Spatial memory and stereotypic behaviour of animals in radial arm mazes

Lanke, Jan; Månsson, Lennart; Bjerkemo, M; Kjellstrand, Per

doi:10.1016/0006-8993(93)91744-d

Cited by 18 publications

(6 citation statements)

References 17 publications

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“…Our behavioral studies with the eight-arm radial maze task demonstrated impairment of spatial working memory, which requires a fully functional hippocampus (Lanke et al, 1993;Hodges, 1996;Pothuizen et al, 2004), in maternally stressed adult offspring. As shown in Figure 2A, the impaired ability of maternally stressed mice to learn to reduce arm-revisiting errors as the training proceeds in the radial arm maze indicates that they have deficits in this one-experience learning.…”

Section: Discussionmentioning

confidence: 74%

“…To examine whether chronic maternal stress has a long-lasting influence on hippocampus-dependent learning and memory, we assessed the effects of maternal stress on the performance of adult offspring in the spatial working memory version of the eight-arm radial maze task, which is known to be dependent on the hippocampus (Lanke et al, 1993;Hodges, 1996). In each session, mice had to visit each of the eight arms only once to earn the greatest reward, because reentry of an arm already visited was not rewarded and was counted as a working memory error.…”

Section: Impaired Spatial Memory But Normal S-r Habit Learning In Matmentioning

confidence: 99%

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Maternal Stress Produces Learning Deficits Associated with Impairment of NMDA Receptor-Mediated Synaptic Plasticity

Geum²,

et al. 2006

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Stress in adulthood can have a profound effect on physiology and behavior, but the extent to which prolonged maternal stress affects the brain function of offspring when they are adult remains primarily unknown. In the present work, chronic immobilization stress to pregnant mice affected fetal growth and development. When pups born from stressed mice were reared to adulthood in an environment identical to that of nonstressed controls, several physiological parameters were essentially unaltered. However, spatial learning and memory was significantly impaired in the maternally stressed offspring in adulthood. Furthermore, electrophysiological examination revealed a significant reduction in NMDA receptor-mediated long-term potentiation in the CA1 area of hippocampal slices. Subsequent biochemical analysis demonstrated a substantial decrease in NR1 and NR2B subunits of the NMDA receptor in synapses of the hippocampus, and the interaction between these two subunits appeared to be reduced. These results suggest that prolonged maternal stress leads to long-lasting malfunction of the hippocampus, which extends to and is manifested in adulthood.

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Section: Discussionmentioning

confidence: 74%

Section: Impaired Spatial Memory But Normal S-r Habit Learning In Matmentioning

confidence: 99%

Maternal Stress Produces Learning Deficits Associated with Impairment of NMDA Receptor-Mediated Synaptic Plasticity

Geum²,

et al. 2006

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“…7) is further evidence of disrupted learning behavior. Impaired spatial/associative learning in rats has been shown to result in animals choosing arms in the maze in a stereotypic manner (sequentially entering adjacent arms), reflecting a shift from the more efficient allocentric stimulusresponse learning strategy (utilizing environmental cues) to a preconditioned ''default'' egocentric strategy (preference of direction) to recover the bait reward (Lanke et al, 1993;Soblosky et al, 1996). Amygdala function is important in mediating this preconditioned approach-reward stereotypic strategy, which does not involve spatial or associative memory or depend upon a learned response (McDonald and White, 1993;White and McDonald, 2002).…”

Section: Discussionmentioning

confidence: 99%

“…the sequence of maze arms entered on each session day. It has been shown that rodents with impaired spatial memory will utilize a stereotypic response strategy (i.e., successively entering adjacent arms) in searching for bait rewards that manifests as preference for choice of direction (Lanke et al, 1993). Here, preweaning Mn-exposed male rats exhibited a stereotypic response strategy on a significantly greater number of session days compared to controls (Kruskal-Wallis Chi-Square 5 8.47, DF 5 2, P 5 0.01) (Fig.…”

Section: Preweaning Mn Exposure Caused a Shift In Goal-oriented Behavmentioning

confidence: 99%

Preweaning manganese exposure causes hyperactivity, disinhibition, and spatial learning and memory deficits associated with altered dopamine receptor and transporter levels

