Anna I. Cowan

Multiple mechanisms govern the dynamics of depression at neocortical synapses of young rats.

Synaptic transmission between pairs of excitatory neurones in layers V (N= 38) or IV (N= 6) of somatosensory cortex was examined in a parasagittal slice preparation obtained from young Wistar rats (14–18 days old). A combined experimental and theoretical approach reveals two characteristics of short‐term synaptic depression. Firstly, as well as a release‐dependent depression, there is a release‐independent component that is evident in smaller postsynaptic responses even following failure to release transmitter. Secondly, recovery from depression is activity dependent and is faster at higher input frequencies. Frequency‐dependent recovery is a Ca2+‐dependent process and does not reflect an underlying augmentation. Frequency‐dependent recovery and release‐independent depression are correlated, such that at those connections with a large amount of release‐independent depression, recovery from depression is faster. In addition, both are more pronounced in experiments performed at physiological temperatures. Simulations demonstrate that these homeostatic properties allow the transfer of rate information at all frequencies, essentially linearizing synaptic responses at high input frequencies.

Ionic basis of membrane potential changes induced by anoxia in rat dorsal vagal motoneurones.

1. The effects of anoxia on membrane properties of 119 dorsal vagal motoneurones (DVMs) were investigated in an in vitro slice preparation of the rat medulla. 2. Membrane potential was unaffected by anoxia in 11% of DVMs. An hyperpolarization accompanied by a decrease in input resistance occurred in 44% of DVMs; the remaining 45% depolarized with either an increase (60%) or decrease in input resistance (40%). TTX at a concentration of 0.3‐1 microM did not significantly affect these responses. 3. Anoxic artificial cerebrospinal fluid (ACSF) containing 20 mM‐TEA reversed the response of DVMs that hyperpolarized in standard ACSF to reveal a depolarization of 7.4 +/‐ 2.1 mV, and increased the anoxic depolarization from 5.0 +/‐ 0.7 to 8.7 +/‐ 1.4 mV. 4. Anoxic depolarization was converted to an hyperpolarization of 7.3 +/‐ 2.1 mV in ACSF containing 5 mM‐4‐aminopyridine (4‐AP) and 1 microM‐TTX. A residual depolarization of 4.5 +/‐ 3.5 mV was then observed in ACSF containing 5 mM‐4‐AP, 1 microM‐TTX and 20 mM‐TEA. Anoxic hyperpolarization was increased from 7.8 +/‐ 1.8 to 10.0 +/‐ 3.9 mV in 5 mM‐4‐AP and 1 microM‐TTX and converted to a depolarization of 5.3 +/‐ 4.5 mV in 5 mM‐4‐AP, 1 microM‐TTX and 20 mM‐TEA. 5. In anoxic ACSF containing TEA, the action potential width was increased from 0.92 +/‐ 0.04 to 8.1 +/‐ 1.1 ms in hyperpolarizing DVMs, and from 0.85 +/‐ 0.01 to 2.4 +/‐ 1.0 ms in depolarizing DVMs. The increase in width was prevented by 2‐3 mM‐Mn2+. 6. The long after‐hyperpolarization (AHP) of DVMs, which is contributed to by both an apamin‐sensitive IK(Ca) and an apamin, charybdotoxin and TEA insensitive IK(Ca) was decreased in duration from 2.59 +/‐ 0.14 to 1.94 +/‐ 0.12 s during anoxia. 7. It is concluded that anoxia enhances the delayed rectifier current (IK(DR)) and an inward current, probably ICa, but suppresses the A currents (IA). In DVMs that hyperpolarize during anoxia, the increase in IK(DR) outweighs the increase in ICa and the decrease in IA. In depolarizing DVMs the decrease in IA and increase in ICa outweight the increase in IK(DR). The change in input resistance is determined by the relative sizes of current enhancement or suppression.

Analysis of NMDA-independent long-term potentiation induced at CA3—CA1 synapses in rat hippocampus in vitro

1 Excitatory postsynaptic currents (EPSCs) were evoked at synapses formed by Schaffer collaterals/commissural (CA3) axons with CA1 pyramidal cells using the rat hippocampal slice preparation. Long‐term potentiation (LTP) was induced at these synapses using a pairing protocol, with 50 μm d,l‐APV present in the artificial cerebrospinal fluid (ACSF). 2 Quantal analysis of the amplitudes of the control and conditioned EPSCs showed that the enhancement of synaptic strength was due entirely to an increase in quantal content of the EPSC. No change occurred in the quantal current. 3 These results were compared with those obtained from a previous quantal analysis of LTP induced in normal ACSF, where both quantal current and quantal content increased. The results suggest that calcium entering via NMDA receptors initiates the signalling cascade that results in enhanced AMPA currents because it is adding to cytoplasmic calcium from other sources to reach a threshold for this signalling pathway, or because calcium entering via NMDA receptors specifically activates this signalling pathway.

Quantifying impacts of short-term plasticity on neuronal information transfer

Short-term changes in efficacy have been postulated to enhance the ability of synapses to transmit information between neurons, and within neuronal networks. Even at the level of connections between single neurons, direct confirmation of this simple conjecture has proven elusive. By combining paired-cell recordings, realistic synaptic modeling, and information theory, we provide evidence that short-term plasticity can not only improve, but also reduce information transfer between neurons. We focus on a concrete example in rat neocortex, but our results may generalize to other systems. When information is contained in the timings of individual spikes, we find that facilitation, depression, and recovery affect information transmission in proportion to their impacts upon the probability of neurotransmitter release. When information is instead conveyed by mean spike rate only, the influences of short-term plasticity critically depend on the range of spike frequencies that the target network can distinguish (its effective dynamic range). Our results suggest that to efficiently transmit information, the brain must match synaptic type, coding strategy, and network connectivity during development and behavior.