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A M Thierry

Publications and source records attributed to A M Thierry.

At least 19 recordsLinked to original sources

Dendritic arborizations of the rat substantia nigra pars reticulata neurons: spatial organization and relation to the lamellar compartmentation of striato-nigral projections.

The cerebral cortex provides a major source of inputs to the basal ganglia. As has been well documented, the topography of corticostriatal projections subdivides the striatum into a mosaic of functionally distinct sectors. How information flow from these striatal sectors remains segregated or not within basal ganglia output nuclei has to be established. Electrophysiologically identified neurons of the rat substantia nigra pars reticulata were labeled by juxtacellular injection of Neurobiotin, and the spatial organization of their dendritic arborizations was analyzed in relation to the projection fields of individual striatal sectors. Thirty-nine nigral neurons located in the projection territory of the distinct striatal sensorimotor sectors were reconstructed. The data show that the dendritic arborizations of nigral neurons conform to the geometry of striato-nigral projections. Like striatal projections, the arborizations formed a series of curved laminas enveloping a dorsolaterally located core. Although dendritic fields of the neurons lying in the laminae were flat, those located in the core were spherical or cylindrical, thereby conforming to the shape of the striatal projection fields. This remarkable alignment between the dendritic arborizations of nigral neurons and the projection fields from individual striatal districts supports the concept of a parallel architecture of the striato-nigral circuits. However, pars reticulata neurons usually extend part of their dendrites within adjacent striatal projection fields, thereby ensuring a continuum between channels. The extension of the dendritic arborizations within the striatal projection fields suggests that nigral neurons integrate the information that is relevant for the completion of the specific motor behavior they control.

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Segregation and convergence of information flow through the cortico-subthalamic pathways.

Cortico-basal ganglia circuits are organized in parallel channels. Information flow from functionally distinct cortical areas remains segregated within the striatum and through its direct projections to basal ganglia output structures. Whether such a segregation is maintained in trans-subthalamic circuits is still questioned. The effects of electrical stimulation of prefrontal, motor, and auditory cortex were analyzed in the subthalamic nucleus as well as in the striatum of anesthetized rats. In the striatum, cells (n = 300) presenting an excitatory response to stimulation of these cortical areas were located in distinct striatal territories, and none of the cells responded to two cortical stimulation sites. In the subthalamic nucleus, both prefrontal and motor cortex stimulations induced early and late excitatory responses as a result of activation of the direct cortico-subthalamic pathway and of the indirect cortico-striato-pallido-subthalamic pathway, respectively. Stimulation of the auditory cortex, which does not send direct projection to the subthalamic nucleus, induced only late excitatory responses. Among the subthalamic responding cells (n = 441), a few received both prefrontal and motor cortex (n = 19) or prefrontal and auditory cortex (n = 10) excitatory inputs, whereas a larger number of cells were activated from both motor and auditory cortices (n = 48). The data indicate that the segregation of cortical information flow originating from prefrontal, motor, and auditory cortices that occurred in the striatum is only partly maintained in the subthalamic nucleus. It can be proposed that the existence of specific patterns of convergence of information flow from these functionally distinct cortical areas in the subthalamic nucleus allows interactions between parallel channels.

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Hippocampo-prefrontal cortex pathway: anatomical and electrophysiological characteristics.

The hippocampus, the prefrontal cortex, and interconnected neural circuits are implicated in several aspects of cognitive and memory processes. The present review is dedicated to the description of the anatomo-functional characteristics of the hippocampo-prefrontal pathway and related neuronal circuits in the rat. This pathway, which originates from the hippocampal CA1/subiculum fields, innervates the prelimbic/medial orbital areas of the prefrontal cortex (PL/MO). Its synaptic influence on cortical pyramidal neurons consists in an early monosynaptic excitation followed by an inhibition and, in some cases, a late excitation. These later effects are likely due to the subsequent activation of the local cortical network. PL/MO areas and the CA1/subiculum both send projections to the nucleus accumbens, a region of the ventral striatum which is particularly implicated in goal-directed behavior. Therefore, emphasis is placed on respective projections from PL/MO areas and from the CA1/subiculum on the "core" and the "shell" regions of the nucleus accumbens, as well as on their interconnected circuits. Signals which are directed to the prefrontal cortex through these circuits might modulate hippocampo-prefrontal inputs. Finally, the direct and/or indirect relationships of the hippocampus, prefrontal cortex, and nucleus accumbens with the ventral tegmental area/substantia nigra pars compacta complex (VTA/SNC) (where dopamine neurons are located) will also be described, because these neurons are known to modulate synaptic transmission and plasticity in their target structures and to play a fundamental role in motivational processes.

