Preferential localization of self-stimulation sites in striosomes/patches in the rat striatum

White, Norman M.; Hiroi, Noboru

doi:10.1073/pnas.95.11.6486

Cited by 125 publications

(101 citation statements)

References 80 publications

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“…Although the rodent dorsolateral striatum is typically considered to be a motor area, lesions in the caudodorsal striatum have been demonstrated to decrease basal PPI (Kodsi and Swerdlow, 1995), suggesting that haloperidol-mediated increases in neuronal activity in this region could influence PPI. In fact, although the majority of evidence has implicated NT in the nucleus accumbens as mediating the antipsychotic-like effects of NT, NT seems to play a more important role in haloperidol-evoked Fos expression in the striatal patch compartment , which has been implicated in affective and cognitive functions (Moratalla et al, 1992;White and Hiroi, 1998;Canales and Graybiel, 2000). These observations suggest that the defect in haloperidol-mediated striatal activation in NT Ϫ/Ϫ mice may explain the inability of this drug to increase PPI in these mice.…”

Section: Discussionmentioning

confidence: 58%

Neurotensin-Deficient Mice Have Deficits in Prepulse Inhibition: Restoration by Clozapine but Not Haloperidol, Olanzapine, or Quetiapine

Kinkead¹,

Dobner²,

Egnatashvili³

et al. 2005

J Pharmacol Exp Ther

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Prepulse inhibition (PPI) of the acoustic startle reflex is a commonly used measure of preattentive sensorimotor gating. Disrupted PPI in rodents represents an animal model of the sensorimotor gating deficits characteristic of schizophrenia. The neurotensin (NT) system is implicated in the pathophysiology of schizophrenia, and NT has been hypothesized to act as an endogenous antipsychotic. In rats, NT receptor agonists restore PPI disrupted by dopamine receptor agonists and Nmethyl-D-aspartate receptor antagonists, and pretreatment with an NT receptor antagonist blocks restoration of isolation rearing induced deficits in PPI by some antipsychotic drugs. The current studies further scrutinized the role of the NT system in the regulation of PPI and in antipsychotic drug-induced restoration of PPI using NT-null mutant mice (NT Ϫ/Ϫ ). NT Ϫ/Ϫ mice exhibited significantly higher pulse alone startle amplitudes and disrupted PPI compared with NT ϩ/ϩ mice. Haloperidol (0.1 mg/kg) and quetiapine (0.5 mg/kg) administered 30 min before PPI testing significantly increased PPI in NT ϩ/ϩ mice but had no effect on PPI in NT Ϫ/Ϫ mice. In contrast, clozapine (1.0 mg/kg) significantly increased PPI in both NT Ϫ/Ϫ and NT ϩ/ϩ mice, whereas olanzapine (0.5 mg/kg) had no effect on PPI in either NT Ϫ/Ϫ or NT ϩ/ϩ mice. In a separate experiment, amphetamine (2.0 mg/kg i.p.) significantly disrupted PPI in NT ϩ/ϩ mice but not NT Ϫ/Ϫ mice. These results provide evidence that the effects of antipsychotic drugs (APDs) may be differentially affected by the state of NT neurotransmission and, moreover, that APDs differ in their dependence on an intact NT system.

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Section: Discussionmentioning

confidence: 58%

Neurotensin-Deficient Mice Have Deficits in Prepulse Inhibition: Restoration by Clozapine but Not Haloperidol, Olanzapine, or Quetiapine

Kinkead¹,

Dobner²,

Egnatashvili³

et al. 2005

J Pharmacol Exp Ther

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“…This inhibitory pathway from the striosomes to the GPh/EPh may also be present in mammals, because striosome neurons have been reported to innervate the rostral entopeduncular nucleus, where the EPh neurons are primarily located (10). The striosomes in mammals have also been implicated in reward-related behavior (39,40), further suggesting that the striosomes-EPh projection may be responsible for inhibiting the EPh neurons in response to prediction of reward.…”

Section: Striosomal Inhibition Of Gph Decreases the Activity In Respomentioning

confidence: 99%

Independent circuits in the basal ganglia for the evaluation and selection of actions

