Mediodorsal thalamic evoked responses in the rat prefrontal cortex

Pirot, Sylvain; Głowiński, J.; Thierry, Anne‐Marie

doi:10.1097/00001756-199605310-00023

Cited by 35 publications

(17 citation statements)

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“…The existence of glutamatergic thalamocortical pathways has been previously reported (Greengard et al, 1991;Kirkwood et al, 1993;Hedberg and Stanton, 1995;Wei et al, 1999). Findings from several electrophysiological studies indicate that these thalamic inputs are the primary source of glutamatergic input to cingulate neurons (Greengard et al, 1991;Gigg et al, 1992;Kirkwood et al, 1993;Hedberg and Stanton, 1995;Pirot et al, 1996;Wei et al, 1999;Gemmell and O'Mara, 2002;Kung and Shyu, 2002). EPSPs and action potentials in cingulate pyramidal neurons were blocked by CNQX and APV in our previous in vitro study, indicating that both AMPA/kainate and NMDA receptors mediate the thalamic excitation of ACC neurons (Lee et al, 2007).…”

Section: Discussionsupporting

confidence: 59%

“…Nociceptive-specific neurons in layers V and VI of the ACC were demonstrated in several studies (Sikes and DeFrance, 1985;Yamamura et al, 1996;Tsai et al, 2004). Subsequent sink currents in deeper layers have a longer latency, indicating a polysynaptic connection, possibly from layer VI neurons that have axon collaterals that terminate on layer V neurons (Branchereau et al, 1996;Pirot et al, 1996). This recurrent excitation may contribute to the late deep-layer sink current, resulting in long-duration recurrent excitation in cingulate neurons.…”

Section: Discussionmentioning

confidence: 95%

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Temporal and spatial dynamics of thalamus-evoked activity in the anterior cingulate cortex

2012

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Section: Discussionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 95%

Temporal and spatial dynamics of thalamus-evoked activity in the anterior cingulate cortex

2012

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“…This differential modulation was an intrinsic property of the voltage dependencies and kinetic properties of the conductances affected by DA and thus was related to the stability-enhancing effect of DA. There is some indirect evidence for this hypothesis: Sawaguchi et al (1988Sawaguchi et al ( , 1990a found that DA strongly increases task-related activity in PFC neurons during working memory, whereas, in contrast, other researchers (Ferron et al 1984;Godbout et al 1991;Mantz et al 1988;Pirot et al 1992Pirot et al , 1996 found that stimulation of the ventral tegmental area or local DA application in the PFC caused a transient suppression of activity in anesthetized animals outside a behavioral context. Thus the observations in the latter studies might correspond to the suppression of spontaneous activity that occurred in the network model in the high DA condition.…”

Section: Experimental Predictions Of the Modelmentioning

confidence: 98%

Dopamine-Mediated Stabilization of Delay-Period Activity in a Network Model of Prefrontal Cortex

Durstewitz

Seamans

Sejnowski

2000

Journal of Neurophysiology

555

412

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jnowski. Dopamine-mediated stabilization of delay-period activity in a network model of prefrontal cortex. J. Neurophysiol. 83: 1733Neurophysiol. 83: -1750Neurophysiol. 83: , 2000. The prefrontal cortex (PFC) is critically involved in working memory, which underlies memory-guided, goal-directed behavior. During working-memory tasks, PFC neurons exhibit sustained elevated activity, which may reflect the active holding of goal-related information or the preparation of forthcoming actions. Dopamine via the D1 receptor strongly modulates both this sustained (delay-period) activity and behavioral performance in working-memory tasks. However, the function of dopamine during delay-period activity and the underlying neural mechanisms are only poorly understood. Recently we proposed that dopamine might stabilize active neural representations in PFC circuits during tasks involving working memory and render them robust against interfering stimuli and noise. To further test this idea and to examine the dopamine-modulated ionic currents that could give rise to increased stability of neural representations, we developed a network model of the PFC consisting of multicompartment neurons equipped with Hodgkin-Huxley-like channel kinetics that could reproduce in vitro whole cell and in vivo recordings from PFC neurons. Dopaminergic effects on intrinsic ionic and synaptic conductances were implemented in the model based on in vitro data. Simulated dopamine strongly enhanced high, delay-type activity but not low, spontaneous activity in the model network. Furthermore the strength of an afferent stimulation needed to disrupt delay-type activity increased with the magnitude of the dopamine-induced shifts in network parameters, making the currently active representation much more stable. Stability could be increased by dopamine-induced enhancements of the persistent Na ϩ and N-methyl-D-aspartate (NMDA) conductances. Stability also was enhanced by a reduction in AMPA conductances. The increase in GABA A conductances that occurs after stimulation of dopaminergic D1 receptors was necessary in this context to prevent uncontrolled, spontaneous switches into high-activity states (i.e., spontaneous activation of task-irrelevant representations).In conclusion, the dopamine-induced changes in the biophysical properties of intrinsic ionic and synaptic conductances conjointly acted to highly increase stability of activated representations in PFC networks and at the same time retain control over network behavior and thus preserve its ability to adequately respond to task-related stimuli. Predictions of the model can be tested in vivo by locally applying specific D1 receptor, NMDA, or GABA A antagonists while recording from PFC neurons in delayed reaction-type tasks with interfering stimuli.

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“…The modulatory interactions of dopamine with other transmitters has also been the subject of intense investigation. Dopamine applied iontophoretically or released by VTA stimulation, suppressed spontaneous, as well as presumed glutamate-mediated (Pirot et al 1994) mediodorsal thalamic-evoked firing in the rat PFC in vivo (Bunney and Aghajanian 1976; Ferron et al 1984;Godbout et al 1991;Pirot et al 1994Pirot et al , 1996Yang and Mogenson 1990). In contrast, PFC neuronal firing induced by iontophoretic application of acetylcholine or NMDA is enhanced by very low doses of iontophoretically applied dopamine (Cépeda et al 1992a;Yang and Mogenson 1990).…”

Section: Electrophysiological Actions Of Dopamine On Pfc Neuronsmentioning

confidence: 99%

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

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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 ...

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Mediodorsal thalamic evoked responses in the rat prefrontal cortex

Cited by 35 publications

References 0 publications

Temporal and spatial dynamics of thalamus-evoked activity in the anterior cingulate cortex

Temporal and spatial dynamics of thalamus-evoked activity in the anterior cingulate cortex

Dopamine-Mediated Stabilization of Delay-Period Activity in a Network Model of Prefrontal Cortex

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

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