Monoaminergic Neuromodulation of Sensory Processing (original) (raw)
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A matter of focus: monoaminergic modulation of stimulus coding in mammalian sensory networks
Current Opinion in Neurobiology, 2004
Although the presence of neuromodulators in mammalian sensory systems has been noted for some time, a groundswell of evidence has now begun to document the scope of these regulatory mechanisms in several sensory systems, highlighting the importance of neuromodulation in shaping feature extraction at all levels of neural processing. The emergence of more sophisticated models of sensory encoding and of the interaction between sensory and regulatory regions of the brain will challenge sensory neurobiologists to further incorporate a concept of sensory network function that is contingent on neuromodulatory and behavioral state.
The Neuroscientist, 2020
How do monoamines influence the perceptual and behavioral aspects of brain function? A library of information regarding the genetic, molecular, cellular, and function of monoamines in the nervous system and other organs has accumulated. We briefly review monoamines' anatomy and physiology and discuss their effects on the target neurons and circuits. Monoaminergic cells in the brain stem receive inputs from sensory, limbic, and prefrontal areas and project extensively to the forebrain and hindbrain. We review selected studies on molecular, cellular, and electrophysiological effects of monoamines on the brain's target areas. The idea is that monoamines, by reversibly modulating the "primary" information processing circuits, regulate and switch the functions of brain networks and can reversibly alter the "brain states," such as consciousness, emotions, and movements. Monoamines, as the drivers of normal motor and sensory brain operations, including housekeeping, play essential roles in pathogenesis of neuropsychiatric diseases.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001
Deficiency in the monoamine degradation enzyme monoamine oxidase A (MAOA) or prenatal exposure to the monoamine uptake inhibitor cocaine alters behavior in humans and rodents, but the mechanisms are unclear. In MAOA knock-out mice, inhibiting serotonin synthesis during development can prevent abnormal segregation of axons in the retinogeniculate and somatosensory thalamocortical systems. To investigate this effect, we crossed MAOA knock-outs with mice lacking the serotonin transporter 5-HTT or the 5-HT1B receptor, two molecules present in developing sensory projections. Segregation was abnormal in 5-HTT knock-outs and MAOA/5-HTT double knock-outs but was normalized in MAOA/5-HT1B double knock-outs and MAOA/5-HTT/5-HT1B triple knock-outs. This demonstrates that the 5-HT1B receptor is a key factor in abnormal segregation of sensory projections and suggests that serotonergic drugs represent a risk for the development of these projections. We also found that the 5-HT1B receptor has an a...
Frontiers in Behavioral Neuroscience, 2012
single cell level, facilitation of evoked responses, increases in signal-to-noise ratio, and improved functional properties of sensory cortex neurons have been reported in the visual, auditory, and somatosensory modality. At the map level, massive cortical reorganizations have been described when repeated activation of a neuromodulatory system are associated with a particular sensory stimulus. In reviewing our knowledge concerning the way the noradrenergic and cholinergic system control sensory cortices, I will point out that the differences between the protocols used to reveal these effects most likely reflect different assumptions concerning the role of the neuromodulators. More importantly, a gap still exists between the descriptions of neuromodulatory effects and the concepts that are currently applied to decipher the neural code operating in sensory cortices. Key examples that bring this gap into focus are the concept of cell assemblies and the role played by the spike timing precision (i.e., by the temporal organization of spike trains at the millisecond time-scale) which are now recognized as essential in sensory physiology but are rarely considered in experiments describing the role of neuromodulators in sensory cortices. Thus, I will suggest that several lines of research, particularly in the field of computational neurosciences, should help us to go beyond traditional approaches and, ultimately, to understand how neuromodulators impact on the cortical mechanisms underlying our perceptual abilities.
