Abstract
Noradrenergic modulation from the locus coerulus is often associated with the regulation of sensory signal-to-noise ratio. In the olfactory system, noradrenergic modulation affects both bulbar and cortical processing, and has been shown to modulate the detection of low concentration stimuli. We here implemented a computational model of the olfactory bulb and piriform cortex, based on known experimental results, to explore how noradrenergic modulation in the olfactory bulb and piriform cortex interact to regulate odor processing. We show that as predicted by behavioral experiments in our lab, norepinephrine can play a critical role in modulating the detection and associative learning of very low odor concentrations. Our simulations show that bulbar norepinephrine serves to pre-process odor representations to facilitate cortical learning, but not recall. We observe the typical non-uniform dose—response functions described for norepinephrine modulation and show that these are imposed mainly by bulbar, but not cortical processing.
Highlights
Both the olfactory bulb (OB) and the piriform cortex (PC) are innervated by the locus coeruleus (LC), which releases the catecholamine neuromodulator norepinephrine (NE)
The non-linearity arises from differential effects of NE on α1 and α2 receptors in the OB (Nai et al, 2009, 2010; Figure 1B), first decreasing inhibition due to α2 receptor activation, and increasing inhibition due to α1 receptor activation, paired with increased excitation of mitral cells at medium NE levels
Rats were habituated to mineral oil (MO), the carrier that odorants are diluted in, during three 1 min trials separated by 5 min intertrial intervals (Figure 2Ci)
Summary
Both the olfactory bulb (OB) and the piriform cortex (PC) are innervated by the locus coeruleus (LC), which releases the catecholamine neuromodulator norepinephrine (NE). Odor representations in the olfactory bulb are modulated by olfactory learning (Mandairon and Linster, 2009), both with respect to mitral cell firing rates (Kay and Laurent, 1999; Doucette and Restrepo, 2008), oscillatory dynamics (reviewed in Kay et al, 2009), and synchronization properties (Doucette et al, 2011) This type of plasticity can be assumed to be heavily dependent on neuromodulatory inputs, including those from the LC (Doucette et al, 2011). Brain slice physiology paired with computational modeling work supports the idea that NE modulation in the olfactory cortex can modulate cortical associative memory function (Hasselmo et al, 1997) by regulating signal to noise ratios as well as synaptic transmission between pyramidal cells. Cortical and bulbar NE cooperate to enhance the learning of odorants in the cortical network, NE impairs the recall of learned odor patterns in cortex
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