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.