Action of Olanzapine in Rodents

Ugale

Hirani

Morelli

et al. 2004

Neuropsychopharmacol

View full text Add to dashboard Cite

Olanzapine increases brain allopregnanolone (ALLO) levels sufficiently to modulate neuronal activity by allosterically regulating GABA A receptors. Recently, we reported the antipsychotic-like profile of ALLO in rodents. The present study examined the hypothesis that olanzapine-induced elevation of endogenous neurosteroid ALLO is vital for its neuroleptic-like action. The conditioned avoidance response (CAR) and apomorphine-induced climbing behavioral paradigms were used in rodents. Administration of ALLO (1 mg, intracerebroventricular (i.c.v.)) or neurosteroidogenic agents such as the mitochondrial diazepam binding inhibitor receptor agonist, FGIN 1-27 (0.5 mg, i.c.v.) or the ALLO precursor, progesterone (10 mg/kg, i.p.) significantly potentiated olanzapine-induced blockade of CAR and apomorphine-induced climbing. In contrast, these agents failed to alter the antipsychotic-like effect of risperidone and haloperidol. On the other hand, inhibition of the endogenous biosynthesis of neurosteroids by the 3b-hydroxysteroid dehydrogenase inhibitor, trilostane (30 mg/kg, i.p.), the 3a-hydroxysteroid oxidoreductase inhibitor, indomethacin (5 mg/kg, i.p.), or the GABA A receptor antagonist bicuculline (1 mg/kg, i.p.) and dehydroepiandrosterone sulfate (DHEAS) (1 mg/kg, i.p.) blocked the effect of olanzapine, but not of risperidone and haloperidol. Socially isolated animals, known to exhibit decreased brain ALLO and GABA A receptor functions, displayed a shortening in the muscimol-induced loss of righting reflex and an increased susceptibility to apomorphine-induced climbing. Administration of olanzapine, but not of haloperidol and risperidone, normalized the duration of muscimol-elicited loss of righting reflex. Although all three antipsychotics proved capable of antagonizing the apomorphine-induced climbing, a dose almost five times higher of olanzapine was required in socially isolated animals. The data obtained suggest that enhancement of the GABAergic tone plays a key role in the antipsychotic-like effect exerted by olanzapine in rodents, likely as a consequence of augmented levels of neuroactive steroids, in particular ALLO, in the brain. The present findings provide the first specific behavioral evidence in support of the hypothesis that neuroactive steroid ALLO-mediated GABAergic modulation is essential for the antipsychotic-like action of olanzapine.

show abstract

Excitation of rat prefrontal cortical neurons by dopamine: An in vitro electrophysiological study

Cited by 189 publications

References 22 publications

Developing a Neuronal Model for the Pathophysiology of Schizophrenia Based on the Nature of Electrophysiological Actions of Dopamine in the Prefrontal Cortex

Developing a Neuronal Model for the Pathophysiology of Schizophrenia Based on the Nature of Electrophysiological Actions of Dopamine in the Prefrontal Cortex

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

Role of Neuroactive Steroid Allopregnanolone in Antipsychotic-like Action of Olanzapine in Rodents

Contact Info

Product

Resources

About