Differential Effects of Suicide Transport Lesions of the Striatonigral or Striatopallidal Pathways on Subsets of Striatal Neurons

Roberts, Rosalinda C.; Harrison, Madaline B.; Francis, Sarah M.N.; Wiley, Ronald G.

doi:10.1006/exnr.1993.1194

Cited by 13 publications

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“…In other experiments, neurotoxic non-selective agents were injected in target nuclei of the striatum efferent populations (i.e., the SNr or the LGP) to selectively kill the striatonigral or the striatopallidal neurons by axonal transport (Harrison et al, 1990; Hervé et al, 1993; Roberts et al, 1993). While this strategy can lead to modest reduction of striatopallidal or striatonigral neuron number (Roberts et al, 1993), it lacks striatum specificity since the neurotoxin can be axonally transported from the injection site to multiple areas.…”

Section: First Experimental Tools To Target Striatal Subpopulationsmentioning

confidence: 99%

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Targeting Neuronal Populations of the Striatum

Durieux¹,

Schiffmann²,

d’Exaerde³

2011

Front. Neuroanat.

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The striatum is critically involved in motor and motivational functions. The dorsal striatum, caudate–putamen, is primarily implicated in motor control and the learning of habits and skills, whereas the ventral striatum, the nucleus accumbens, is essential for motivation and drug reinforcement. The GABA medium-sized spiny neurons (MSNs, about 95% of striatal neurons), which are targets of the cerebral cortex and the midbrain dopaminergic neurons, form two pathways. The dopamine D1 receptor-positive (D1R) striatonigral MSNs project to the medial globus pallidus and substantia nigra pars reticulata (direct pathway) and co-express D1R and substance P, whereas dopamine D2 receptor-positive (D2R) striatopallidal MSNs project to the lateral globus pallidus (indirect pathway) and co-express D2R, adenosine A2A receptor (A2AR) and enkephalin (Enk). The specific role of the two efferent pathways in motor and motivational control remained poorly understood until recently. Indeed, D1R striatonigral and D2R striatopallidal neurons, are intermingled and morphologically indistinguishable, and, hence, cannot be functionally dissociated with techniques such as chemical lesions or surgery. In view of the still debated respective functions of projection D2R striatopallidal and D1R striatonigral neurons and striatal interneurons, both in motor control and learning but also in more cognitive processes such as motivation, the present review sum up the development of new models and techniques (bacterial artificial chromosome transgenesis, optogenetic, viral transgenesis) allowing the selective targeting of these striatal neuronal populations in adult animal brain to understand their specific roles.

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Section: First Experimental Tools To Target Striatal Subpopulationsmentioning

confidence: 99%

“…While this strategy can lead to modest reduction of striatopallidal or striatonigral neuron number (Roberts et al, 1993), it lacks striatum specificity since the neurotoxin can be axonally transported from the injection site to multiple areas.…”

Section: First Experimental Tools To Target Striatal Subpopulationsmentioning

confidence: 99%

Targeting Neuronal Populations of the Striatum

Durieux¹,

Schiffmann²,

d’Exaerde³

2011

Front. Neuroanat.

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“…Microinjections of ibotenic acid destroy the neurons at the injection site, leaving the neuropil and fibres of passage intact. Volkensin is a highly toxic lectin derived from the roots of the Adenia volkensii plant (Stirpe et al ., 1985) which, in addition to destroying neurons at the injections site, is transported retrogradely from terminal endings to the perikarya of origin, where it inhibits protein synthesis and produces cell death within 10 days (Wiley & Stirpe, 1988; Harrison et al ., 1992; Roberts et al ., 1993, 1995). Therefore, by microinjecting this toxin directly into the NAc SHELL , not only will there be a lesion at the injection site, but also over the course of 10 days the individual perikarya that innervate this region, located throughout the brain, will be eliminated.…”

Section: Introductionmentioning

confidence: 99%

Neither ibotenic acid nor volkensin lesions of the nucleus accumbens shell affect the expression of cocaine sensitization

Todtenkopf

Stellar

Melloni

2002

Eur J of Neuroscience

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Studies have shown that the nucleus accumbens shell plays an integral role in the expression of psychostimulant-induced behavioural sensitization. Dopaminergic regulation of excitatory amino acid inputs in this region of the brain could be a key factor in the neural influence of this phenomenon. Alterations in the dopaminergic innervation patterns in the shell have been demonstrated in rats that received repeated cocaine injections. Furthermore, lesions of brain regions that send projections to the shell alter psychostimulant-induced locomotion, both acutely and in sensitization paradigms. A previous study from our laboratory demonstrated that lesions of the shell before repeated cocaine treatment decrease the locomotor response to cocaine during the induction phase of behavioural sensitization. To better understand the role of this brain region during the expression phase of behavioural sensitization, the present study examined the effects of two forms of cytotoxic lesions of the shell. Rats received a sensitization-inducing regimen of cocaine (bi-daily injections of 15 mg/kg i.p. for 5 consecutive days). Two days after the last injection, rats demonstrating behavioural sensitization received one of three bilateral microinjections into the shell: (i) 0.5 micro L 0.9% saline; (ii) 2.5 micro g/0.5 micro L ibotenic acid (which lesions the cell bodies at the injection site); or (iii), 0.5 ng/0.2 micro L of volkensin (a retrograde suicide transport lectin). Upon challenge with cocaine (15 mg/kg) 12 days after surgery, neither ibotenic acid- nor volkensin-lesioned rats showed any difference in their locomotor response compared with sham controls. These data indicate that bilateral shell lesions do not affect the long-term expression of behavioural sensitization in cocaine-sensitized rats.

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“…(2) Plastic (secondary) changes often occur in the surrounding unaffected neurons, and these changes may also be of importance. Typically, the secondary effects develop more slowly than the primary effect of failure of the target neuron population (Harrison et al, 1993;Roberts et al, 1993). Thus, repeated observations over the first 2 weeks (or more) after toxin injection may be needed to distinguish primary effects from secondary plastic effects of the lesion.…”

Section: Strategic Planningmentioning

confidence: 99%

Targeted Toxins

Wiley

Lappi

2001

CP Neuroscience

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Molecular neurosurgery can be used to make selective neural lesions by targeting cytotoxins to specific populations of neurons based on their common expression of a particular surface molecule. The targeted toxins employed in this unit consist of a targeting moiety (vector) and an effector moiety (cytotoxin). In all cases discussed in this unit, the cytotoxic moiety is an enzyme that catalytically inactivates the large ribosomal subunit, irreversibly inhibiting protein synthesis and resulting in cell death. These toxins appear to kill in an all-or-none fashion, indicating that one molecule of free cytotoxin in the cytoplasm of a cell is sufficient to kill the cell. Three general molecular neurosurgery protocols are presented in this unit. The first describes suicide transport, which refers to the use of targeted toxins to make anatomically restricted lesions based on retrograde axonal transport of the toxin. The second involves immunolesioning and uses anti-neuronal immunotoxins to make type-selective and anatomically restricted lesions. The final protocol uses neuropeptide-toxin conjugates to selectively destroy neurons expressing the receptor for the specific neuropeptide.

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Differential Effects of Suicide Transport Lesions of the Striatonigral or Striatopallidal Pathways on Subsets of Striatal Neurons

Cited by 13 publications

References 0 publications

Targeting Neuronal Populations of the Striatum

Targeting Neuronal Populations of the Striatum

Neither ibotenic acid nor volkensin lesions of the nucleus accumbens shell affect the expression of cocaine sensitization

Targeted Toxins

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