Afferent projections to the reticular thalamic nucleus from the globus pallidus and the substantia nigra in the rat

Gandia, J A; Heras, Silvano de las; García, Maribel Osorio; Giménez‐Amaya, José Manuel

doi:10.1016/0361-9230(93)90199-l

Cited by 74 publications

(41 citation statements)

References 21 publications

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“…In the rat, the paraventricular, lateral habenular and mediodorsal nuclei are also targets of the globus pallidus (see references in Heimer et al, 1995). Interestingly, the pallidoreticular projections in the rat are also segregated from the nigral afferents to the reticular thalamic nucleus (Gandia et al, 1993). These results illustrate the existence of another important route through which the basal ganglia, via their output nuclei, may control the thalamic flow towards the cerebral cortex or towards brainstem structures like the superior colliculus, and may also control the intrathalamic neural communication (see references in Gandia et al, 1993).…”

Section: The Output Organization Of the Basal Ganglia To The Thalamusmentioning

confidence: 82%

“…Finally, the external segment of the globus pallidus projects to the reticular thalamic nucleus (see Parent, 1991, andGandia et al, 1993 and references therein). In the rat, the paraventricular, lateral habenular and mediodorsal nuclei are also targets of the globus pallidus (see references in Heimer et al, 1995).…”

Section: The Output Organization Of the Basal Ganglia To The Thalamusmentioning

confidence: 99%

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Thalamic interaction between the input and the output systems of the basal ganglia

Mengual

Heras

Erro

et al. 1999

Journal of Chemical Neuroanatomy

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The striatal return through the thalamus is largely neglected in current studies dealing with basal ganglia function, and its role within this circuitry remains obscure. In this contribution the thalamus is regarded as an important place of interaction between the input and the output organization of the basal ganglia. In support of this idea, a brief overview is provided of some of the most recent findings concerning the thalamus in relation to the basal ganglia circuitry. In particular, we have focused on the thalamostriatal projections themselves, on the output of the basal ganglia to the thalamus and also on the overlapping territories between the thalamic projection of the output nuclei and the thalamostriatal neurons. These data support the existence of several thalamic feedback circuits within the basal ganglia neural system. Finally, some considerations are provided upon the functional significance of these thalamic feedback circuits in the overall organization of the basal ganglia.

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Section: The Output Organization Of the Basal Ganglia To The Thalamusmentioning

confidence: 82%

Section: The Output Organization Of the Basal Ganglia To The Thalamusmentioning

confidence: 99%

Thalamic interaction between the input and the output systems of the basal ganglia

Mengual

Heras

Erro

et al. 1999

Journal of Chemical Neuroanatomy

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“…In some studies, next to those afferents, GABAergic, inhibitory projections from the globus pallidus to the RTN were found. 26,27 This finding of a direct connection between the basal ganglia and the RTN, which does not exist between the basal ganglia and the VPN, provides an additional route by which RTN neurons can be influenced. MCAO leads not only to cortical infarction but also to infarction of the globus pallidus, and thus the inhibitory GABAergic input to the RTN is reduced.…”

Section: Dihné Et Al Secondary Thalamic Damage After Focal Ischemia 3009mentioning

confidence: 98%

Different Mechanisms of Secondary Neuronal Damage in Thalamic Nuclei After Focal Cerebral Ischemia in Rats

Dihné

Grommes

Lutzenburg

et al. 2002

Stroke

116

106

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Background and Purpose-After focal cerebral ischemia, depending on its localization and extent, secondary neuronal damage may occur that is remote from the initial lesion. In this study differences in secondary damage of the ventroposterior thalamic nucleus (VPN) and the reticular thalamic nucleus (RTN) were investigated with the use of different ischemia models. Methods-Transient middle cerebral artery occlusion (MCAO) leads to cortical infarction, including parts of the basal ganglia such as the globus pallidus, and to widespread edema. Photothrombotic ischemia generates pure cortical infarcts sparing the basal ganglia and with only minor edema. Neuronal degeneration was quantified within the ipsilateral RTN and VPN 14 days after ischemia. Glial reactions were studied with the use of immunohistochemistry. Results-MCAO resulted in delayed neuronal cell loss of the ipsilateral VPN and RTN. Glial activation occurred in both nuclei beginning after 24 hours. Photothrombotic ischemia resulted in delayed neuronal cell loss only within the VPN. Even 2 weeks after photothrombotic ischemia, glial activation could only be seen within the VPN. Conclusions-Pure cortical infarcts after photothrombotic ischemia, without major edema and without effects on the globus pallidus of the basal ganglia, only lead to secondary VPN damage that is possibly due to retrograde degeneration. MCAO, which results in infarction of cortex and globus pallidus and which causes widespread edema, leads to secondary damage in the VPN and RTN. Thus, additional RTN damage may be due to loss of protective GABAergic input from the globus pallidus to the RTN or due to the extensive edema. Retrograde degeneration is not possible because the RTN, in contrast to the VPN, has no efferents to the cortex.