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Relationships between the prefrontal cortex and the basal ganglia in the rat: physiology of the cortico-nigral circuits.

The prelimbic/medial orbital areas (PL/MO) of the rat prefrontal cortex are connected to substantia nigra pars reticulata (SNR) through three main circuits: a direct nucleus accumbens (NAcc)-SNR pathway, an indirect NAcc-SNR pathway involving the ventral pallidum (VP) and the subthalamic nucleus (STN), and a disynaptic cortico-STN-SNR pathway. The present study was undertaken to characterize the effect of PL/MO stimulation on SNR cells and to determine the contribution of these different pathways. The major pattern of responses observed in the SNR was an inhibition preceded by an early excitation and followed or not by a late excitation. The inhibition resulted from the activation of the direct NAcc-SNR pathway because it disappeared after acute blockade of the glutamatergic cortico-striatal transmission by CNQX application into the NAcc. The late excitation resulted from the activation of the indirect NAcc-VP-STN-SNR pathway via a disinhibition of the STN because it disappeared after either CNQX application into the NAcc or blockade of the GABAergic striato-pallidal transmission by bicuculline application into the VP. The early excitation, which was markedly decreased after blockade of the cortico-STN transmission by CNQX application into the STN, resulted from the activation of the disynaptic cortico-STN-SNR pathway. Finally, the blockade of the cortico-STN-VP circuit by CNQX application into STN or VP modified the influence of the trans-striatal circuits on SNR cells. This study suggests that, in the prefrontal cortex-basal ganglia circuits, the trans-subthalamic pathways, by their excitatory effects, participate in the shaping of the inhibitory influence of the direct striato-nigral pathway on SNR neurons.

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Effect of a functional impairment of corticostriatal transmission on cortically evoked expression of c-Fos and zif 268 in the rat basal ganglia.

The activity-dependent induction of immediate-early genes is commonly used to map activated neuronal networks. In a previous analysis of the cortico-basal ganglia circuits, we have shown that a cortical stimulation produces Fos protein expression in the striatum and the subthalamic nucleus, with a pattern which conforms to the anatomical organization of cortical projections [Sgambato V. et al. (1996) Neuroscience 81, 93-112]. In the present study, we examined the effects of a unilateral blockade of the corticostriatal transmission on c-fos and zif 268 messenger RNA expression evoked in the substantia nigra pars reticulata and the subthalamic nucleus following stimulation of the ipsilateral motor cortex. The blockade of the corticostriatal pathway was performed either by an excitotoxic striatal lesion or by an application of the AMPA/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione within the striatum. After application of the glutamate receptor antagonist, which prevented the cortical stimulation activating the GABAergic striatonigral pathway, the induction of both c-fos and zif 268 messenger RNAs was facilitated in the ipsilateral substantia nigra pars reticulata. In the subthalamic nucleus ipsilateral to the application of 6-cyano7-nitroquinoxaline-2,3-dione, the cellular discharges evoked by stimulation of the cortex were considerably shortened as a result of the blockade of the disinhibitory striato-pallido-subthalamic circuit. However, a strong expression of immediate-early genes was still induced by the cortical stimulation. By contrast, after unilateral kainate lesion of the striatum, the cortical stimulation was no longer able to induce c-fos and zif 268 messenger RNA expression in the ipsilateral subthalamic nucleus and in the substantia nigra pars reticulata bilaterally. The lack of immediate-early gene induction strongly contrasted with the neuronal discharges evoked in these nuclei by the cortical stimulation. Comparison between the cortically evoked neuronal activities and the pattern of immediate-early gene expression suggests that the induction of immediate-early genes in the basal ganglia mainly reflects the level of synaptic activity rather than the frequency of discharge of the postsynaptic neurons. Moreover, the results stress that modifications of immediate-early gene expression observed in the basal ganglia after an acute or a chronic interruption of the corticostriatal transmission are not superimposable.

