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Long-term plasticity is well documented in synapses between glutamatergic principal cells in the cortex both in vitro and in vivo. Long-term potentiation (LTP) and -depression (LTD) have also been reported in glutamatergic connections to hippocampal GABAergic interneurons expressing parvalbumin (PV+) or nitric oxide synthase (NOS+) in brain slices, but plasticity in these cells has not been tested in vivo. We investigated synaptically-evoked suprathreshold excitation of identified hippocampal neurons in the CA1 area of urethane-anaesthetized rats. Neurons were recorded extracellularly with glass microelectrodes, and labelled with neurobiotin for anatomical analyses. Single-shock electrical stimulation of afferents from the contralateral CA1 elicited postsynaptic action potentials with monosynaptic features showing short delay (9.95 ± 0.41 ms) and small jitter in 13 neurons through the commissural pathway. Theta-burst stimulation (TBS) generated LTP of the synaptically-evoked spike probability in pyramidal cells, and in a bistratified cell and two unidentified fast-spiking interneurons. On the contrary, PV+ basket cells and NOS+ ivy cells exhibited either LTD or LTP. An identified axo-axonic cell failed to show long-term change in its response to stimulation. Discharge of the cells did not explain whether LTP or LTD was generated. For the fast-spiking interneurons, as a group, no correlation was found between plasticity and local field potential oscillations (1-3 or 3-6 Hz components) recorded immediately prior to TBS. The results demonstrate activity-induced long-term plasticity in synaptic excitation of hippocampal PV+ and NOS+ interneurons in vivo. Physiological and pathological activity patterns in vivo may generate similar plasticity in these interneurons. [ABSTRACT FROM AUTHOR]

Rapid memory formation relies, at least in part, on long-term potentiation (LTP) of excitatory synapses. Inhibitory interneurons of the hippocampus, which are essential for information processing, have recently been found to exhibit not one, but two forms of LTP. One form resembles LTP that occurs in pyramidal neurons, which depends on N-methyl-D-aspartate receptors and is triggered by coincident pre- and postsynaptic activity. The other depends on Ca2+ influx through glutamate receptors that preferentially open when the postsynaptic neuron is at rest. Here we review these contrasting forms of LTP and describe how they are mirrored by two forms of long-term depression. We further discuss how the remarkable plasticity of glutamatergic synapses on interneurons greatly enhances the computational capacity of the cortical microcircuit. [ABSTRACT FROM AUTHOR]

Cortical information processing requires a delicate balance of excitatory and inhibitory signaling. How is this balance preserved during hippocampal memory encoding, which involves NMDA receptor–dependent long term potentiation (LTP)? This form of LTP occurs at synapses between pyramidal neurons but has not been detected in feed-forward inhibitory interneurons. We show that paired pre- and postsynaptic activity evokes pathway-specific LTP in half of rat stratum radiatum interneurons if cytoplasmic integrity is preserved. LTP occurs in aspiny feed-forward interneurons and propagates to pyramidal neurons as an enhancement of disynaptic inhibition. We also show that when LTP is restricted to synapses on pyramidal neurons, the temporal fidelity of synaptic integration and action potential generation in pyramidal cells is compromised. However, when LTP also occurs at synapses on feed-forward interneurons, temporal fidelity is preserved. We propose that Hebbian LTP at synapses driving disynaptic inhibition is necessary to maintain information processing without degradation during memory encoding. [ABSTRACT FROM AUTHOR]

Presents research which explores how the K+/Cl- co-transporter KCC2 renders gamma-aminobutyric acid (GABA) hyperpolarizing during neuronal maturation in the rat hippocampus. Developmental induction of the expression of the neuronal Cl- extruding K+/Cl- co-transporter, KCC2; Production of a marked positive shift in the reversal potential of GABA- responses of antisense oligonucleotide with inhibition of KCC2 expression; Implications.