Warning! Dopaminergic Modulation of the Superior Colliculus

Essig, Jaclyn; Felsen, Gidon

doi:10.1016/j.tins.2015.12.002

Cited by 21 publications

(12 citation statements)

References 9 publications

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“…The special lack of correlations for 18 F-fallypride uptake in the colliculi also points towards a functional separation of dopamine neurons that project to the colliculi compared to other target regions. Both of these ideas are consistent with the seemingly specific role for dopamine signalling in the colliculi in behavioural responses to aversive or fearful stimuli [15] [16]. Our experiment examined well-handled subjects in a nonfearful environment.…”

Section: Resultssupporting

confidence: 82%

Using Tandem Behaviour-PET to Examine Dopaminergic Signalling Underlying Exploration

Herde

Ioanas

Boss

et al. 2017

Matters

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Section: Resultssupporting

confidence: 82%

Using Tandem Behaviour-PET to Examine Dopaminergic Signalling Underlying Exploration

Herde

Ioanas

Boss

et al. 2017

Matters

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“…Recent studies in our laboratory showed that intranasal dopamine application reduced escape behavior in two tests of unconditioned fear (i.e., escape from bright light and ultrasonic vocalization response to immobilization) 80 , attenuated footshock-induced freezing in training, test, and retest sessions in fear extinction conditioning, and reduced PSF following electrical stimulation of the dPAG at the escape threshold 81 . Dopamine neurons in the zona incerta (A13 zone) have been suggested to be the possible source of dopaminergic input that is involved in modulating the neural substrates of fear in the midbrain tectum 82,83 .…”

Section: Pharmacological Strategies To Inhibit the Transfer Of Aversimentioning

confidence: 99%

Role of the dorsal periaqueductal gray in posttraumatic stress disorder: mediation by dopamine and neurokinin

Brandão

Lovick

2019

Transl Psychiatry

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In susceptible individuals, exposure to intensely traumatic life events can lead to the development of posttraumatic stress disorder (PTSD), including long-term dysregulation of the contextual processing of aversive stimuli, the overgeneralization of learned fear, and impairments in the ability to learn or respond to safety signals. The neuropathophysiological changes that underlie PTSD remain incompletely understood. Attention has focused on forebrain structures associated with fear processing. Here we consider evidence from human and animal studies that long-lasting changes in functional connectivity between the midbrain periaqueductal gray (dPAG) and amygdala may be one of the precipitating events that contribute to PTSD. Long-lasting neuroplastic changes in the dPAG can persist after a single aversive stimulation and are pharmacologically labile. The early stage (at least up to 24 h poststimulation) involves neurokinin-1 receptor-mediated events in the PAG and amygdala and is also regulated by dopamine, both of which are mainly involved in transferring ascending aversive information from the dPAG to higher brain structures, mainly the amygdala. Changes in the functional connectivity within the dPAG-amygdala circuit have been reported in PTSD patients. We suggest that further investigations of plasticity and pharmacology of the PAGamygdala network provide a promising target for understanding pathophysiological circuitry that underlies PTSD in humans and that dopaminergic and neurokininergic drugs may have a potential for the treatment of psychiatric disorders that are associated with a dysfunctional dPAG.

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“…To assess which ZI neuron type(s) contribute to fear-memory conditioning, we injected double-floxed, Cre-dependent TetTox into the ZI of Cre-driver mouse lines expressing Crerecombinase selectively in tyrosine hydroxylase-positive (TH + ), somatostatin-positive (SST + ) or parvalbumin-positive (PV + ) neurons. TH + -neurons of the ZI were proposed to modulate responses to aversive stimuli 16 ; however, silencing ZI TH + -neurons caused no significant impairment of fear conditioning (Figure 1i-1l). SST + -neurons in the ZI are thought to function in cortical neuronal development 17 .…”

mentioning

confidence: 99%

A central amygdala to zona incerta projection is required for acquisition and remote recall of conditioned fear memory

et al. 2018

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Formation and retrieval of conditioned fear memories critically depend on the amygdala. Here, we identify an inhibitory projection from somatostatin-positive neurons in the central amygdala to parvalbumin-positive neurons in the zona incerta that is required for both recent and remote fear memories. Thus, amygdala inhibitory input to parvalbumin-positive neurons in the zona incerta, a nucleus not previously implicated in fear memory, is an essential component of the fear-memory circuitry.

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Warning! Dopaminergic Modulation of the Superior Colliculus

Cited by 21 publications

References 9 publications

Using Tandem Behaviour-PET to Examine Dopaminergic Signalling Underlying Exploration

Using Tandem Behaviour-PET to Examine Dopaminergic Signalling Underlying Exploration

Role of the dorsal periaqueductal gray in posttraumatic stress disorder: mediation by dopamine and neurokinin

A central amygdala to zona incerta projection is required for acquisition and remote recall of conditioned fear memory

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