Changes in striatal dopamine neurotransmission assessed with microdialysis following recovery from a bilateral 6-OHDA lesion: variation as a function of lesion size

Castañeda, Edward; Whishaw, Ian Q.; Robinson, Terry E.

doi:10.1523/jneurosci.10-06-01847.1990

Cited by 184 publications

(78 citation statements)

References 42 publications

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“…Neurochemical analysis showed a 95% decrease in the striatum. Thus, the early and persistent behavioral deficits are consistent with the observation that animals with less than 5-10% of their terminals remaining in the striatum are not able to maintain normal extracellular DA levels even in the presence of enhanced neuronal processes (Robinson and Whishaw 1988;Zhang et al 1988;Abercrombie et al 1990;Castañeda et al 1990;Parsons et al 1991;Robinson et al 1994). Furthermore, even in the presence of enhanced neuronal processes and supersensitive postsynaptic receptors, these animals do not recover from their behavioral deficits (Zigmond and Stricker 1973;Creese and Snyder 1979;Marshall 1979Marshall , 1984Neve et al 1982Neve et al , 1984.…”

Section: Discussionsupporting

confidence: 77%

“…Previous studies have shown that with sub-maximal striatal depletion of DA, the remaining neurons compensate for the loss with a decrease in the uptake, and an increase in the synthesis, metabolism, and release of DA, thereby maintaining extracellular DA levels (Hefti et al 1980;Altar et al 1987;Stricker and Zigmond 1976;Zigmond et al 1984). Indeed, it has been shown that with less than 80% depletion, the extracellular concentration of DA is maintained in the presence of the remaining terminals (Robinson and Whishaw 1988;Zhang et al 1988;Abercrombie et al 1990;Castañeda et al 1990;Parsons et al 1991;Robinson et al 1994). This compensation could account for the lack of a functional deficit during the first three weeks post-lesion; however, if so, these same mechanisms failed to prevent the appearance of deficits in the fourth and fifth week post-lesion.…”

Section: Discussionmentioning

confidence: 99%

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Effect of Bilateral 6-Hydroxydopamine Lesions of the Medial Forebrain Bundle on Reaction Time

Smith

Amalric²,

Koob

et al. 2002

Neuropsychopharmacology

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Overt symptoms of Parkinson's disease do not manifest themselves until there is a substantial loss of the dopaminergic nigrostriatal projection. However, as neuroprotective strategies are developed, it will be essential to detect the disease in its preclinical phase. Performance on conditioned reaction time tasks is known to be impaired by extensive 6-hydroxydopamine-induced lesions of theThe primary neuropathology of Parkinson's disease is the loss of dopamine (DA) neurons within the substantia nigra (SN) and massive depletion of DA in the striatum, the terminal region of the SN. This loss of DA appears to be responsible for the most prominent symptoms of Parkinson's disease. The degree of neurological deficit is related to the loss of striatal DA (Hornykiewicz and Kish 1987). The neurotoxins 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), used extensively to induce selective loss of DA neurons within the SN, provide animal models that share several of the characteristics of Parkinson's disease (see reviews by Zigmond and Keefe 1997;Jenner and Marsden 1986;Gerlach and Riederer NO . 6 Bilateral 6-OHDA on Reaction Time 7571996; Przedborski and Jackson-Lewis 1998). In addition, whereas intrastriatal injection of indirect DA agonists induces stereotypy (Costall et al. 1973;Statton and Solomon 1984), 6-OHDA lesions of the striatum block this stereotyped behavior (Price and Fibiger 1974). Finally, chronic administration of DA receptor antagonists produce extrapyramidal effects reminiscent of Parkinson's disease, and this is believed to be due to their action at D 2 receptors located in the striatum (Coffin et al. 1989). Although resting tremor and muscular rigidity are generally not reported in rodents after pharmacological manipulation of the nigrostriatal pathway, deficits in movement initiation and execution have been studied using several tests including a conditioned reaction time task. In this task, animals are typically required to respond in a particular way and within a limited period in order to receive a reward, such as a food pellet. This behavioral paradigm is responsive to pharmacological manipulation of dopaminergic neurotransmission mediated by the D 2 subtype of DA receptors Koob 1987, 1989;Amalric et al. 1993Amalric et al. , 1995Smith et al. 2000). For example, we have shown that low dose blockade of D 2 receptors, but not D 1 or D 3 receptors, decreased correct responses in the conditioned reaction time task, increased delayed responses, and lengthened reaction time in a manner suggestive of dysfunctions in movement initiation (Amalric et al. 1993;Smith et al. 2000). Moreover, deficits in reaction time have also been reported in Parkinson's disease (Evarts et al. 1981;Gauntlett-Gilbert and Brown 1998;Berry et al. 1999). These deficits appear to be mediated by the nigrostriatal dopaminergic pathway, as 6-OHDA-induced loss of SN neurons and striatal DA, and not accumbal DA, produces impairments in this task (Amalric and Koob 1987), and intrastriatal infusion...

