Behavioral differences among 129 substrains: Implications for knockout and transgenic mice.

Cook, Melloni N.; Bolivar, Valerie I.; McFadyen, Melanie P.; Flaherty, Lorraine

doi:10.1037/0735-7044.116.4.600

Cited by 103 publications

(118 citation statements)

References 36 publications

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“…However, Cook et al (2002) found that contextual and cued fear conditioning were normal in 129P1/ReJ mice compared with C57BL/6J mice. Thus, it is unlikely that the genetic contribution of 129P1/ReJ to the 9XCA/Wah strain is the sole cause of altered hippocampal synaptic transmission and impaired memory extinction.…”

Section: Discussionmentioning

confidence: 97%

Selective Modification of Short-Term Hippocampal Synaptic Plasticity and Impaired Memory Extinction in Mice with a Congenitally Reduced Hippocampal Commissure

Schimanski¹,

Wahłsten

Nguyen

2002

J. Neurosci.

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The hippocampus is critical for forming new long-term memories, but the contributions of the hippocampal commissure (HC) to memory function and hippocampal synaptic plasticity are unclear. To shed light on this issue, we characterized behavioral memory and hippocampal synaptic plasticity in two inbred mouse strains. BALB/cWah1 mice display a range of corpus callosal defects and an intact HC, whereas 9XCA/Wah mice exhibit a complete absence of corpus callosum and a greatly reduced HC. No differences between strains were found in long-term potentiation (LTP) within two synaptic pathways in hippocampal slices. However, paired-pulse facilitation was deficient in area CA1 of slices from 9XCA/Wah, and it was rescued by decreasing extracellular [Ca 2ϩ ], suggesting that presynaptic calcium dynamics may be altered in this strain. In addition, contextual fear extinction was impaired in 9XCA/Wah mice, but performance on cued fear extinction and on 24 hr memory tests for cued and contextual fear conditioning were not significantly different between strains. Thus, an intact HC is critical for normal extinction of contextual fear. Intact interhemispheric connectivity is not required for acquisition or expression of cued and contextual fear conditioning. LTP was normal in slices from mice that lacked an intact HC, and this was correlated with normal performance on fear conditioning tests. In contrast, impaired short-term synaptic plasticity was correlated with defective contextual memory extinction in mice lacking an intact HC. Thus, the HC in mice is vital for particular aspects of memory function and for short-term synaptic modification in specific hippocampal circuits. Key words: hippocampal commissure; memory; learning; LTP; fear conditioning; extinction; agenesis; mouse strains; synaptic plasticityThe classic case study of H.M., a patient with surgical transection of the medial temporal lobes, demonstrated that the hippocampus is critical for the formation of new declarative memories (Scoville and Milner, 1957). Studies of human commissurotomy patients indicate that the main interhemispheric communication pathway between hippocampi, the hippocampal commissure (HC), is important for normal memory function. Indeed, patients with a transected HC show greater recognition memory deficits than those with an intact HC (Phelps et al., 1991). Patients with transection of both the corpus callosum (CC) and the HC also showed poor memory performance (Zaidel and Sperry, 1974). These findings indicate that an intact CC and HC are required for normal memory function.In two common inbred mouse strains, BALB/c and 129, agenesis of the CC occurs in Ͻ50% of these mice, whereas the remainder appear to have normal forebrain commissures (see Fig.

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Section: Discussionmentioning

confidence: 97%

Selective Modification of Short-Term Hippocampal Synaptic Plasticity and Impaired Memory Extinction in Mice with a Congenitally Reduced Hippocampal Commissure

Schimanski¹,

Wahłsten

Nguyen

2002

J. Neurosci.

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“…Symptomatic YAC128 mice also showed deficits in open-field habituation, a simple test of learning and memory (Gerlai et al, 1996;Bolivar et al, 2000;Cook et al, 2002). At 8 months of age, YAC128 mice were hypoactive compared with WT mice.…”

Section: Cognitive Deficits In Symptomatic Yac128 Micementioning

confidence: 99%

Cognitive Dysfunction Precedes Neuropathology and Motor Abnormalities in the YAC128 Mouse Model of Huntington's Disease

