Dopaminergic mechanisms underlying catalepsy, fear and anxiety: Do they interact?

Colombo, Ana Caroline; Oliveira, Amanda Ribeiro de; Reimer, Adriano E.; Brandão, Marcus Lira

doi:10.1016/j.bbr.2013.10.002

Cited by 18 publications

(23 citation statements)

References 53 publications

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“…For example, aversive stimulation of the IC at the escape threshold enhanced dopamine release in the prefrontal cortex [15,30] and intracollicular injections of the non‐selective dopamine receptor antagonist haloperidol enhanced auditory‐evoked potentials (AEPs) that were recorded directly from the IC in rats that were subjected to loud sounds as the US [35]. These results support previous studies from our laboratory that showed that systemic injections of sulpiride enhanced escape responses in rats that in the switch‐off procedure [36] and increased the frequency of ultrasonic vocalizations during the training sessions in a fear conditioning test [14]. These data are in sharp contrast to other studies on the association between enhanced dopamine transmission and conditioned fear.…”

Section: Dopamine In Unconditioned Fearsupporting

confidence: 84%

“…Depending on the type of threatening condition (i.e., conditioned or unconditioned), dopamine D 2 receptor antagonists may reduce or heighten the aversiveness of the situation. Intra‐BLA injections of these compounds clearly reduce conditioned fear in rats that are subjected to animal models of anxiety [20,21,14,23]. To test the hypothesis that dopamine plays a modulatory role in the neural substrates of fear in periventricular structures, we microinjected dopamine receptor antagonists into the IC to inhibit D 2 receptor‐mediated mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…As mentioned above, the EAS is a multifaceted neural circuit that involves several neurotransmitters (GABA, serotonin, excitatory amino acids, and neurokinins, among others) and plays a role in modulating the organization, elaboration, and expression of defense reactions. However, the use of tests of unconditioned fear has generated experimental results that do not always fit the hypothesis of dopamine's anxiogenic role [36,14,22,35]. Studies that used aversive USs that decisively activate brainstem structures, such as the IC, to elicit defensive behavior in rats has led to the suggestion that dopamine exerts an antiaversive action in this brain region [35,22].…”

Section: Integrated Viewmentioning

confidence: 99%

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Dual role of dopamine D₂‐like receptors in the mediation of conditioned and unconditioned fear

et al. 2015

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a b s t r a c tA reduction of dopamine release or D 2 receptor blockade in the terminal fields of the mesolimbic system, particularly the amygdala, clearly reduces conditioned fear. Similar D 2 receptor antagonism in the neural substrates of fear in the midbrain tectum attenuates the processing of unconditioned aversive information. However, the implications of the interplay between opposing actions of dopamine in the rostral and caudal segments of the dopaminergic system are still unclear. Previous studies from this laboratory have reported the effects of dopaminergic drugs on behavior in rats in the elevated plus maze, auditory-evoked potentials (AEPs) recorded from the midbrain tectum, fear-potentiated startle, and conditioned freezing. These findings led to an interesting framework on the functional roles of dopamine in both anxiety and fear states. Dopamine D 2 receptor inhibition in the terminal fields of the mesolimbic dopamine system generally causes anxiolytic-like effects, whereas the activity of midbrain substrates of unconditioned fear are enhanced by D 2 receptor antagonists, suggesting that D 2 receptor-mediated mechanisms play opposing roles in fear/anxiety processes, depending on the brain region under study. Dopamine appears to mediate conditioned fear by acting at rostral levels of the brain and regulate unconditioned fear at the midbrain level, likely by reducing the sensorimotor gating of aversive events.

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Section: Dopamine In Unconditioned Fearsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Section: Integrated Viewmentioning

confidence: 99%

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Dual role of dopamine D₂‐like receptors in the mediation of conditioned and unconditioned fear

et al. 2015

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“…Indirect support for these results was previously provided by studies that demonstrated that systemic injections of the DA receptor antagonist sulpiride increased the switch-off response to light presented as an aversive US and enhanced fear-like behavior in the open arms of the EPM [17], [65]. Moreover, our recent study found that systemic administration of haloperidol strongly reduced ultrasonic vocalizations emitted during the testing session of a contextual fear conditioning paradigm [66], but increased the magnitude of AEPs in response to the unconditioned auditory aversive stimulation [16].…”

