Escape behavior — brainstem and spinal cord circuitry and function

Korn, Henri; Faber, Donald S.

doi:10.1016/s0959-4388(96)80034-1

Cited by 39 publications

(21 citation statements)

References 47 publications

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“…The lateral periaqueductal gray activates these motor patterns by stimulating premotor centers in the pons and the medulla (LeDoux et al, ; Zhang, Bandler, & Carrive, ; for a review, see Benarroch, ). These premotor centers subsequently project to motor networks in the brainstem and the spinal cord to induce the active defensive response in rodents (Heckman, Lee, & Brownstone, ; Korn & Faber, ; for a review, see Holstege, ).…”

Section: Fight‐or‐flightmentioning

confidence: 99%

The effects of trauma on brain and body: A unifying role for the midbrain periaqueductal gray

Terpou

Harricharan

McKinnon

et al. 2019

J of Neuroscience Research

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Post-traumatic stress disorder (PTSD), a diagnosis that may follow the experience of trauma, has multiple symptomatic phenotypes. Generally, individuals with PTSD display symptoms of hyperarousal and of hyperemotionality in the presence of fearful stimuli. A subset of individuals with PTSD; however, elicit dissociative symptomatology (i.e., depersonalization, derealization) in the wake of a perceived threat. This pattern of response characterizes the dissociative subtype of the disorder, which is often associated with emotional numbing and hypoarousal. Both symptomatic phenotypes exhibit attentional threat biases, where threat stimuli are processed preferentially leading to a hypervigilant state that is thought to promote defensive behaviors during threat processing. Accordingly, PTSD and its dissociative subtype are thought to differ in their proclivity to elicit active (i.e., fight, flight) versus passive (i.e., tonic immobility, emotional shutdown) defensive responses, which are characterized by the increased and the decreased expression of the sympathetic nervous system, respectively. Moreover, active and passive defenses are accompanied by primarily endocannabinoid-and opioid-mediated analgesics, respectively. Through critical review of the literature, we apply the defense cascade model to better understand the pathological presentation of defensive responses in PTSD with a focus on the functioning of lower-level midbrain and extended brainstem systems. K E Y W O R D Sbrainstem, dissociation, periaqueductal gray, PTSD, trauma | INTRODUC TI ONIn this review, we integrate literature from trauma experiences, the defense cascade, and the threat-response neurocircuitry within a framework of post-traumatic stress disorder (PTSD). We begin by introducing the concepts of the hypothalamic-pituitary-adrenal (HPA) axis, general PTSD, and defensive responses. Following these primers, we discuss the influences of trauma onset and prolonged exposure to trauma and their effects on the development of PTSD and the dissociative subtype of PTSD. Next, we introduce the defense cascade model and its underlying neurocircuitry as described in the animal literature and relate it to PTSD. In addition, we discuss the current state of the neuroimaging literature, which Edited by Sandra Chanraud.All peer review communications can be found with the online version of the article. | 1111TERPOU ET al. suggests that functional alterations are detectable in the midbrain of individuals with PTSD and its dissociative subtype as compared to healthy controls. We conclude by presenting directions for future research and the clinical implications for treatment of persons with PTSD that arise from this review of the extant literature.

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Section: Fight‐or‐flightmentioning

confidence: 99%

The effects of trauma on brain and body: A unifying role for the midbrain periaqueductal gray

Terpou

Harricharan

McKinnon

et al. 2019

J of Neuroscience Research

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“…This complexity has motivated the search for more accessible startle circuits such as the touch-reflex circuit of Tritonia (Frost et al 2003) and the startle-escape circuit of fish (see below and Neumeister et al 2008) where pre-and postsynaptic cellular mechanisms mediating PPI-type phenomena have been identified. Indeed, the auditory startle pathway is conserved in fish and mammals, involving a direct disynaptic pathway from the hair cell receptors to brain stem neurons that integrate multimodal inputs and activate downstream motor circuits with comparable latencies (10 -15 ms; Korn and Faber 1996). Fish and mammals also show comparable temporal characteristics for effective prepulse/pulse interstimulus intervals (ISIs; 30 -500 ms) during behavioral PPI of the auditory startle response (Braff et al 1978 …”

mentioning

confidence: 99%

Dopaminergic-induced changes in Mauthner cell excitability disrupt prepulse inhibition in the startle circuit of goldfish