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Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Effect of Bilateral 6-Hydroxydopamine Lesions of the Medial Forebrain Bundle on Reaction Time

Smith

Amalric²,

Koob

et al. 2002

Neuropsychopharmacology

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“…Similar discrepancies have been noted in pigeons, where N-methyl-D-aspartate receptor blockade with AP-5 in the prefrontal cortex produced deficits in extinction learning, but lesions did not (Lissek and Gunturkun, 2003). Abundant evidence suggests that neuroadaptations in multiple cellular functions occur following lesions, including presynaptic increases in synthesis, metabolism, and fractional release of DA in the remaining terminals (Abercrombie et al, 1990;Castaneda et al, 1990;Robinson and Whishaw, 1988;Touchet and Bennett, 1989;Zhang et al, 1988), and post-synaptic DA-receptor supersensitivity (Creese et al, 1977;Mishra et al, 1974;Neve et al, 1982). Therefore, while lesion-induced deficits in certain paradigms are well-documented, the lack of deficits in some lesion studies makes them difficult to interpret, given the likely recovery of function.…”

Section: Discrepancies Between Pharmacological and Lesion Studiesmentioning

confidence: 56%

Instrumental learning, but not performance, requires dopamine D1-receptor activation in the amygdala

2005

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Substantial experimental evidence exists suggesting a critical role for dopamine in reinforcer-related processes, such as learning and drug addiction. Dopamine receptors, and in particular D1 receptors, are widely considered as modulators of synaptic plasticity. The amygdala contains both dopamine terminals and dopamine D1 receptors and is intimately involved in motivation and learning. However, little is known about the involvement of D1 receptor activation in two subnuclei of the mammalian amygdala, the central nucleus and basolateral complex in instrumental learning. Following recovery from surgery and preliminary training, rats with bilateral indwelling cannulae aimed at the central nucleus or basolateral complex were trained to lever-press for sucrose pellets over 12 sessions. Infusion of the selective D1 antagonist R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride (0.3 nmol and 3.0 nmol) prior to the first five training sessions dose-dependently impaired instrumental learning when compared with vehicleinfused controls. All rats were then exposed to five sessions drug-free; lever-pressing quickly reached equal levels across groups. A drug infusion prior to an 11th session revealed no effect on performance. Control experiments indicated that basic motivational processes and general motor responses were intact, such as spontaneous feeding and locomotor activity. These results show an essential role for D1-receptor activation in both the central nucleus and basolateral complex on the acquisition of lever pressing for sucrose pellets in rats, but not the performance of the behavior once conditioned. We propose that instrumental learning is dependent on plasticity in the central nucleus and basolateral complex amygdala, and that D1 receptor activation participates in transcriptional processes that underlie this plasticity.Keywords instrumental learning; amygdala; dopamine; D1; plasticity; rats Biologically important events, such as procurement of food, escape from predation, and access to sexual partners, often require flexible patterns of behavior in order to produce themforaging, vigilance, and defense, for example. Important biological reinforcers (Reinf), in turn, change the behavior that produced them, illustrating a form of adaptability termed "instrumental learning." Many Reinf-related processes are mediated by the mesocorticolimbic dopamine (DA) system, consisting of DA neurons in the ventral tegmental area and their projections to the nucleus accumbens, medial prefrontal cortex, striatum, amygdala and other *Corresponding author. Tel: +1-608-262-9332. E-mail address: mandrzejewsk@wisc.edu (M. E. Andrzejewski). (Beninger and Miller, 1998;Cardinal et al., 2002;Kelley and Berridge, 2002). Specifically, studies have shown that D1 receptor activation throughout this corticolimbicstriatal network plays a critical role in learning (Beninger and Gerdjikov, 2004). Indeed, D1 receptor activation is thought to serve a crucial modulatory function in the induction o...

