The brain dynamically changes its input-output relationship depending on the behavioral state and context in order to optimize information processing. At the molecular level, cholinergic/monoaminergic transmitters have been extensively studied as key players for the state/context-dependent modulation of brain function. In this paper, we review how cortical visual information processing in the primary visual cortex (V1) of macaque monkey, which has a highly differentiated laminar structure, is optimized by serotonergic and cholinergic systems by examining anatomical and in vivo electrophysiological aspects to highlight their similarities and distinctions. We show that these two systems have a similar layer bias for axonal fiber innervation and receptor distribution. The common target sites are the geniculorecipient layers and geniculocortical fibers, where the appropriate gain control is established through a geniculocortical signal transformation. Both systems exert activity-dependent response gain control across layers, but in a manner consistent with the receptor subtype. The serotonergic receptors 5-HT1B and 5HT2A modulate the contrast-response curve in a manner consistent with bi-directional response gain control, where the sign (facilitation/suppression) is switched according to the firing rate and is complementary to the other. On the other hand, cholinergic nicotinic/muscarinic receptors exert mono-directional response gain control without a sign reversal. Nicotinic receptors increase the response magnitude in a multiplicative manner, while muscarinic receptors exert both suppressive and facilitative effects. We discuss the implications of the two neuromodulator systems in hierarchical visual signal processing in V1 on the basis of the developed laminar structure.

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Serotonin (5-HT) is a neuromodulator secreted from serotonergic neurons located in the pons and upper brain stem in a behavioral context-dependent manner. The serotonergic axon terminals innervate almost the whole brain, causing modulatory actions on various brain functions including vision. Our previous study demonstrated the visual responses of neurons in the primary visual cortex (V1) of anesthetized monkeys were modulated by the activation of 5-HT receptors depending on the response magnitude, in which 5-HT2A receptor-selective agonists enhanced weak visual responses but not strong responses. This observation suggests that the activation of serotonergic receptors modulates neuronal visual information processing to improve the behavioral detectability of a stimulus. However, it remains unknown if 5-HT improves visual detectability at the behavioral level. To investigate this point, visual detectability was measured as contrast sensitivity (CS) in freely moving rats using a two-alternative forced-choice visual detection task (2AFC-VDT) combined with the staircase method. The grating contrast was decreased or increased step by step after a correct choice (hit) or incorrect choice (miss), respectively. CS was evaluated as an inverse value of the visual contrast threshold. The effect of the intraperitoneal administration of fluoxetine (FLX, 5 mg/kg), a selective serotonin reuptake inhibitor, on CS was tested. The CS of rats was significantly higher in FLX than control conditions, and the drug effect showed specificity for the spatial frequency (SF) of a grating stimulus, in which CS improvement was observed at optimal SF but not non-optimal high SF. Thus, we conclude that endogenously-secreted serotonin in the brain improves visual detectability, which may be mediated by vision-related neurons acquiring SF information of the visual stimulus. PLOS ONEPLOS ONE | https://doi.org/10.

Rationale Noradrenaline (NA) is a neuromodulator secreted from noradrenergic neurons in the locus coeruleus to the whole brain depending on the physiological state and behavioral context. It regulates various brain functions including vision via three major adrenergic receptor (AR) subtypes. Previous studies investigating the noradrenergic modulations on vision reported different effects, including improvement and impairment of perceptual visual sensitivity in rodents via β-AR, an AR subtype. Therefore, it remains unknown how NA affects perceptual visual sensitivity via β-AR and what neuronal mechanisms underlie it. Objectives The current study investigated the noradrenergic modulation of perceptual and neuronal visual sensitivity via β-AR in the primary visual cortex (V1). Methods We performed extracellular multi-point recordings from V1 of rats performing a go/no-go visual detection task under the head-fixed condition. A β-AR blocker, propranolol (10 mM), was topically administered onto the V1 surface, and the drug effect on behavioral and neuronal activities was quantified by comparing pre-and post-drug administration. Results The topical administration of propranolol onto the V1 surface significantly improved the task performance. An analysis of the multi-unit activity in V1 showed that propranolol significantly suppressed spontaneous activity and facilitated the visual response of the recording sites in V1. We further calculated the signal-to-noise ratio (SNR), finding that the SNR was significantly improved after propranolol administration. Conclusions Pharmacological blockade of β-AR in V1 improves perceptual visual detectability by modifying the SNR of neuronal activity.