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  • Title: Deletion of connexin45 in mouse neurons disrupts one-trial object recognition and alters kainate-induced gamma-oscillations in the hippocampus.
    Author: Zlomuzica A, Reichinnek S, Maxeiner S, Both M, May E, Wörsdörfer P, Draguhn A, Willecke K, Dere E.
    Journal: Physiol Behav; 2010 Sep 01; 101(2):245-53. PubMed ID: 20471991.
    Abstract:
    Neuronal gap junctions, allowing fast intercellular electrotonic signal transfer, have been implicated in mechanisms governing learning and memory processes. We have examined conditional neuron-directed (Cx45fl/fl:Nestin-Cre) connexin45 deficient mice in terms of behavioral and electrophysiological correlates of learning and memory. Behavioral habituation to a novel environment and motor learning were not changed in these mice. Novel object recognition after delays of up to 60min was impaired in neuronal Cx45 deficient mice. However, object-place recognition was not significantly different from controls. Analysis of enhanced green fluorescent reporter protein expression controlled by the endogenous mouse Cx45 promoter in the brain of neuronal Cx45 deficient mice suggested that Cx45 is expressed in the perirhinal cortex and the CA3 subregion of the hippocampus. The neuronal Cx45 deficient mice were also examined for aberrations in the generation and synchronization of network oscillations in the hippocampus. General excitability, synaptic short time plasticity, and spontaneous high-frequency oscillations (sharp-wave ripples) in the hippocampus were not different from controls. However, bath stimulation of hippocampal slices with kainate induced significantly lower gamma-oscillation amplitudes in the CA3, but not in the CA1 subfield of the neuronal Cx45 deficient mice. Additionally, they exhibited a significantly larger full width half maximum of the frequency distribution in the CA1 subfield as compared to the controls. In conclusion, the neuron-directed deletion of Cx45 impaired one-trial novel object recognition and altered kainate-induced gamma-oscillations possibly via the disruption of inter-neuronal gap junctional communication in the hippocampus or perirhinal cortex.
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