Effects of neonatal dopamine depletion on sensory inhibition in the rat
Pharmacology Biochemistry and Behavior, 1996
of neonotuldopamine depletion on sensory inhibition in the ruf. PHARMACOL BIOCHEM BEHAV 53(4) 817-823, 1996.-Central dopamine systems appear to play an important role in sensory information processing. In particular, the filtering (or gating) of repetitive auditory stimuli is modulated by pharmacological manipulations that affect dopaminergic neurotransmission. The present study further addressed the role of dopamine in auditory gating. Three-day-old male Sprague-Dawley rats, pretreated with desipramine, received intracisternal injections of 6-hydroxydopamine (6-OHDA; 75 pg in 10 ~1) or the vehicle. At 4 months of age the rats were implanted for evoked potential recording and auditory gating was assessed using a paired click paradigm. Neonatally administered 6-OHDA did not alter gating in the adult rats. However, unlike for the control group, systemic amphetamine (1.83 mg/kg, IP) failed to disrupt gating in the treated rats. Apomorphine (1.0 mg/kg, SC) disrupted gating in both groups. Neonatal 6-OHDA treatment caused significant reductions in dopamine levels in the striatum, nucleus accumbens, and substantia nigra/ventral tegmental regions. There was an inverse relationship between substantia nigra/ ventral tegmental area dopamine levels and auditory gating. Overall, the results suggest that amphetamine-induced auditory gating loss requires presynaptic dopamine release, but that the deficiency occurs through postsynaptic dopamine receptor activation.
Serotonergic development of active sensing
Active sensing requires adaptive motor (positional) control of sensory organs based on contextual, sensory and task requirements, and develops postnatally after the maturation of intracortical circuits. Alterations in sensorimotor network connectivity during this period are likely to impact sensorimotor computation also in adulthood. Serotonin is among the cardinal developmental regulators of network formation, thus changing the serotonergic drive might have consequences for the emergence and maturation of sensorimotor control. Here we tested this hypothesis on an object localization task by quantifying the motor control dynamics of whiskers during tactile navigation. The results showed that sustained alterations in serotonergic signaling in serotonin transporter knockout rats, or the transient pharmacological inactivation of the transporter during early postnatal development, impairs the emergence of adaptive motor control of whisker position based on recent sensory information. A ...
Neuroscience, 2000
The role of monoaminergic neuromodulators in the reorganization of cortical topography following limited sensory deprivation in the adult cat was investigated. The total concentrations of dopamine, noradrenaline, serotonin and their major metabolites were measured in the visual cortex of both normal control and experimental animals using microbore high-performance liquid chromatography coupled with electrochemical detection. The experimental animals were subjected to a binocular retinal lesion corresponding to the central 10Њ of vision and killed two weeks post-lesion. The sensory deprivation was confirmed in area 17 by measuring immediate-early gene zif-268 messenger RNA expression. Following the retinal lesion, the total concentrations of noradrenaline and dopamine were significantly higher in the non-deprived cortex of retinal lesion cats than in the deprived cortex of retinal lesion cats and the cortex of normal animals. This pattern follows the release of the excitatory neurotransmitter glutamate under the same conditions. Serotonin levels were significantly lower in the deprived cortex, and its metabolite 5-hydroxyindole-3acetic acid was significantly higher in the non-deprived cortex than in deprived cortex and normal cortex.
Neuroscience, 2008
A behavioral reaction to sensory stimulation is a basic mechanism which is pivotal to many complex behavioral responses. In previous studies we found that visual stimulation induces a selective serotonergic and dopaminergic activation in the occipital (OccC), but not temporal (TempC) cortex in freely moving rats. In a behavioral study in rats we demonstrate now that visual stimulation (0, 8, 22, 82, 155 or 440 lux) activates behavioral activity in an intensitydependent manner. Behavior activating visual stimulation with 82 lux, but not 22 lux or 82 dB white noise, increased extracellular serotonin (5-HT), but not dopamine (DA), in the medial prefrontal cortex (mPFC) in freely moving animals measured by in vivo microdialysis. There was no effect on 5-HT or DA in the entorhinal and perirhinal cortex. Visual stimulation with 82 lux increased extracellular 5-HT in the mPFC and OccC also in anesthetized animals, but had no effect in the TempC. Auditory stimulation reduced 5-HT in the TempC, but had no effect in the mPFC or OccC. Neither visual nor auditory stimulation had a significant effect on DA in all three cortical areas. We conclude that visual stimulation induces behavioral activation by increasing 5-HT activity in the mPFC and OccC.