Dopamine depletion in a striatal subregion disrupts performance of a skilled motor task in the rat

Sabol, Karen E.; Neill, Darryl B.; Wages, Sherry A.; Church, William H.; Justice, Joseph B.

doi:10.1016/0006-8993(85)90273-2

Cited by 130 publications

(40 citation statements)

References 31 publications

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“…Whatever the explanation of the differences in results of this study and that described by Robbins and Everitt (1982), it is evident that profound DA depletion in the caudate nucleus need not attenuate the enhanced responding for CR seen with d-amphetamine -even though such depletion can produce significant behavioural impairments (Sabol et al 1985). Our emphasis solely on the nucleus accumbens should, however, be tempered with the possibility that other structures in the vicinity of the nucleus accumbens might be responsible for some of the effects, such as parts of the medial caudate-nucleus and perhaps olfactory tubercle, which is also depleted by 6-OHDA lesions of the nucleus accumbens (e.g.…”

Section: Discussioncontrasting

confidence: 76%

“…However, it must be pointed out that although the degree of caudate nucleus and nucleus accumbens DA depletion was similar in the two experiments, the actual sites of 6-OHDA administration within the caudate varied slightly, with the present placement being made more lateral. As Sabol et al (1985) have recently shown, the effects of DA depletion from the caudate nucleus depend critically upon its precise pattern. Thus, DA depletion from ventrolateral caudate nucleus impaired paw-use in a skilled motor task, whereas depletion from more anteromedial regions among other effects also apparently influenced motivational variables.…”

Section: Discussionmentioning

confidence: 99%

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6-Hydroxydopamine lesions of the nucleus accumbens, but not of the caudate nucleus, attenuate enhanced responding with reward-related stimuli produced by intra-accumbens d-amphetamine

1986

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Intra-accumbens d-amphetamine enhances responding for reward-related stimuli (conditioned reinforcers, CRs), whereas intra-caudate d-amphetamine has only weak and variable effects (Taylor and Robbins 1984). The present experiment further examined the involvement of the nucleus accumbens and the role of dopamine (DA) in this effect. Thirsty rats were trained to associate a flash of a light and movement of a dipper (CR) with water. After implantation of permanent guide cannulae aimed at the nucleus accumbens, they were assigned to one of four groups, receiving either bilateral 6-OHDA (4 mg/ml free base in 2 microliters 0.1% ascorbic acid/0.9% saline) or sham (vehicle) infusions into the nucleus accumbens or the caudate nucleus. In the test phase, two novel levers were available. Responding on one lever (CR lever) produced the light and dipper stimuli without water presentation, whereas responding on the other (NCR lever) had no effect. All four groups received four counterbalanced intra-accumbens infusions of d-amphetamine (3, 10, 20 micrograms/2 microliters) or vehicle. On the 5th test day, subjects were pretreated subcutaneously with apomorphine (0.1 mg/kg). Intra-accumbens d-amphetamine in both sham-lesioned groups produced a dose-dependent increase in responding on the CR lever, but no significant change on the NCR lever. No selective increases in responding on either lever were found in animals with 6-OHDA-induced depletion of DA (greater than 80%) in the nucleus accumbens following intra-accumbens d-amphetamine; however, in subjects with DA depletion of the posterior caudate nucleus (greater than 80%).(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussioncontrasting

confidence: 76%

Section: Discussionmentioning

confidence: 99%

6-Hydroxydopamine lesions of the nucleus accumbens, but not of the caudate nucleus, attenuate enhanced responding with reward-related stimuli produced by intra-accumbens d-amphetamine

1986

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“…Acquisition of these forms of nondeclarative memory is impaired after damage to the striatum but characteristically is spared after limbic lesions (Olmstead et al, 1976;Siegfried and Bures, 1980;Martone et al, 1984;Sabol et al, 1985;Whishaw et al, 1986;Heindel et al, 1988Heindel et al, , 1991Phillips et al, 1988;Pisa, 1988;SaintCyr et al, 1988;Knopman and Nissen, 1991;McDonald and White, 1993). These data and reports of nigrostriatal changes as behavior becomes automatic encourage further study of striatal activity during motor learning.…”

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confidence: 93%

Loss of Lever Press-Related Firing of Rat Striatal Forelimb Neurons after Repeated Sessions in a Lever Pressing Task

