Time course of certain behavioral changes after hippocampal damage and their alteration by dopaminergic intervention into nucleus accumbens

Reinstein, Daniel K.; Hannigan, John H.; Isaacson, Robert L.

doi:10.1016/0091-3057(82)90069-7

Cited by 47 publications

(12 citation statements)

References 33 publications

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“…This moderate elevation of activity suggests that the biological changes associated with this e¤ect are not dramatic and do not involve complete changes in neurotransmitter function. However, there appears to be a clear similarity between the increased activity in KA-lesioned animals and animals with site-speciÞc lesions of limbic-cortical areas (Kolb 1977;Devenport et al 1981;Handelmann and Olton 1981;Reinstein et al 1982;Fass 1983;Nyakas et al 1983;Hannigan et al 1984;Emerich and Walsh 1990;Lorenzini et al 1991;Port et al 1991;Whishaw and Mittleman 1991;Burns et al 1993;Lipska et al 1993;Wilkinson et al 1993). These previous studies, along with our own Þndings, suggest that regions such as the hippocampus, amygdala, thalamus, and entorhinal cortex exert a signiÞcant modulatory inßuence over locomotor activity.…”

Section: Discussionsupporting

confidence: 62%

“…The hyperlocomotion observed in animals with limbic-cortical lesions may arise as a direct consequence of limbic-cortical neuronal loss, independent of disruptions in limbic input to subcortical locomotor systems. Alternatively, as many authors have suggested, lesion-induced hypermotility may reßect the loss of limbic input into subcortical brain regions which regulate locomotor behavior (Devenport et al 1981;Reinstein et al 1982;Hannigan et al 1984;Emerich and Walsh 1990;Whishaw and Mittleman 1991;Lipska et al 1993;Wilkinson et al 1993).…”

Section: Discussionmentioning

confidence: 96%

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The effects of kainic acid lesions on locomotor responses to haloperidol and clozapine

Bardgett¹,

Jackson²,

Taylor³

et al. 1998

Psychopharmacology

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Spontaneous and amphetamine-elicited locomotor activity in rats is reduced by most clinically effective antipsychotic drugs. We have recently demonstrated that intracerebroventricular infusion of kainic acid (KA), which produces cell loss in the hippocampus and other limbic-cortical brain regions, increases spontaneous and amphetamine-elicited locomotion. The present study determined if KA lesions alter the suppressive effects of the antipsychotic drugs, haloperidol and clozapine, on spontaneous and amphetamine-elicited locomotor behavior. Young adult male rats (70 days of age) received intracerebroventricular infusions of vehicle or KA, which produced hippocampal pyramidal cell loss in each rat and more variable cell loss or gliosis in the amygdala, piriform cortex, and laterodorsal thalamus. Thirty days post-surgery, lesioned and control rats were tested once a week for locomotor responses to drug treatments. As observed previously, spontaneous locomotor activity and hyperactivity elicited by amphetamine (1.50 mg/kg s.c.) were greater in lesioned animals than controls. In addition, the level of spontaneous activity and/or amphetamine-elicited hyperlocomotion observed in lesioned rats after haloperidol treatment (0.13, 0.35, or 1.50 mg/kg s.c.) was greater than that found in controls. Locomotor responses to low (6.30 mg/kg) and moderate doses of clozapine (20 mg/kg) were similar in lesioned and control rats, although lesioned rats were more active than controls following the administration of a high dose of clozapine (30 mg/kg). These data indicate that the hyperactivity associated with limbic-cortical lesions may be insensitive to reversal by haloperidol, yet uniquely sensitive to suppression by clozapine.