Kern

Stanwood

Smith

2009

Synapse

122

164

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Epidemiological studies in children have reported associations between elevated dietary manganese (Mn) exposure and neurobehavioral and neurocognitive deficits. To better understand the relationship between early Mn exposure and neurobehavioral deficits, we treated neonate rats with oral Mn doses of 0, 25, or 50 mg Mn/kg/d over postnatal day (PND) 1 -21, and evaluated behavioral performance using open arena (PND 23), elevated plus maze (PND 23), and 8-arm radial maze (PND 33-46) paradigms. Brain dopamine D1 and D2-like receptors, and DAT transporter densities were determined on PND 24, and blood and brain Mn levels were measured to coincide with behavioral testing (PND 24, PND 36). Pre-weaning Mn exposure caused hyperactivity and behavioral disinhibition in the open arena, but no altered behavior in the elevated plus maze. Manganese-exposed males committed significantly more reference and marginally more working errors in the radial arm maze compared to controls. Fewer Mn exposed males achieved the radial maze learning criterion, and they required more session days to reach it compared to controls. Manganese-exposed animals also exhibited a greater frequency of stereotypic response strategy in searching for the baited arms in the maze. These behavioral and learning deficits were associated with altered expression of the dopamine D1 and D2 receptors and the dopamine transporter in prefrontal cortex, nucleus accumbens, and dorsal striatum. These data corroborate epidemiological studies in children, and suggest that exposure to Mn during neurodevelopment significantly alters dopaminergic synaptic environments in brain nuclei that mediate control of executive function behaviors, such as reactivity and cognitive flexibility.

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“…For each rat, four randomly selected arms were selected and baited with food; no more than two adjacent arms were baited. The partially baited RAM was preferred over the all-arms-baited RAM to prevent stereotypic behaviors (e.g., visiting arms sequentially; see Lanke et al 1993) and to allow operational measurements of reference and working memory (Olton et al 1979). In the first six sessions, food pellets were placed along the arms as well as at the end of the arms; performance during these trials were not scored.…”

Section: Methodsmentioning

confidence: 99%

Hippocampal CA1 kindling but not long-term potentiation disrupts spatial memory performance

Leung¹,

Shen²

2006

Learn. Mem.

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Long-term synaptic enhancement in the hippocampus has been suggested to cause deficits in spatial performance. Synaptic enhancement has been reported after hippocampal kindling that induced repeated electrographic seizures or afterdischarges (ADs) and after long-term potentiation (LTP) defined as synaptic enhancement without ADs. We studied whether repeated stimulations that gave LTP or ADs resulted in spatial performance deficits on the radial arm maze (RAM) and investigated the minimal number of ADs required for such deficits. Three experimental groups were run as follows: (1) 5 hippocampal ADs in 1 d (5-AD group), (2) 10 hippocampal ADs in 2 d (10-AD group), and (3) 12 θ-frequency primed-burst stimulations (PBSs) in 2 d in order to induce LTP without ADs (LTP group). Each experimental group was run together with a control group during the same time period. Rats were first trained in a spatial task on a radial arm maze with four of the eight arms baited, then given control or experimental treatment, and maze performance was tested in the first week (1-4 d) and fourth week (22-25 d) after treatment. Basal dendritic population excitatory postsynaptic potentials (pEPSPs) and medial perforant path (MPP)-evoked dentate gyrus population spike and polysynaptic CA1 excitation were recorded before and after experimental and control treatment. Spatial memory errors, in particular reference memory errors, were significantly higher in the 10-AD kindled group than any other group on the first and fourth week after treatment. Spatial memory errors were not significantly different in the 5-AD and LTP groups as compared with any control groups at any time. Basal dendritic pEPSP in CA1 was enhanced for about 1 wk after 12 PBSs, 10 ADs, or 5 ADs, while the dentate gyrus population spike and CA1 polysynaptic excitation evoked by MPP was increased for up to 4 wk after 10 ADs, but not 12 PBSs. Thus, distributed alteration of multiple synaptic transmission in the entorhinal-hippocampal circuit, but not LTP at the basal dendritic synapses in CA1, may disrupt spatial performance after 10 hippocampal ADs.

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Spatial memory and stereotypic behaviour of animals in radial arm mazes

Cited by 18 publications

References 17 publications

Maternal Stress Produces Learning Deficits Associated with Impairment of NMDA Receptor-Mediated Synaptic Plasticity

Maternal Stress Produces Learning Deficits Associated with Impairment of NMDA Receptor-Mediated Synaptic Plasticity

Preweaning manganese exposure causes hyperactivity, disinhibition, and spatial learning and memory deficits associated with altered dopamine receptor and transporter levels

Hippocampal CA1 kindling but not long-term potentiation disrupts spatial memory performance

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