1997

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Lateral striatal neurons that fire phasically in relation to active movement of the contralateral forelimb (determined via daily sensorimotor examination) were studied during acquisition of cued lever pressing. Rats were trained to lift the contralateral forepaw from the floor to press a lever in the presence of a tone. The tone was presented 70 times per day (session) for 18 consecutive days. All animals acquired the task, evidenced by gradual improvements across sessions and eventual asymptotic levels in tone discrimination, reaction time, and efficiency of the lever press. Forelimb neurons fired in relation to the lever press during early sessions of acquisition but not after repeated sessions on the task. This difference in firing could not be attributed to differences in forelimb movements during lever pressing or to sampling from different populations of neurons in early versus late sessions. In view of evidence that striatal damage impairs acquisition of motor skills, the change in firing suggests that the striatal activity present in early sessions may be necessary for the acquisition of, but not the automatic performance of, learned motor responses. Key words: striatum; electrophysiology; S-R habit; chronic recording; dopamine; movementThe lateral striatum contains a population of neurons that discharge spontaneously at low rates and phasically in relation to sensorimotor activity of individual body parts. Their functional organization is in register with convergent, patchy somatotopic projections from primary somatosensory and motor cortices (

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“…These lesion types led to distinctly different behavioral patterns: while animals with lesions encompassing also the cortex presented with significant loss of sensorimotor function, exclusively subcortical lesions did not cause sensorimotor deficits. The latter was not anticipated, because the dorsolateral striatum is the main striatal area receiving input from the somatosensory cortex and projecting to the substantia nigra, and has been proven an important structure for sensory and motor function in the rat (Sabol et al, 1985;Whishaw et al, 1986).…”

Section: Introductionmentioning

confidence: 99%

Temporal profile of T₂-Weighted MRI Distinguishes between Pannecrosis and Selective Neuronal Death after Transient Focal Cerebral Ischemia in the Rat

Wegener

Weber

Ramos‐Cabrer

et al. 2005

J Cereb Blood Flow Metab

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Transient middle cerebral artery occlusion (MCAO) by an intraluminal thread leads to primarily subcortical infarctions with little sensorimotor impairment in the Wistar rat strain. We investigated the course of infarct development in this lesion type for 10 weeks using magnetic resonance imaging (MRI) along with histological characterization. MCAO was induced in male Wistar rats (260 to 300 g) for 60 mins. Animals received follow-up T 1 -and T 2 -weighted MRI from day 1 until week 10. Separate groups of animals were analyzed histologically after 2, 6, and 10 weeks. Histology included immunohistochemistry for neuronal and astrocytic markers as well as hematoxylin eosin and luxol fast blue-cresyl violet staining. In contrast to lesions involving the cortex, exclusively subcortical infarctions were characterized by a complete resolution of initially increased T 1 and T 2 relaxation times by 10 weeks. Between 2 and 10 weeks, neuronal death and gliosis as well as a dense inflammatory infiltrate were evident in these lesions, without damage to fiber tracts or development of cystic cavities. Exclusively subcortical lesions in Wistar rats are characterized by normalization of T 1 and T 2 relaxation times, which might, however, not be mistaken for tissue recovery. Despite this MRI normalization, selective neuronal death and gliosis develop. Although MRI at individual time points might therefore be ambiguous, the temporal profile of relaxation time changes over the chronic time period allows discrimination of the lesion development into selective neuronal death or pannecrosis.

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Dopamine depletion in a striatal subregion disrupts performance of a skilled motor task in the rat

Cited by 130 publications

References 31 publications

6-Hydroxydopamine lesions of the nucleus accumbens, but not of the caudate nucleus, attenuate enhanced responding with reward-related stimuli produced by intra-accumbens d-amphetamine

6-Hydroxydopamine lesions of the nucleus accumbens, but not of the caudate nucleus, attenuate enhanced responding with reward-related stimuli produced by intra-accumbens d-amphetamine

Loss of Lever Press-Related Firing of Rat Striatal Forelimb Neurons after Repeated Sessions in a Lever Pressing Task

Temporal profile of T₂-Weighted MRI Distinguishes between Pannecrosis and Selective Neuronal Death after Transient Focal Cerebral Ischemia in the Rat

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Dopamine depletion in a striatal subregion disrupts performance of a skilled motor task in the rat

Cited by 130 publications

References 31 publications

6-Hydroxydopamine lesions of the nucleus accumbens, but not of the caudate nucleus, attenuate enhanced responding with reward-related stimuli produced by intra-accumbens d-amphetamine

6-Hydroxydopamine lesions of the nucleus accumbens, but not of the caudate nucleus, attenuate enhanced responding with reward-related stimuli produced by intra-accumbens d-amphetamine

Loss of Lever Press-Related Firing of Rat Striatal Forelimb Neurons after Repeated Sessions in a Lever Pressing Task

Temporal profile of T2-Weighted MRI Distinguishes between Pannecrosis and Selective Neuronal Death after Transient Focal Cerebral Ischemia in the Rat

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Temporal profile of T₂-Weighted MRI Distinguishes between Pannecrosis and Selective Neuronal Death after Transient Focal Cerebral Ischemia in the Rat