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Differential noradrenergic modulation of the rat somatosensory and prefrontal cortex

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons84393

van Keulen,  S
Department Empirical Inference, Max Planck Institute for Biological Cybernetics, Max Planck Society;
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons84063

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

http://pubman.mpdl.mpg.de/cone/persons/resource/persons83895

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

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Citation

van Keulen, S., Logothetis, N., & Eschenko, O. (2011). Differential noradrenergic modulation of the rat somatosensory and prefrontal cortex. Poster presented at 12th Conference of Junior Neuroscientists of Tübingen (NeNA 2011), Heiligkreuztal, Germany.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0013-B9B8-F
Abstract
Noradrenaline (NE) is known to modulate sensory processing by increasing the signal-tonoise ratio (SNR). Pre- and postsynaptic mechanisms acting on cortical adrenoreceptors have been implicated. The noradrenergic nucleus Locus Coeruleus (LC) is activated by sensory stimulation. However, the contribution of the sensory-evoked discharge in LC to modulation of cortical sensory responses is not well understood. We compared the effects of systemic or local (in LC) application of clonidine, an alpha2-receptor agonist, which is known to inhibit LC-NE neurons, on sensory responses in two cortical targets of LC. Simultaneous recordings in LC, primary Somatosensory (S1) and medial Prefrontal Cortex (mPFC) were performed in the urethane-anesthetized rat. Electrical foot shocks (FS) of the contralateral hind paw served as somatosensory stimuli (0.5ms, 5mA). The LC responses to FS differed dramatically after local and systemic clonidine administration. Iontophoretic application of clonidine (50nA, 50μl/ml, 20min) into LC resulted in complete cessation of both spontaneous and evoked activity of LC-NE neurons. Systemic clonidine (50 μl/ml, i.p.) produced a decrease in LC firing (less than 50 baseline for 30 min), however the LC responses to FS were preserved. Both local and systemic clonidine administration increased spontaneous activity in S1 and mPFC. The evoked responses in S1 were unchanged under condition of complete inhibition of the ipsilateral LC by local application of clonidine (n=13) and decreased during systemic clonidine condition (n=13). In mPFC, 8 units (40) increased and 9 units (45) decreased the response amplitude following local inhibition of LC. Four out of 24 mPFC neurons showed increased responses after systemic clonidine injection. Strikingly, 20 of initially non-responsive mPFC neurons became responsive (n=7) in case of local inhibition of LC. The same phenomenon was observed during systemic clonidine in 58 of cases (n=14). Thus, blocking the LC sensory-evoked discharge differentially affected signal processing in S1 and mPFC. The responses in S1 were preserved, while responses of a large proportion of mPFC neurons ( 50) were affected. We observed the opposite effects in S1 (decrease SNR) and mPFC (increased signaling) after activation of the alpha2 receptors in the entire brain. Overall, we conclude that alpha2 receptors are involved in sensory signal processing in both cortical regions, but mPFC receives a stronger NE neuromodulatory input.