Monitoring serotonin signaling on a subsecond time scale

Dankoski, Elyse C.; Wightman, R. Mark

doi:10.3389/fnint.2013.00044

Cited by 58 publications

(63 citation statements)

References 104 publications

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“…The technique relies on a non-enzymatic oxidation of monoamines to quinones upon passing specific ramp currents through the carbon fiber electrode (CFE) placed in a monoamine-containing milieu, such as brain tissue or a solution. By measuring the oxidation rate, the amount of monoamine released is inferred (Dankoski et al, 2016; Dankoski and Wightman, 2013; Herr et al, 2012; Park et al, 2009; Park et al, 2011; Wood and Hashemi, 2013). The procedure was performed as previously described by our group (Kumar et al, 2016; Mazarati et al, 2008; Pineda et al, 2014; Pineda et al, 2011) with further optimization for directly calculating the amount of the released transmitter.…”

Section: Subjects Materials and Methodsmentioning

confidence: 99%

Galanin contributes to monoaminergic dysfunction and to dependent neurobehavioral comorbidities of epilepsy

Medel-Matus

Shin

Sankar

et al. 2017

Experimental Neurology

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Status epilepticus (SE) in rats, along with chronic epilepsy, leads to the development of behavioral impairments resembling depressive disorder and/or attention deficit/hyperactivity disorder (ADHD), thus reflecting respective comorbidities in epilepsy patients. Suppressed neurotransmitter tone in the raphe nucleus (RN)-prefrontal cortex (PFC) serotonergic pathway and in the locus coeruleus (LC)-PFC noradrenergic pathway underlies depressive- and impulsive- like behavioral deficits respectively. We examined possible mechanisms leading to the monoamine dysfunction in brainstem efferents, namely modulatory effects of the neuropeptide galanin on serotonin (5-HT) and norepinephrine (NE) signaling. SE was induced in young adult male Wistar rats by LiCl and pilocarpine. Epileptic rats were categorized vis-à-vis behavioral deficits as not impaired, “depressed” and “impulsive”. Depressive- and impulsive- like behaviors were examined in the forced swimming test (FST). The strength of serotonergic transmission in RN-PFC and of noradrenergic transmission in LC-PFC was analyzed using in vivo fast scan cyclic voltammetry. Galanin receptor type 1 (GalR1) / type 2 (GalR2) antagonist M40, and a preferential GalR2 antagonist M871 were administered over 3 days locally into either RN or LC by means of ALZET osmotic minipumps connected to locally implanted infusion cannulas. Intra-RN injection of M40 improved serotonergic tone and depressive-like behavior in epileptic “depressed” rats. Intra-LC injection of M40 improved noradrenergic tone and impulsive-like behavior in epileptic “impulsive” rats. The effects of M40 were only observed in impaired subjects. The treatment did not modify neurotransmission and behavior in naïve and epileptic not impaired rats; in “depressed” rats the effects were limited to serotonergic transmission and immobility, while in “impulsive” rats – to noradrenergic transmission and struggling behavior. Intra-RN administration of M871 exacerbated depressive-like behavior, but had no effects on any other of the examined parameters in any category of animals. These findings suggest that endogenous galanin, acting through GalR1 may be involved in the pathophysiology of epilepsy-associated depression and ADHD via inhibiting RN-PFC serotonergic and LC-PFC noradrenergic transmissions respectively.

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Section: Subjects Materials and Methodsmentioning

confidence: 99%

Galanin contributes to monoaminergic dysfunction and to dependent neurobehavioral comorbidities of epilepsy

Medel-Matus

Shin

Sankar

et al. 2017

Experimental Neurology

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“…In this range, the current amplitude changes linearly with concentration (Dankoski and Wightman, 2013). For a typical electrode used in our recordings, each nanoampere of current corresponded to an ∼80 n m change in 5-HT concentration.…”

Section: Methodsmentioning

confidence: 99%

“…The pattern of 5-HT release in LS, and its relation with chirp production, however, remains elusive. In this study, we used fast-scan cyclic voltammetry (FSCV; Dankoski and Wightman, 2013) to detect electrosensory modulation of 5-HT release in the LS, and characterized its relation to chirping behavior.…”