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Nicotinic receptors in the rat prefrontal cortex: increase in glutamate release and facilitation of mediodorsal thalamo-cortical transmission.

The modulatory influence of nicotinic acetylcholine receptor (nAChRs) on thalamocortical transmission was characterized in the prelimbic area (PrL) of the rat prefrontal cortex. In the first experiment, rats received a unilateral excitotoxic lesion centred on the mediodorsal thalamic nucleus (MD), and were sacrificed 1 week later. The lesion resulted in a 40% reduction of 3H-nicotine autoradiographic labelling in the ipsilateral prefrontal cortex, particularly in areas that are innervated by the MD. Electrophysiological experiments were subsequently performed in non-lesioned anaesthetized animals, in order to study modulation of short- and long-latency responses of PrL neurons evoked by electrical stimulation of the MD. The short-latency responses result from activation of the MD-PrL pathway and are mediated via AMPA-type glutamatergic receptors, whereas the long-latency responses reflect activation of the recurrent collaterals of cortical pyramidal neurons, Iontophoretic application of nicotinic agonists (nicotine, DMPP) facilitated both types of response. Local application of the nAChR antagonists dihydro-beta-erythroidine, mecamylamine and methyllycaconitine, prevented both kinds of facilitation. Finally, intracerebral microdialysis experiments were performed in order to test for nicotinic modulation of extracellular glutamate concentrations in the PrL. Direct application of nicotine via the dialysis probe increased glutamate levels in a dose-dependent manner. This effect was blocked by local perfusion of dihydro-beta-erythroidine. These findings therefore provide anatomical and functional evidence for nAChR-mediated modulation of thalamocortical input to the prefrontal cortex. Such a mechanism may be relevant to the cognitive effects of nicotine and nicotinic antagonists.

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Relationships between the prefrontal cortex and the basal ganglia in the rat: physiology of the corticosubthalamic circuits.

The prelimbic-medial orbital areas (PL/MO) of the prefrontal cortex are connected to the medial part of the subthalamic nucleus (STN) through a direct projection and an indirect circuit that involves the core of the nucleus accumbens (NAcc) and the ventral pallidum (VP). In the present study, the influence of the PL/MO on the discharge of STN cells has been characterized. The major pattern of the responses observed after stimulation of PL/MO consisted of two excitatory peaks often separated by a brief inhibitory period. The early excitation was most likely to be caused by the activation of direct cortical inputs because its latency matches the conduction time of the prefrontal STN projections. The late excitation resulted from the activation of the indirect PL/MO-STN pathway that operates through a disinhibitory process. Indeed, the late excitation was no longer observed after acute blockade of the glutamatergic corticostriatal transmission by CNQX application into the NAcc. A similar effect was obtained after the blockade of the GABAergic striatopallidal transmission by bicuculline application into the VP. Finally, the brief inhibition that followed the early excitation was likely to result from the activation of a feedback inhibitory loop through VP because this inhibition was no longer observed after the blockade of STN inputs by CNQX application into the VP. This study further indicates the implication of STN in prefrontal basal ganglia circuits and underlines that in addition to a direct excitatory input, medial STN receives an indirect excitatory influence from PL/MO through an NAcc-VP-STN disinhibitory circuit.

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Prefrontal cortex-basal ganglia circuits in the rat: involvement of ventral pallidum and subthalamic nucleus.

The core of the nucleus accumbens (NAcc core) is the principal input structure to the basal ganglia circuitry for the prelimbic and medial orbital areas (PL/MO) of the prefrontal cortex. As is now well recognized in the rat, the main basal ganglia output of this prefrontal channel is the dorsomedial part of the substantia nigra pars reticulata (SNR) and not the ventral pallidum as previously suggested. There is evidence suggesting that the ventral pallidum is rather involved with the subthalamic nucleus (STN) in an indirect NAcc-SNR pathway. Indeed, we have recently shown that the NAcc core sends an inhibitory input to the lateral ventral pallidum (VPl), which projects to the medial STN. In the present study, we injected biocytin into the medial STN, at a site where neurons presented an inhibitory response to VPl stimulation. This produced anterogradely labelled fibres in the medial SNR and in the VPl. Furthermore, the stimulation of the VPl induced an inhibition in a majority of the STN cells identified, by the antidromic activation method, as projecting to SNR (76.6%) and/or back to the VPl (72.7%). In conclusion, these data further demonstrate the existence of an indirect striato-nigral pathway in the PL/MO channel and indicate that VPl is involved in an inhibitory feedback circuit, which modulates the discharge of medial STN. These results indicate that the medial STN is implicated in the limbic/cognitive functions of the basal ganglia.

