The Neuroanatomical Organization of the Basal Ganglia

Gerfen, C. R.; Bolam, J. Paul

doi:10.1016/b978-0-12-802206-1.00001-5

Cited by 62 publications

(79 citation statements)

References 201 publications

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“…In the corticostriatal pathway, medium spiny neurons (MSN) of the striatum receive extensive excitatory input from cortical projection neurons (Gerfen and Bolam, 2010), prompting us to compare the degree of retrograde transsynaptic transfer from striatal to cortical neurons. To restrict priming infection we used mice expressing Cre-recombinase under the control of an adenosine receptor 2A (Adora2A) promoter, which is active in approximately half of all MSNs (Gong et al, 2007) (Figure 2B,C).…”

Section: Resultsmentioning

confidence: 99%

Rabies Virus CVS-N2c ΔG Strain Enhances Retrograde Synaptic Transfer and Neuronal Viability

Reardon

Murray

Túri

et al. 2016

Neuron

254

321

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Summary Virally-based transsynaptic tracing technologies are powerful experimental tools for neuronal circuit mapping. The glycoprotein-deletion variant of the SAD-B19 vaccine strain rabies virus (RABV) has been the reagent of choice in monosynaptic tracing, since it permits the mapping of synaptic inputs to genetically marked neurons. Since its introduction, new helper viruses and reagents that facilitate complementation have enhanced the efficiency of SAD-B19ΔG transsynaptic transfer, but there has been little focus on improvements to the core RABV strain. Here we generate a new deletion-mutant strain, CVS-N2cΔG, and examine its neuronal toxicity and efficiency in directing retrograde transsynaptic transfer. We find that by comparison with SAD-B19ΔG, the CVS-N2cΔG strain exhibits a reduction in neuronal toxicity and a marked enhancement in transsynaptic neuronal transfer. We conclude that the CVS-N2cΔG strain provides a more effective means of mapping neuronal circuitry and of monitoring and manipulating neuronal activity in vivo in the mammalian central nervous system.

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Section: Resultsmentioning

confidence: 99%

Rabies Virus CVS-N2c ΔG Strain Enhances Retrograde Synaptic Transfer and Neuronal Viability

Reardon

Murray

Túri

et al. 2016

Neuron

254

321

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“…In the STR, GABAergic spiny projection neurons and interneurons are the majority (~90%) while the cholinergic interneurons are the remainder [31]. Terminals within the STR can arise from these interneurons as well as dopaminergic or glutamatergic projection neurons from the substantia nigra and cortex, respectively [31,32].…”

Section: Discussionmentioning

confidence: 99%

“…Terminals within the STR can arise from these interneurons as well as dopaminergic or glutamatergic projection neurons from the substantia nigra and cortex, respectively [31,32]. In a previous experiment ERα and GPER1 were not observed in dopaminergic neurons in the STR, and a low proportion of these receptors were observed in cholinergic interneurons (~10%) [7].…”

Section: Discussionmentioning

confidence: 99%

Estrogen receptor α and G-protein coupled estrogen receptor 1 are localized to GABAergic neurons in the dorsal striatum

Almey

Milner

Brake

2016

Neuroscience Letters

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Estrogens affect dopamine transmission in the striatum, increasing dopamine availability, maintaining D2 receptor density, and reducing the availability of the dopamine transporter. Some of these effects of estrogens are rapid, suggesting that they are mediated by membrane associated receptors. Recently our group demonstrated that there is extra-nuclear labeling for ERα, ERβ, and GPER1 in the striatum, but that ERα and GPER1 are not localized to dopaminergic neurons in this region. GABAergic neurons are the most common type of neuron in the striatum, and changes in GABA transmission affect dopamine transmission. Thus, to determine whether ERα or GPER1 are localized to GABAergic neurons, we double labeled the striatum with antibodies for ERα or GPER1 and GABA and examined them using electron microscopy. Ultrastructural analysis revealed that ERα and GPER1 are localized exclusively to extranuclear sites in the striatum, and ~35% of the dendrites and axon terminals labeled for these receptors contain GABA immunoreactivity. Binding at membrane-associated ERα and GPER1 could account for rapid estrogen-induced decreases in GABA transmission in the striatum, which, in turn, could affect dopamine transmission in this region.

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“…Castanon et al, 2000; Hoplight et al, 2007). Alternatively, 5-HT1B-mediated inhibition of GABA release from local striatal axon terminals of striatal projection neurons (Gerfen and Bolam, 2010) may directly disinhibit striatal neurons. Either mechanism could thus be expected to produce potentiated (disinhibited) gene induction in striatal neurons.…”

Section: Discussionmentioning

confidence: 99%

Fluoxetine potentiation of methylphenidate-induced gene regulation in striatal output pathways: Potential role for 5-HT1B receptor

et al. 2015

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Drug combinations that include the psychostimulant methylphenidate plus a selective serotonin reuptake inhibitor (SSRI) such as fluoxetine are increasingly used in children and adolescents. For example, this combination is indicated in the treatment of attention-deficit/hyperactivity disorder and depression comorbidity and other mental disorders. Such co-exposure also occurs in patients on SSRIs that use methylphenidate as a cognitive enhancer. The neurobiological consequences of these drug combinations are poorly understood. Methylphenidate alone can produce gene regulation effects that mimic addiction-related gene regulation by cocaine, consistent with its moderate addiction liability. We have previously shown that combining SSRIs with methylphenidate potentiates methylphenidate-induced gene regulation in the striatum. The present study investigated which striatal output pathways are affected by the methylphenidate+fluoxetine combination, by assessing effects on pathway-specific neuropeptide markers, and which serotonin receptor subtypes may mediate these effects. Our results demonstrate that a 5-day repeated treatment with fluoxetine (5 mg/kg) potentiates methylphenidate (5 mg/kg)-induced expression of both dynorphin (direct pathway marker) and enkephalin (indirect pathway). These changes were accompanied by correlated increases in the expression of the 5-HT1B, but not 5-HT2C, serotonin receptor in the same striatal regions. A further study showed that the 5-HT1B receptor agonist CP94253 (3-10 mg/kg) mimics the fluoxetine potentiation of methylphenidate-induced gene regulation. These findings suggest a role for the 5-HT1B receptor in the fluoxetine effects on striatal gene regulation. Given that 5-HT1B receptors are known to facilitate addiction-related gene regulation and behavior, our results suggest that SSRIs may enhance the addiction liability of methylphenidate by increasing 5-HT1B receptor signaling.

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The Neuroanatomical Organization of the Basal Ganglia

Cited by 62 publications

References 201 publications

Rabies Virus CVS-N2c ΔG Strain Enhances Retrograde Synaptic Transfer and Neuronal Viability

Rabies Virus CVS-N2c ΔG Strain Enhances Retrograde Synaptic Transfer and Neuronal Viability

Estrogen receptor α and G-protein coupled estrogen receptor 1 are localized to GABAergic neurons in the dorsal striatum

Fluoxetine potentiation of methylphenidate-induced gene regulation in striatal output pathways: Potential role for 5-HT1B receptor

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