Avoidance and escape behavior following striatal lesions in the rat
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Cited by (65)
Neural bases of frustration-aggression theory: A multi-domain meta-analysis of functional neuroimaging studies
2023, Journal of Affective DisordersChronic pain and pain processing in Parkinson's disease
2018, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :Dopamine is a key neurotransmitter in the modulation of pain perception, and rodent experiments showed that dopamine is involved in the descending antinociception mediated in the rostral agranular insular cortex (Burkey et al., 1999). Lesions of the rat caudate nucleus impaired the behavioral response in a pain avoidance task (Kirkby and Kimble, 1968). Deep pain may arise in humans following focal lenticular infarction, but the integrity of nearby pathways is difficult to ascertain in such cases (Russmann et al., 2003).
Neurobiology of Procedural Learning in Animals
2017, Learning and Memory: A Comprehensive ReferenceThe role of the hippocampus in approach-avoidance conflict decision-making: Evidence from rodent and human studies
2016, Behavioural Brain ResearchCitation Excerpt :A substantial number of early studies revealed that another form of avoidance learning, known as ‘two-way active avoidance’, which requires animals to actively shuttle between two conjoined compartments to avoid shocks being delivered in one, is consistently facilitated in HPC-lesioned animals [e.g. 43–46] [47][for review see 47]. In contrast, the effects of HPC lesions on ‘one-way’ active avoidance, in which only one of the compartments is designated as ‘safe’, and the other as the ‘dangerous’ shock-associated compartment, have been unclear (i.e. no effect or deficit observed) [e.g. 45,48–51]. It has been suggested that rodent HPC lesion-induced deficits in one-way active avoidance occur only when the two compartments are distinguishable on the basis of extra-maze (distal, spatial), but not intra-maze (proximal, non-spatial) cues [47].
Nucleus accumbens core lesions enhance two-way active avoidance
2014, NeuroscienceCitation Excerpt :Here, we examine this issue by asking how bilateral NAc lesions impact performance on a two-way active avoidance task. Previous work has shown that escape-avoidance depends on the dorsal striatum (DS) (Kirkby and Kimble, 1968; Allen and Davison, 1973; Winocur, 1974; Prado-Alcala et al., 1975; Viaud and White, 1989; White and Viaud, 1991) and normal dopamine levels in the striatum (Cooper et al., 1974; Neill et al., 1974; Jackson et al., 1977; Schwarting and Carey, 1985; Wadenberg et al., 1990; McCullough et al., 1993), but it is less clear what specific role the NAc plays in these types of paradigms (Gal et al., 2005; Pothuizen et al., 2005, 2006). Original reports suggest that electrolytic lesions of the rat nuclei accumbens septi improves performance on conditioned avoidance (Lorens et al., 1970), but it is unclear if excitotoxic lesions to the NAc will have the same effect during performance of a two-way active avoidance task.
Role of Basal Ganglia in Habit Learning and Memory: Rats, Monkeys, and Humans
2010, Handbook of Behavioral NeuroscienceCitation Excerpt :In rats, early lesion studies conducted prior to the advent of the multiple memory systems approach can be considered consistent with the hypothesis that the basal ganglia play a role in habit learning. Thus, basal ganglia damage impairs acquisition of one-way and two-way active avoidance (e.g., Kirkby and Kimble, 1968; Winocur and Mills, 1969; Neill and Grossman, 1971; Mitcham and Thomas, 1972; Kirkby and Polgar, 1974; Winocur, 1974), and straight-alley runway behavior (Kirkby et al., 1981). However, the first study to directly assess this hypothesis in rats employed dissociation methodology to compare the effects of basal ganglia lesions on acquisition of both cognitive and habit learning tasks in a radial maze (Packard et al., 1989).
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This research was partially supported by USPHS grant No. 08545-03 to D. P. Kimble, and by research funds to R. J. Kirkby from the New South Wales Department of Health, with whose permission the paper is published. The authors express their appreciation for the technical assistance of Ruth BreMiller and Allan S. Tollow.