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Alpha1-adrenergic, D1, and D2 receptors interactions in the prefrontal cortex: implications for the modality of action of different types of neuroleptics.

The activation of rat mesocortical dopaminergic (DA) neurons evoked by the electrical stimulation of the ventral tegmental area (VTA) induces a marked inhibition of the spontaneous activity of prefrontocortical cells. In the present study, it was first shown that systemic administration of either clozapine (a mixed antagonist of D1, D2, and alpha1-adrenergic receptors) (3-5 mg/kg, i.v.), prazosin (an alpha1-adrenergic antagonist) (0.2 mg/kg, i.v.), or sulpiride (a D2 antagonist) (30 mg/kg, i.v.), but not SCH 23390 (a D1 antagonist) (0.2 mg/kg, i.v.), reversed this cortical inhibition. Second, it was found that following the systemic administration of prazosin, the VTA-induced cortical inhibition reappeared when either SCH 23390 or sulpiride was applied by iontophoresis into the prefrontal cortex. Third, it was seen that, whereas haloperidol (0.2 mg/kg, i.v.), a D2 antagonist which also blocks alpha1-adrenergic receptors, failed to reverse the VTA-induced inhibition, the systemic administration of haloperidol plus SCH 23390 (0.2 mg/kg, i.v.) blocked this inhibition. Finally, it was verified that the cortical inhibitions obtained following treatments with either "prazosin plus sulpiride" or "prazosin plus SCH 23390" were blocked by a superimposed administration of either SCH 23390 or sulpiride, respectively. These data indicate that complex interactions between cortical D2, D1, and alpha1-adrenergic receptors are involved in the regulation of the activity of prefrontocortical cells innervated by the VTA neurons. They confirm that the physiological stimulation of cortical alpha1-adrenergic receptors hampers the functional activity of cortical D1 receptors and suggest that the stimulations of cortical D1 and D2 receptors exert mutual inhibition on each other's transmission.

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Position of the ventral pallidum in the rat prefrontal cortex-basal ganglia circuit.

The ventral pallidum receives major inputs from the nucleus accumbens, a striatal region related to the prefrontal cortex. The ventral pallidum, through its projections to the mediodorsal nucleus of the thalamus, has been considered as the main output structure of the prefrontal-basal ganglia circuits. However, as shown recently, the ventral pallidum also sends efferents to the subthalamic nucleus and the substantia nigra, suggesting that it could participate in intrinsic basal ganglia circuits. The aim of the present investigation was to determine the position of the ventral pallidum in the prefrontal-basal ganglia circuit originating from the prelimbic and medial orbital areas. Following injections of biocytin (an anterograde tracer) into the region of the core of the nucleus accumbens receiving excitatory inputs from the prelimbic and medial orbital areas, axonal terminal fields were observed in a delineated dorsal region of the ventral pallidum. When the biocytin injections were made into this ventral pallidal region, anterogradely labelled fibres were observed in both the dorsomedial substantia nigra pars reticulata and the medial subthalamic nucleus, but not in the mediodorsal nucleus of the thalamus. Confirming these anatomical observations, electrical stimulation of the core of the nucleus accumbens induced an inhibition of the spontaneous activity (D=34.9+/-13.3 ms, L=9.2+/-3.3 ms) in 46.5% of the ventral pallidal cells. Among these responding cells, 43% were antidromically driven from the subthalamic nucleus, 30% from the substantia nigra pars reticulata and only 6% from the mediodorsal nucleus of the thalamus. These data demonstrate that the region of the ventral pallidum involved in the prefrontal cortex-basal ganglia circuit originating from the prelimbic and medial orbital areas represents essentially a ventral subcommissural extension of the external segment of the globus pallidus since it exhibits similar extrinsic connections and functional characteristics. In conclusion, in this prelimbic and medial orbital channel, the ventral pallidum cannot be considered as a major output structure but is essentially involved in intrinsic basal ganglia circuits.

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Mediodorsal thalamic evoked responses in the rat prefrontal cortex: influence of the mesocortical DA system.