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“…The ANOVA showed that there was a significant effect of side, but no Treatment Group ϫ Side interaction. It can be seen that levels of both metabolites were significantly lower on the lesioned side in all groups, indicating that all groups sustained lesions of similar magnitude (Robinson and Whishaw, 1988;Castañeda et al, 1990). See legend of Figure 2 for results of statistical analyses.…”

Section: Dopac and Hvamentioning

confidence: 85%

“…Behavioral recovery after partial unilateral lesions of the nigrostriatal pathway is accompanied by gradual normalization of extracellular dopamine (DA) in the striatum measured using microdialysis (Robinson and Whishaw, 1988;Zhang et al, 1988;Abercrombie et al, 1990;Castañeda et al, 1990;Robinson et al, 1994). We showed recently that daily injections of NMDA receptor antagonists given in the first week after such lesions block behavioral recovery and normalization of extracellular DA in striatum measured 1 week after the last drug injections using microdialysis (Emmi et al, 1996).…”

mentioning

confidence: 99%

Behavioral and Neurochemical Recovery from Partial 6-Hydroxydopamine Lesions of the Substantia Nigra Is Blocked by Daily Treatment with D1/D5, But Not D2, Dopamine Receptor Antagonists

1997

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To determine whether D1/D5 dopamine (DA) receptors play a role in normalization of DA extracellular levels of striatal DA and behavioral recovery after partial 6-OHDA lesions of the substantia nigra, animals were treated on days 1-8 after lesioning with the D1/D5 DA receptor antagonists SCH 23390 (0.1 mg/ kg, s.c.) and SCH 39166 (1.0 mg/kg, s.c.), the inactive enantiomer SCH 23388 (0.1 mg/kg, s.c.), the D2 antagonist eticlopride (0.1 mg/kg, i.p.), or saline. Spontaneous turning behavior was assessed on days 3 and 15. Basal extracellular DA and metabolites were measured in both striata using microdialysis on days 16 and 17, 8 -9 d after termination of drug treatments. On day 3, all animals turned ipsilateral to the lesion. On day 15, animals previously treated with either saline, eticlopride, or SCH 23388 showed no behavioral asymmetries, whereas animals treated with SCH 23390 or SCH 39166 turned ipsilaterally. On days 16 and 17, extracellular DA did not differ on the two sides in animals treated with saline or eticlopride and were higher on the lesioned side after SCH 23388. In animals treated with the D1/D5 receptor antagonists, however, basal levels of DA were lower on the lesioned side, showing no evidence of normalization. These results suggest a role for the D1/D5 DA receptor in the development of compensatory changes in the DA neurons that accompany behavioral recovery from partial lesions of nigrostriatal DA system.

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Changes in striatal dopamine neurotransmission assessed with microdialysis following recovery from a bilateral 6-OHDA lesion: variation as a function of lesion size

Cited by 184 publications

References 42 publications

Effect of Bilateral 6-Hydroxydopamine Lesions of the Medial Forebrain Bundle on Reaction Time

Effect of Bilateral 6-Hydroxydopamine Lesions of the Medial Forebrain Bundle on Reaction Time

Instrumental learning, but not performance, requires dopamine D1-receptor activation in the amygdala

Behavioral and Neurochemical Recovery from Partial 6-Hydroxydopamine Lesions of the Substantia Nigra Is Blocked by Daily Treatment with D1/D5, But Not D2, Dopamine Receptor Antagonists

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