Stephenson-Jones

Kardamakis

Robertson

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

100

116

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The basal ganglia are critical for selecting actions and evaluating their outcome. Although the circuitry for selection is well understood, how these nuclei evaluate the outcome of actions is unknown. Here, we show in lamprey that a separate evaluation circuit, which regulates the habenula-projecting globus pallidus (GPh) neurons, exists within the basal ganglia. The GPh neurons are glutamatergic and can drive the activity of the lateral habenula, which, in turn, provides an indirect inhibitory influence on midbrain dopamine neurons. We show that GPh neurons receive inhibitory input from the striosomal compartment of the striatum. The striosomal input can reduce the excitatory drive to the lateral habenula and, consequently, decrease the inhibition onto the dopaminergic system. Dopaminergic neurons, in turn, provide feedback that inhibits the GPh. In addition, GPh neurons receive direct projections from the pallium (cortex in mammals), which can increase the GPh activity to drive the lateral habenula to increase the inhibition of the neuromodulatory systems. This circuitry, thus, differs markedly from the "direct" and "indirect" pathways that regulate the pallidal (e.g., globus pallidus) output nuclei involved in the control of motion. Our results show that a distinct reward-evaluation circuit exists within the basal ganglia, in parallel to the direct and indirect pathways, which select actions. Our results suggest that these circuits are part of the fundamental blueprint that all vertebrates use to select actions and evaluate their outcome.striosomes | reward/aversion | pallium/cortex | evolution T o achieve a goal, animals need to select actions and evaluate their outcome to determine whether their goal was achieved. In mammals, the basal ganglia play a key role in the selection of actions (1-3) and have more recently been suggested to additionally contribute to predicting and evaluating the outcome of the selected actions (4-8).The so-called "direct" and "indirect" pathways through the basal ganglia are present in all vertebrates and act together to select actions by decreasing tonic inhibition of the basal ganglia output nuclei [globus pallidus interna (GPi) and substantia nigra pars reticulata (SNr)] on a selected motor program and increasing the inhibition onto other competing actions. The output of these selection circuits target brainstem and thalamic motor areas, and neurons within this circuit are modulated by various aspect of movement kinetics related to the initiation and modulation of ongoing actions.In addition to the output neurons that project to motor areas, a separate subpopulation of pallidal neurons projects to the lateral habenula (9-12), a structure involved in evaluating and predicting the motivational value of actions. Recent in vivo recordings in primates have shown that the activity of these habenula-projecting pallidal neurons is modulated by the cues that predict the availability of reward (13,14) and not by aspects of movements. The majority of these pallidal neurons, as with latera...

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“…An example of such structures could be striosomes, which are a neurochemically distinct compartment in the striatum [11,15]. Striosomes have different electrophysiology [54] and metabolic activity [4] than the surrounding matrix. However, the authors are unaware of permeability measurements within striosomes.…”

Section: Nanoparticle Distribution Volumementioning

confidence: 99%

Dilation and degradation of the brain extracellular matrix enhances penetration of infused polymer nanoparticles

et al. 2007

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This study investigates methods of manipulating the brain extracellular matrix (ECM) to enhance the penetration of nanoparticle drug carriers in convection-enhanced delivery (CED). A probe was fabricated with two independent microfluidic channels to infuse, either simultaneously or sequentially, nanoparticles and ECM-modifying agents. Infusions were performed in the striatum of the normal rat brain. Monodisperse polystyrene particles with a diameter of 54 nm were used as a model nanoparticle system. Because the size of these particles is comparable to the effective pore size of the ECM, their transport may be significantly hindered compared with the transport of low molecular weight molecules. To enhance the transport of the infused nanoparticles, we attempted to increase the effective pore size of the ECM by two methods: dilating the extracellular space and degrading selected constituents of the ECM. Two methods of dilating the extracellular space were investigated: co-infusion of nanoparticles and a hyperosmolar solution of mannitol, and pre-infusion of an isotonic buffer solution followed by infusion of nanoparticles. These treatments resulted in an increase in the nanoparticle distribution volume of 50% and 123%, respectively. To degrade hyaluronan, a primary structural component of the brain ECM, a pre-infusion of hyaluronidase (20,000 U/mL) was followed after 30 min by infusion of nanoparticles. This treatment resulted in an increase in the nanoparticle distribution of 64%. Our results suggest that both dilation and enzymatic digestion can be incorporated into CED protocols to enhance nanoparticle penetration.

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Preferential localization of self-stimulation sites in striosomes/patches in the rat striatum

Cited by 125 publications

References 80 publications

Neurotensin-Deficient Mice Have Deficits in Prepulse Inhibition: Restoration by Clozapine but Not Haloperidol, Olanzapine, or Quetiapine

Neurotensin-Deficient Mice Have Deficits in Prepulse Inhibition: Restoration by Clozapine but Not Haloperidol, Olanzapine, or Quetiapine

Independent circuits in the basal ganglia for the evaluation and selection of actions

Dilation and degradation of the brain extracellular matrix enhances penetration of infused polymer nanoparticles

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