The prefrontal cortex (PFC) receives a dopaminergic (DA) innervation from the ventral tegmental area (VTA) and is reciprocally connected with the mediodorsal thalamic nucleus (MD). The present study was performed in anaesthetized rats to determine the influence of the mesocortical DA system on excitatory responses evoked in the PFC by stimulation of MD: (1) short latency (< 4 ms) responses resulting from activation of the MD-PFC pathway; (2) long latency responses (> 10 ms) resulting from activation of recurrent collaterals of PFC neurons projecting to MD. Local DA application and VTA stimulation did not affect short latency responses but blocked long latency responses. These results suggest that the mesocortical DA system inhibits excitations by recurrent collaterals of the PFC-MD neurones but not the excitatory MD inputs to the PFC.

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Prefrontal cortex inputs of the nucleus accumbens-nigro-thalamic circuit.

The functional organization of the cortico-nucleus accumbens-substantia nigra pars reticulata circuit was investigated in the rat using combined anatomical and electrophysiological approaches. The nucleus accumbens neurons which project to the substantia nigra pars reticulata are located in a circumscribed region of the core immediately adjacent and extending dorsally to the anterior commissure. As shown by retrograde and anterograde transports of wheatgerm agglutinin conjugated to horseradish peroxidase, the region of the nucleus accumbens related to the substantia nigra was found to receive bilateral inputs from restricted areas of the medial and lateral prefrontal cortex, i.e., prelimbic/medial orbital and dorsal agranular insular areas. The electrical stimulation of these medial and lateral prefrontal cortical areas induced excitatory responses in nucleus accumbens neurons projecting to the dorsomedial substantia nigra pars reticulata. Interestingly, an important proportion (61%) of the nucleus accumbens-nigral cells responding to the stimulation of the lateral prefrontal cortex were also excited by the stimulation of the medial prefrontal cortex, demonstrating the existence of a convergent influence of these cortical areas on single nucleus accumbens cells. Furthermore, the present data also show that the stimulation of the medial prefrontal cortex results in a powerful inhibition of the tonic firing of the substantia nigra pars reticulata neurons. In conclusion, this study reveals the existence of a functional link between the prefrontal cortex (prelimbic/medial orbital and agranular insular areas) and the nucleus accumbens neurons which innervate the dorsomedial region of the substantia nigra pars reticulata. Since the dorsomedial region of substantia nigra pars reticulata is known to project to subfields of the mediodorsal and ventromedial thalamic nuclei related to the prefrontal cortex, the present data further demonstrate the existence of a prefrontal-nucleus accumbens-thalamo-cortical circuit involving the substantia nigra pars reticulata.

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Excitatory responses evoked in prefrontal cortex by mediodorsal thalamic nucleus stimulation: influence of anaesthesia.

The prefrontal cortex and the mediodorsal thalamic nucleus are reciprocally connected through excitatory amino acid pathways. Cortical excitatory responses resulting from activation of either the mediodorsal thalamic nucleus-prefrontal cortex pathway (short latency) or the recurrent collaterals of prefrontal cortex-mediodorsal thalamic nucleus neurons (long latency) can be discriminated mainly by their latency. The present study was undertaken to compare the effects of halothane and ketamine anaesthesia on these cortical excitatory responses and to establish their pharmacological characteristics using microiontophoretic application of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and D,L-2-amino-5-phosphonovaleric acid (APV), the specific antagonists of D,L-alpha-amino-3-hydroxy-5-methyl-4-isoxalone propionic acid (AMPA) and N-methyl-D-aspartic acid (NMDA) receptors respectively. The number of prefrontal cortex cells which presented short or long latency excitatory responses was smaller in halothane- than in ketamine-anaesthetized rats. Whatever the anaesthetic used, short latency responses were blocked by CNQX and not affected by APV. Long latency responses were mainly blocked by APV and occasionally by CNQX in halothane-anaesthetized rats, while they were only blocked by CNQX in ketamine-anaesthetized animals. Therefore, halothane seems to preferentially reduce evoked responses mediated by AMPA receptors while ketamine completely abolishes evoked responses involving NMDA receptors. Moreover, the present data confirm that excitatory responses resulting from the activation of the mediodorsal thalamic nucleus-prefrontal cortex pathway are mainly mediated by AMPA receptors. In addition, they demonstrate that cortical responses linked to the activation of recurrent collaterals from prefrontal cortex-mediodorsal thalamic nucleus neurons involve both AMPA and NMDA receptors.