Section: Introductionmentioning

confidence: 99%

Subsecond Sensory Modulation of Serotonin Levels in a Primary Sensory Area and Its Relation to Ongoing Communication Behavior in a Weakly Electric Fish

Fotowat

Harvey‐Girard

Cheer

et al. 2016

eNeuro

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Serotonergic neurons of the raphe nuclei of vertebrates project to most regions of the brain and are known to significantly affect sensory processing. The subsecond dynamics of sensory modulation of serotonin levels and its relation to behavior, however, remain unknown. We used fast-scan cyclic voltammetry to measure serotonin release in the electrosensory system of weakly electric fish, Apteronotus leptorhynchus. These fish use an electric organ to generate a quasi-sinusoidal electric field for communicating with conspecifics. In response to conspecific signals, they frequently produce signal modulations called chirps. We measured changes in serotonin concentration in the hindbrain electrosensory lobe (ELL) with a resolution of 0.1 s concurrently with chirping behavior evoked by mimics of conspecific electric signals. We show that serotonin release can occur phase locked to stimulus onset as well as spontaneously in the ELL region responsible for processing these signals. Intense auditory stimuli, on the other hand, do not modulate serotonin levels in this region, suggesting modality specificity. We found no significant correlation between serotonin release and chirp production on a trial-by-trial basis. However, on average, in the trials where the fish chirped, there was a reduction in serotonin release in response to stimuli mimicking similar-sized same-sex conspecifics. We hypothesize that the serotonergic system is part of an intricate sensory–motor loop: serotonin release in a sensory area is triggered by sensory input, giving rise to motor output, which can in turn affect serotonin release at the timescale of the ongoing sensory experience and in a context-dependent manner.

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“…Third, single unit recordings 22,29 show that rewarding and aversive events activate the same individual DRN neurons and are thus not generated by distinct populations. Finally, because individual 5-HT neurons have broad projection fields 42 and transmit primarily by volume conduction 43 , heterogeneity will tend to be averaged out through pooling by downstream targets.…”

Section: Figure 1 | Inhibition Of Drn 5-mentioning

confidence: 99%

Firing patterns of serotonin neurons underlying cognitive flexibility

Matias

Lottem

Dugué

et al. 2016

Preprint

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Serotonin is implicated in mood and affective disorders 1,2 but growing evidence suggests that its core endogenous role may be to promote flexible adaptation to changes in the causal structure of the environment 3-8 . This stems from two functions of endogenous serotonin activation: inhibiting learned responses that are not currently adaptive 9,10 and driving plasticity to reconfigure them 11-13 . These mirror dual functions of dopamine in invigorating reward-related responses 14,15 and promoting plasticity that reinforces new ones 16,17 . However, while dopamine neurons are known to be activated by reward prediction errors 18,19 , consistent with theories of reinforcement learning 18,20 , the reported firing patterns of serotonin neurons 21-23 do not accord with any existing theories 1,24,25 . Here, we used long-term photometric recordings in mice to study a genetically-defined population of dorsal raphe serotonin neurons whose activity we could link to normal reversal learning. We found that these neurons are activated by both positive and negative prediction errors, thus reporting the kind of surprise signal proposed to promote learning in conditions of uncertainty 26,27 . Furthermore, by comparing cue responses of serotonin and dopamine neurons we found differences in learning rates that could explain the importance of serotonin in inhibiting perseverative responding. Together, these findings show how the firing patterns of serotonin neurons support a role in cognitive flexibility and suggest a revised model of dopamine-serotonin opponency with potential clinical implications.

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Monitoring serotonin signaling on a subsecond time scale

Cited by 58 publications

References 104 publications

Galanin contributes to monoaminergic dysfunction and to dependent neurobehavioral comorbidities of epilepsy

Galanin contributes to monoaminergic dysfunction and to dependent neurobehavioral comorbidities of epilepsy

Subsecond Sensory Modulation of Serotonin Levels in a Primary Sensory Area and Its Relation to Ongoing Communication Behavior in a Weakly Electric Fish

Firing patterns of serotonin neurons underlying cognitive flexibility

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