Medan

Preuss

2011

Journal of Neurophysiology

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Medan V, Preuss T. Dopaminergic-induced changes in Mauthner cell excitability disrupt prepulse inhibition in the startle circuit of goldfish. J Neurophysiol 106: 3195-3204, 2011. First published September 28, 2011 doi:10.1152/jn.00644.2011.-Prepulse inhibition (PPI) is a widespread sensorimotor gating phenomenon characterized by a decrease in startle magnitude if a nonstartling stimulus is presented 20 -1,000 ms before a startling stimulus. Dopaminergic agonists disrupt behavioral PPI in various animal models. This provides an important neuropharmacological link to schizophrenia patients that typically show PPI deficits at distinct (60 ms) prepulsepulse intervals. Here, we study time-dependent effects of dopaminergic modulation in the goldfish Mauthner cell (M-cell) startle network, which shows PPI-like behavioral and physiological startle attenuations. The unique experimental accessibility of the M-cell system allows investigating the underlying cellular mechanism with physiological stimuli in vivo. Our results show that the dopaminergic agonist apomorphine (2 mg/kg body wt) reduced synaptic M-cell PPI by 23.6% (n ϭ 18; P ϭ 0.009) for prepulse-pulse intervals of 50 ms, whereas other intervals showed no reduction. Consistently, application of the dopamine antagonist haloperidol (0.4 mg/kg body wt) restored PPI to control level. Current ramp injections while recording M-cell membrane potential revealed that apomorphine acts through a postsynaptic, time-dependent mechanism by deinactivating a M-cell membrane nonlinearity, effectively increasing input resistance close to threshold. This increase is most pronounced for prepulse-pulse intervals of 50 ms (47.9%, n ϭ 8; P Ͻ 0.05) providing a timedependent, cellular mechanism for dopaminergic disruption of PPI. These results provide, for the first time, direct evidence of dopaminergic modulation of PPI in the elementary startle circuit of vertebrates and reemphasize the potential of characterizing temporal aspects of PPI at the physiological level to understand its underlying mechanisms.sensorimotor-gating; dopamine; cellular mechanisms; input resistance; time-specific neuromodulation THE CENTRAL NERVOUS SYSTEM has to filter the overwhelming stream of information provided by the various sense organs while optimizing detection of behaviorally relevant information. One prominent filtering phenomenon is prepulse inhibition (PPI), which is thought of as an early sensory gate that reduces the sensory information of a secondary event (pulse) while a preceding event (prepulse) is being processed (Graham 1975;Hoffman and Ison 1980;Koch 1999). Experimentally, PPI is produced when a startling stimulus (pulse) is preceded within 20 -1,000 ms by a subthreshold stimulus (prepulse) of the same or another modality (Graham 1975;Hoffman and Ison 1980;Koch 1999). The multimodal nature of PPI distinguishes it from unimodal synaptic modulations such as pairedpulse depression and short-term habituation (Aubert et al. 2006;Campeau and Davis 1995;Simons-Weidenmaier et al. 2006). The majority ...

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“…The M-cell is one of the RSNs, which together constitute a phylogenetically conserved descending system across vertebrates (Nieuwenhuys et al, 1998;Butler and Hodos, 2005) that integrates sensory inputs to generate spinal motor commands (Rossignol et al, 2006;Grillner et al, 2008). In addition, the neuronal components and basic characteristics of fast escape in teleosts are strikingly similar to those of acoustic startle in higher vertebrates (Korn and Faber, 1996;Burgess and Granato, 2007). Thus, the switch in the effective sensory input to RSNs that elicits teleost fast escape may serve as a common physiological process underlying early sensorimotor development of vertebrates: developing nervous systems expand their ability to respond to a variety of sensory stimuli by dedicating a subcomponent of the preexisting sensorimotor circuit to late-developing modalities.…”

Section: M-cells As a Model For Studying Neuronal Basis Of Sensorimotmentioning

confidence: 99%

Effective Sensory Modality Activating an Escape Triggering Neuron Switches during Early Development in Zebrafish

Kohashi

Nakata²,

Oda³

2012

J. Neurosci.

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Escape behavior — brainstem and spinal cord circuitry and function

Cited by 39 publications

References 47 publications

The effects of trauma on brain and body: A unifying role for the midbrain periaqueductal gray

The effects of trauma on brain and body: A unifying role for the midbrain periaqueductal gray

Dopaminergic-induced changes in Mauthner cell excitability disrupt prepulse inhibition in the startle circuit of goldfish

Effective Sensory Modality Activating an Escape Triggering Neuron Switches during Early Development in Zebrafish

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