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Inhibition of hippocampoprefrontal cortex excitatory responses by the mesocortical DA system.

The prefrontal cortex (PFC) receives dopaminergic (DA) afferents from the ventral tegmental area (VTA) and excitatory inputs from the hippocampal formation. The present electrophysiological experiments performed in anaesthetized rats demonstrate that activation of the mesocortical DA system blocked the spontaneous activity of PFC neurones and the excitatory responses induced by hippocampal stimulation. These data indicate that there is a convergence in the effects of hippocampal and DA mesocortical afferents on common PFC neurones. Furthermore, a population of PFC neurones responding to hippocampal stimulation could be identified as projecting to either the nucleus accumbens and/or the VTA, suggesting that the hippocampus exerts an indirect influence on these two structures through the PFC.

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Anatomical and electrophysiological evidence for an excitatory amino acid pathway from the thalamic mediodorsal nucleus to the prefrontal cortex in the rat.

This study was undertaken to identify the neurotransmitter of the projection from the thalamic mediodorsal nucleus (MD) to the prefrontal cortex (PFC) using both retrograde transport of D-[3H]aspartate and electrophysiological approaches in the rat. Unilateral microinjections of D-[3H]aspartate performed into the prelimbic area of the PFC resulted in dense labelling of numerous cells in the ipsilateral MD. Excitatory responses were observed in PFC neurons after electrical stimulation of the MD. However, since cortical neurons project to the MD, these excitatory responses could have resulted either from the activation of the MD-PFC pathway and/or from the activation of recurrent collaterals of antidromically driven cortico-thalamic fibres. The conduction time of each of these two reciprocal pathways was determined by antidromic activation. Short latency excitatory responses resulted from activation of the MD-PFC pathway. They were predominantly observed in PFC neurons located in layer III and evoked at low frequency stimulation (0.3-1 Hz). These excitatory responses disappeared or were replaced by longer latency responses when higher frequency stimulations (3-10 Hz) were used. MD-evoked responses were blocked by the iontophoretic application of the AMPA receptor antagonist CNQX into the PFC. These results indicate that the MD-PFC pathway utilizes glutamate and/or aspartate as the neurotransmitter and that its activation induces excitation in PFC neurons through AMPA receptors. Even though the local application of the NMDA receptor antagonist APV was ineffective, a contribution of these receptors in MD-PFC transmission cannot be excluded.

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Indirect nucleus accumbens input to the prefrontal cortex via the substantia nigra pars reticulata: a combined anatomical and electrophysiological study in the rat.

The nucleus accumbens is a major component of the ventral striatum through which most of the limbic affiliated cortical areas gain access to the basal ganglia circuitry. In this study, the organization of the pathways linking the nucleus accumbens to the thalamus, via the substantia nigra pars reticulata, was examined in the rat using anatomical and electrophysiological methods. Use of anterograde and retrograde transport of wheatgerm agglutinin conjugated to horseradish peroxidase has established that the core of the nucleus accumbens innervates a dorsal region of the substantia nigra pars reticulata which projects to subfields of the mediodorsal and ventral medial thalamic nuclei. These subfields consist of the rostral pole of the mediodorsal nucleus with the exception of its central segment and a region of the ventral medial nucleus, medial to the mammillothalamic tract. Confirming the existence of a nucleus accumbens nigrothalamic link, we have observed that electrical or chemical stimulation of the nucleus accumbens induces an inhibition of the spontaneous discharges of the nigral cells which project to the mediodorsal and ventral medial thalamic nuclei. Finally, the cortical projections of the thalamic subfields involved in the nucleus accumbens nigrothalamic circuit were determined using the anterograde and retrograde axonal transport of wheatgerm agglutinin conjugated with horseradish peroxidase. These subfields innervate mainly the prelimbic and to a lesser degree the orbital areas of the prefrontal cortex. The present data show that the substantia nigra pars reticulata is a major link between the core of the nucleus accumbens and the prefrontal cortex and provide further evidence for the concept of a parallel architecture in the basal ganglia thalamocortical circuits of the ventral striatum.

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