English
 
User Manual Privacy Policy Disclaimer Contact us
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Poster

Burst-like stimulation of the locus coeruleus leads to thalamo-cortical activation and hippocampal suppression: implication for competing networks

MPS-Authors
/persons/resource/persons83895

Eschenko,  O
Max Planck Institute for Biological Cybernetics, Max Planck Society;
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

/persons/resource/persons84105

Neves,  RM
Max Planck Institute for Biological Cybernetics, Max Planck Society;
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

/persons/resource/persons192674

Yang,  M
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

/persons/resource/persons84063

Logothetis,  NK
Max Planck Institute for Biological Cybernetics, Max Planck Society;
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

Locator

Link
(Any fulltext)

Fulltext (public)
There are no public fulltexts available
Supplementary Material (public)
There is no public supplementary material available
Citation

Eschenko, O., Neves, R., Yang, M., & Logothetis, N. (2016). Burst-like stimulation of the locus coeruleus leads to thalamo-cortical activation and hippocampal suppression: implication for competing networks. Poster presented at 46th Annual Meeting of the Society for Neuroscience (Neuroscience 2016), San Diego, CA, USA.


Cite as: http://hdl.handle.net/21.11116/0000-0000-7AE8-2
Abstract
Diffusely projecting noradrenergic (NE) neurons of the brainstem nucleus locus coeruleus (LC) regulate excitatory/inhibitory balance in their multiple forebrain targets. The net effect of LC activation depends on the amount of NE released and mediated by different types of adrenergic receptors. It has been long recognized that a predominant effect of NE in cortex is suppression of spontaneous firing, which increases a signal-to-noise ratio of sensory transmission. However, we have recently reported that a brief phasic activation of LC transiently increases gamma power and spike probability in the prefrontal cortex (PFC). Research on NE effects in hippocampus mainly focused on synaptic plasticity. The vast experimental evidence shows that NE release in hippocampus creates a temporal window of heightened synaptic plasticity, but both potentiation and depression effects have been documented. Here, we recorded simultaneously extracellular activity in multiple cortical and subcortical projection targets of LC including sensory and associative thalamic nuclei, hippocampus, sensory cortex and PFC in the urethane-anesthetized rat using high-density multi-electrode arrays. We quantified the effects of LC phasic activation (direct electric current: 0.5mA, at 50-100Hz for 100-200 ms) on neural activity using band-limited power (BLP) analysis. Briefly, a wide-band (0.1Hz-8kHz) signal was band-pass filtered in different frequency ranges; the BLP for each band was normalized to pre-stimulus values and the magnitude of power modulation was extracted over 1s post-stimulus period. Power increase/decrease in the gamma frequency range was indicative for excitatory/inhibitory net effect, respectively. The LC stimulation produced remarkable dissociation between thalamo-cortical activation and strong suppression of neural activity in hippocampus. The neuromodulatory effects were transient and lasted for 1-3 s post-stimulation. This result suggests that LC phasic activation in response to salient stimuli potentiates broadcasting within thalamo-cortical circuit, while suppresses potentially competing hippocampal-cortical network, which support ‘off-line’ information processing. Present results also consistent with our recent findings that LC stimulation at times of hippocampal ripples after learning reduced the efficiency of ‘off-line’ memory consolidation, possibly by activating a competing thalamo-cortical network and therefore causing interference for hippocampal-cortical communication.