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Section: Discussionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 96%

The effects of kainic acid lesions on locomotor responses to haloperidol and clozapine

Bardgett¹,

Jackson²,

Taylor³

et al. 1998

Psychopharmacology

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“…Many studies have reported that lesions of the ventral hippocampus alter behavioural, pharmacological, or neurochemical indices of dopaminergic transmission and that such alterations emerge days or weeks following lesions (Springer & Isaacson, 1982; Lipska et al ., 1992, 1995). For instance, hippocampal lesions increase exploration and investigatory stereotypes produced by injections of dopamine agonists (Reinstein et al ., 1982; Lipska & Weinberger, 1993; Mittleman et al ., 1993), augment elevations in NAS dopamine evoked by amphetamine (Wilkinson et al ., 1993), and enhance the behavioural suppressant effects of antipsychotic drugs (Lipska & Weinberger, 1993). On the other hand, neither basal tissue levels of the dopamine metabolite 3‐methoxytyramine (Lipska et al ., 1995) nor basal levels of extracellular dopamine (Wilkinson et al ., 1993) in the NAS of lesioned rats are altered following ventral hippocampal lesions.…”

Section: Discussionmentioning

confidence: 99%

Novelty‐evoked elevations of nucleus accumbens dopamine: dependence on impulse flow from the ventral subiculum and glutamatergic neurotransmission in the ventral tegmental area

Legault

Wise

2001

Eur J of Neuroscience

168

115

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In vivo microdialysis in freely moving rats was used to monitor novelty-evoked elevations in extracellular dopamine in the nucleus accumbens septi (NAS) and to examine the role of the ventral subiculum of the hippocampus and glutamatergic transmission in the ventral tegmental area (VTA) on these elevations. Exposure to novel stimuli evoked investigatory activity and increased nucleus accumbens dopamine. Unilateral injections of the sodium channel blocker tetrodotoxin (0.16 ng/0.5 microL) into the ventral subiculum ipsilateral to the dialysed NAS abolished novelty-evoked elevations in dopamine. Injections of tetrodotoxin into the contralateral VS did not prevent novelty-evoked elevations in nucleus accumbens dopamine. Unilateral perfusion (via microdialysis) of the ionotropic glutamate receptor antagonists kynurenic acid (1 mM) into the ipsilateral but not the contralateral VTA blocked novelty-evoked elevations in nucleus accumbens dopamine. Neither unilateral injections of tetrodotoxin nor unilateral perfusion of kynurenic acid disrupted investigatory behaviour. These data indicate that phasic elevations in nucleus accumbens dopamine evoked by exposure to unconditioned novel stimuli are dependent on impulse flow from the hippocampus and glutamatergic transmission in the VTA.

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“…This behavioral pattern might have its origin in ventral striatal dysfunction. Indeed, the ventral striatum has long been recognized as a central node of the motivation system (Mogenson et al, 1980; Reinstein et al, 1982). Both appetitive and fearful motivation involve dopamine and glutamate in the nucleus accumbens (for review Carlezon and Thomas (2009)).…”

Section: Striatum and Motivationmentioning

confidence: 99%

Striatum on the anxiety map: Small detours into adolescence

et al. 2017

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Adolescence is the most sensitive period for the development of pathological anxiety. Moreover, specific neural changes associated with the striatum might be related to adolescent vulnerability to anxiety. Up to now, the study of anxiety has primarily focused on the amygdala, bed nucleus of the stria terminalis (BNST), hippocampus and ventromedial prefrontal cortex (vmPFC), while the striatum has typically not been considered as part of the anxiety system. This review proposes the addition of the striatum, a complex, multi-component structure, to the anxiety network by underscoring two lines of research. First, the co-occurrence of the adolescent striatal development with the peak vulnerability of adolescents to anxiety disorders might potentially reflect a causal relationship. Second, the recognition of the role of the striatum in fundamental behavioral processes that do affect anxiety supports the putative importance of the striatum in anxiety. These behavioral processes include (1) attention, (2) conditioning/prediction error, and (3) motivation. This review proposes a simplistic schematic representation of the anxiety circuitry that includes the striatum, and aims to promote further work in this direction, as the role of the striatum in shaping an anxiety phenotype during adolescence could have critical implications for understanding and preventing the peak onset of anxiety disorders during this period.

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Time course of certain behavioral changes after hippocampal damage and their alteration by dopaminergic intervention into nucleus accumbens

Cited by 47 publications

References 33 publications

The effects of kainic acid lesions on locomotor responses to haloperidol and clozapine

The effects of kainic acid lesions on locomotor responses to haloperidol and clozapine

Novelty‐evoked elevations of nucleus accumbens dopamine: dependence on impulse flow from the ventral subiculum and glutamatergic neurotransmission in the ventral tegmental area

Striatum on the anxiety map: Small detours into adolescence

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