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Gain control in CA1 pyramidal cells using changes in somatic conductance.

ABSTRACT: Gain modulation is an important feature of neural activity. Previous work has focused on the ability of background synaptic noise to modulate the slope (i.e., gain) of the frequency-current (f-I) relationship in neurons. To date, demonstrations of gain control that are independent of synaptic noise have been limited. We investigated the effects of increasing somatic conductance in the form of tonic inhibition on the initial and steady-state f-I relationship of CA1 pyramidal cells. We find that increasing membrane conductance reduces the gain of the steady-state f-I relationship through a graded increase in the magnitude of spike frequency adaptation. Increased adaptation arises through a conductance-induced depolarization of spike voltage threshold. Thus, by increasing the magnitude of spike frequency adaptation, added conductance can reduce the gain of the steady-state f-I relationship in the absence of random background membrane fluctuations.

SUBMITTER: Fernandez FR

PROVIDER: S-EPMC2865889 | biostudies-other | 2010 Jan

REPOSITORIES: biostudies-other

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Gain control in CA1 pyramidal cells using changes in somatic conductance.

Fernandez Fernando R FR White John A JA

The Journal of neuroscience : the official journal of the Society for Neuroscience 20100101 1

Gain modulation is an important feature of neural activity. Previous work has focused on the ability of background synaptic noise to modulate the slope (i.e., gain) of the frequency-current (f-I) relationship in neurons. To date, demonstrations of gain control that are independent of synaptic noise have been limited. We investigated the effects of increasing somatic conductance in the form of tonic inhibition on the initial and steady-state f-I relationship of CA1 pyramidal cells. We find that i ...[more]

PMID: 20053905

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Project description:CA1 pyramidal neurons receive two distinct excitatory inputs that are each capable of influencing hippocampal output and learning and memory. The Schaffer collateral (SC) input from CA3 axons onto the more proximal dendrites of CA1 is part of the trisynaptic circuit, which originates in Layer II of the entorhinal cortex (EC). The temporoammonic (TA) pathway to CA1 provides input directly from Layer III of the EC onto the most distal dendrites of CA1 pyramidal cells, and is involved in spatial memory and memory consolidation. We have previously described a developmental decrease in short-term facilitation from juvenile (P13-18) to young adult (P28-42) rats at SC synapses that is due to feedback inhibition via synaptically activated mGluR1 on CA1 interneurons. It is not known how short-term changes in synaptic strength are regulated at TA synapses, nor is it known how short-term plasticity is balanced at SC and TA inputs during development. Here we describe a novel developmental increase in short-term facilitation at TA synapses, which is the opposite of the decrease in facilitation occurring at SC synapses. Although short-term facilitation is much lower at TA synapses when compared with SC synapses in juveniles, short-term plasticity at SC and TA synapses converges at similar levels of paired-pulse facilitation in the young adult rat. However, in young adults CA3-CA1 synapses still exhibit more facilitation than TA-CA1 synapses during physiologically-relevant activity, suggesting that the two pathways are each poised to uniquely modulate CA1 output in an activity-dependent manner. Finally, we show that there is a developmental decrease in the initial release probability at TA synapses that underlies their developmental decrease in facilitation, but no developmental change in release probability at SC synapses. This represents a fundamental difference in the presynaptic function of the two major inputs to CA1, which could alter the flow of information in hippocampus during development.

Dataset Information

Gain control in CA1 pyramidal cells using changes in somatic conductance.

Publications

Gain control in CA1 pyramidal cells using changes in somatic conductance.

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