Raamsdonk¹,

Pearson²,

Slow³

et al. 2005

J. Neurosci.

284

232

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Huntington's disease (HD) is an adult-onset neurodegenerative disorder involving motor dysfunction, cognitive deficits, and psychiatric disturbances that result from underlying striatal and cortical dysfunction and neuropathology. The YAC128 mouse model of HD reproduces both the motor deficits and selective degeneration observed in the human disease. However, the presence of cognitive impairment in this model has not been determined. Here, we report mild cognitive deficits in YAC128 mice that precede motor onset and progressively worsen with age. Rotarod testing revealed a motor learning deficit at 2 months of age that progresses such that by 12 months of age, untrained YAC128 mice are unable to learn the rotarod task. Additional support for cognitive dysfunction is evident in a simple swimming test in which YAC128 mice take longer to find the platform than wild-type (WT) controls beginning at 8 months of age. YAC128 mice also have deficits in open-field habituation and in a swimming T-maze test at this age. Strikingly, in the reversal phase of the swimming T-maze test, YAC128 mice take twice as long as WT mice to locate the platform, indicating a difficulty in changing strategy. At 12 months of age, YAC128 mice show decreased prepulse inhibition and habituation to acoustic startle. The clear pattern of cognitive dysfunction in YAC128 mice is similar to the symptoms and progression of cognitive deficits in human HD and provides both the opportunity to examine the relationship between cognitive dysfunction, motor impairment, and neuropathology in HD and to assess whether potential therapies for HD can restore cognitive function.

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“…This is an element of context that only a handful of laboratories have used (Cook et al 2002;Wrenn et al 2002;Balogh and Wehner 2003;Bothe et al 2004;Gould et al 2004), and we believe it reduced effects unrelated to tone-shock associations by making the contexts more distinguishable. Although the visual (checkered vs. solid colored walls) and tactile elements (smooth vs. grid floor; square vs. octagon shape) yielded discriminable contexts in the Initial Protocol, as reflected in the different levels of freezing to the two contexts in the initial study, the addition of odor to one of the two contexts during the Final Protocol provided a distinguishing element in a sensory modality that is highly salient to mice (Doty 1986;Beauchamp and Yamazaki 2003;Breer 2003).…”

Section: Modification Of Experimental Parameters Reduced Nonassociatimentioning

confidence: 99%

Genetic background differences and nonassociative effects in mouse trace fear conditioning

Smith¹,

Gallagher²,

Stanton³

2007

Learn. Mem.

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Fear conditioning, including variants such as delay and trace conditioning that depend on different neural systems, is widely used to behaviorally characterize genetically altered mice. We present data from three strains of mice, C57/BL6 (C57), 129/SvlmJ (129), and a hybrid strain of the two (F 1 hybrids), trained on various versions of a trace fear-conditioning protocol. The initial version was taken from the literature but included unpaired control groups to assess nonassociative effects on test performance. We observed high levels of nonassociative freezing in both contextual and cued test conditions. In particular, nonassociative freezing in unpaired control groups was equivalent to freezing shown by paired groups in the tests for trace conditioning. A number of pilot studies resulted in a new protocol that yielded strong context conditioning and low levels of nonassociative freezing in all mouse strains. During the trace-CS test in this protocol, freezing in unpaired controls remained low in all strains, and both the C57s and F 1 hybrids showed reliable associative trace fear conditioning. Trace conditioning, however, was not obtained in the 129 mice. Our findings indicate that caution is warranted in interpreting mouse fear-conditioning studies that lack control conditions to address nonassociative effects. They also reveal a final set of parameters that are important for minimizing such nonassociative effects and demonstrate strain differences across performance in mouse contextual and trace fear conditioning.

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Behavioral differences among 129 substrains: Implications for knockout and transgenic mice.

Cited by 103 publications

References 36 publications

Selective Modification of Short-Term Hippocampal Synaptic Plasticity and Impaired Memory Extinction in Mice with a Congenitally Reduced Hippocampal Commissure

Selective Modification of Short-Term Hippocampal Synaptic Plasticity and Impaired Memory Extinction in Mice with a Congenitally Reduced Hippocampal Commissure

Cognitive Dysfunction Precedes Neuropathology and Motor Abnormalities in the YAC128 Mouse Model of Huntington's Disease

Genetic background differences and nonassociative effects in mouse trace fear conditioning

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