Section: Discussionsupporting

confidence: 72%

Dopamine D2-Like Receptors Modulate Unconditioned Fear: Role of the Inferior Colliculus

et al. 2014

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BackgroundA reduction of dopamine release or D2 receptor blockade in the terminal fields of the mesolimbic system clearly reduces conditioned fear. Injections of haloperidol, a preferential D2 receptor antagonist, into the inferior colliculus (IC) enhance the processing of unconditioned aversive information. However, a clear characterization of the interplay of D2 receptors in the mediation of unconditioned and conditioned fear is still lacking.MethodsThe present study investigated the effects of intra-IC injections of the D2 receptor-selective antagonist sulpiride on behavior in the elevated plus maze (EPM), auditory-evoked potentials (AEPs) to loud sounds recorded from the IC, fear-potentiated startle (FPS), and conditioned freezing.ResultsIntra-IC injections of sulpiride caused clear proaversive effects in the EPM and enhanced AEPs induced by loud auditory stimuli. Intra-IC sulpiride administration did not affect FPS or conditioned freezing.ConclusionsDopamine D2-like receptors of the inferior colliculus play a role in the modulation of unconditioned aversive information but not in the fear-potentiated startle response.

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“…However, this increase can not be considered an index of merely enhanced anxiety, because it was heavily influenced by the confounding factor haloperidol-dependent motor slowdown. These findings are consistent with the hypothesis that a fear/anxiety state does not underlie haloperidol-induced catalepsy (Colombo et al, 2013). Similarly, there is no evidence of a relationship between catalepsy and fear/anxiety state in congenic mouse strains (Kondaurova et al, 2011).…”

Section: Discussionsupporting

confidence: 92%

Behavioral and electrophysiological effects of endocannabinoid and dopaminergic systems on salient stimuli

Laricchiuta

Musella

Rossi

et al. 2014

Front. Behav. Neurosci.

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Rewarding effects have been related to enhanced dopamine (DA) release in corticolimbic and basal ganglia structures. The DAergic and endocannabinoid interaction in the responses to reward is described. This study investigated the link between endocannabinoid and DAergic transmission in the processes that are related to response to two types of reward, palatable food and novelty. Mice treated with drugs acting on endocannabinoid system (ECS) (URB597, AM251) or DAergic system (haloperidol) were submitted to approach-avoidance conflict tasks with palatable food or novelty. In the same mice, the cannabinoid type-1 (CB1)-mediated GABAergic transmission in medium spiny neurons of the dorsomedial striatum was analyzed. The endocannabinoid potentiation by URB597 magnified approach behavior for reward (food and novelty) and in parallel inhibited dorsostriatal GABAergic neurotransmission. The decreased activity of CB1 receptor by AM251 (alone or with URB597) or of DAergic D2 receptor by haloperidol had inhibitory effects toward the reward and did not permit the inhibition of dorsostriatal GABAergic transmission. When haloperidol was coadministered with URB597, a restoration effect on reward and reward-dependent motor activity was observed, only if the reward was the palatable food. In parallel, the coadministration led to restoring inhibition of CB1-mediated GABAergic transmission. Thus, in the presence of simultaneous ECS activation and inhibition of DAergic system the response to reward appears to be a stimulus-dependent manner.

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Dopaminergic mechanisms underlying catalepsy, fear and anxiety: Do they interact?

Cited by 18 publications

References 53 publications

Dual role of dopamine D₂‐like receptors in the mediation of conditioned and unconditioned fear

Dual role of dopamine D₂‐like receptors in the mediation of conditioned and unconditioned fear

Dopamine D2-Like Receptors Modulate Unconditioned Fear: Role of the Inferior Colliculus

Behavioral and electrophysiological effects of endocannabinoid and dopaminergic systems on salient stimuli

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Dopaminergic mechanisms underlying catalepsy, fear and anxiety: Do they interact?

Cited by 18 publications

References 53 publications

Dual role of dopamine D2‐like receptors in the mediation of conditioned and unconditioned fear

Dual role of dopamine D2‐like receptors in the mediation of conditioned and unconditioned fear

Dopamine D2-Like Receptors Modulate Unconditioned Fear: Role of the Inferior Colliculus

Behavioral and electrophysiological effects of endocannabinoid and dopaminergic systems on salient stimuli

Contact Info

Product

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Dual role of dopamine D₂‐like receptors in the mediation of conditioned and unconditioned fear

Dual role of dopamine D₂‐like receptors in the mediation of conditioned and unconditioned fear