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“…Alterations in thalamic DA receptors are also implicated in various neurological and psychiatric disorders (Behrendt 2006;Buchsbaum et al 2006;Di Chiara 2002;Kane et al 2009;Takahashi et al 2006;Yasuno et al 2004). Anatomical studies have shown that TRN receives a dopaminergic innervation from the substantia nigra pars compacta (SNc) (Anaya-Martinez et al 2006;Gandia et al 1993;Garcia-Cabezas et al 2007Sanchez-Gonzalez et al 2005) and expresses DA receptors (Khan et al 1998;Mrzljak et al 1996). In addition, TRN receives GABAergic projections from globus pallidus (GP), substantia nigra pars reticulata (SNr), and basal forebrain (Anaya-Martinez et al 2006;Asanuma and Porter 1990;Asanuma 1994;Bickford et al 1994;Gandia et al 1993;Hazrati and Parent 1991;Pare et al 1990).…”

Section: Introductionmentioning

confidence: 99%

“…Anatomical studies have shown that TRN receives a dopaminergic innervation from the substantia nigra pars compacta (SNc) (Anaya-Martinez et al 2006;Gandia et al 1993;Garcia-Cabezas et al 2007Sanchez-Gonzalez et al 2005) and expresses DA receptors (Khan et al 1998;Mrzljak et al 1996). In addition, TRN receives GABAergic projections from globus pallidus (GP), substantia nigra pars reticulata (SNr), and basal forebrain (Anaya-Martinez et al 2006;Asanuma and Porter 1990;Asanuma 1994;Bickford et al 1994;Gandia et al 1993;Hazrati and Parent 1991;Pare et al 1990). Inhibitory innervations within TRN arise from local collaterals (Deleuze and Huguenard 2006;Lam et al 2006;Shu and McCormick 2002).…”

Section: Introductionmentioning

confidence: 99%

Regulation of Inhibitory Synapses by Presynaptic D₄ Dopamine Receptors in Thalamus

Govindaiah

Wang

Gillette

et al. 2010

Journal of Neurophysiology

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Govindaiah G, Wang T, Gillette MU, Crandall SR, Cox CL. Regulation of inhibitory synapses by presynaptic D 4 dopamine receptors in thalamus. J Neurophysiol 104: 2757-2765. First published September 8, 2010 doi:10.1152/jn.00361.2010 receptors are the principal targets of drugs used in the treatment of schizophrenia. Among the five DA receptor subtypes, the D 4 subtype is of particular interest because of the relatively high affinity of the atypical neuropleptic clozapine for D 4 compared with D 2 receptors. GABA-containing neurons in the thalamic reticular nucleus (TRN) and globus pallidus (GP) express D 4 receptors. TRN neurons receive GABAergic afferents from globus pallidus (GP), substantia nigra pars reticulata (SNr), and basal forebrain as well as neighboring TRN neuron collaterals. In addition, TRN receives dopaminergic innervations from substantia nigra pars compacta (SNc); however, the role of D 4 receptors in neuronal signaling at inhibitory synapses is unknown. Using whole cell recordings from in vitro pallido-thalamic slices, we demonstrate that DA selectively suppresses GABA A receptor-mediated inhibitory postsynaptic currents (IPSCs) evoked by GP stimulation. The D 2 -like receptor (D 2,3,4 ) agonist, quinpirole, and selective D 4 receptor agonist, PD168077, mimicked the actions of DA. The suppressive actions of DA and its agonists were associated with alterations in paired pulse ratio and a decrease in the frequency of miniature IPSCs, suggesting a presynaptic site of action. GABA A receptor agonist, muscimol, induced postsynaptic currents in TRN neurons were unaltered by DA or quinpirole, consistent with the presynaptic site of action. Finally, DA agonists did not alter intra-TRN inhibitory signaling. Our data demonstrate that the activation of presynaptic D 4 receptors regulates GABA release from GP efferents but not TRN collaterals. This novel and selective action of D 4 receptor activation on GP-mediated inhibition may provide insight to potential functional significance of atypical antipsychotic agents. These findings suggest a potential heightened TRN neuron activity in certain neurological conditions, such as schizophrenia and attention deficit hyperactive disorders.

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Afferent projections to the reticular thalamic nucleus from the globus pallidus and the substantia nigra in the rat

Cited by 74 publications

References 21 publications

Thalamic interaction between the input and the output systems of the basal ganglia

Thalamic interaction between the input and the output systems of the basal ganglia

Different Mechanisms of Secondary Neuronal Damage in Thalamic Nuclei After Focal Cerebral Ischemia in Rats

Regulation of Inhibitory Synapses by Presynaptic D₄ Dopamine Receptors in Thalamus

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Afferent projections to the reticular thalamic nucleus from the globus pallidus and the substantia nigra in the rat

Cited by 74 publications

References 21 publications

Thalamic interaction between the input and the output systems of the basal ganglia

Thalamic interaction between the input and the output systems of the basal ganglia

Different Mechanisms of Secondary Neuronal Damage in Thalamic Nuclei After Focal Cerebral Ischemia in Rats

Regulation of Inhibitory Synapses by Presynaptic D4 Dopamine Receptors in Thalamus

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Regulation of Inhibitory Synapses by Presynaptic D₄ Dopamine Receptors in Thalamus