Synaptic depression and short-term habituation are located in the sensory part of the mammalian startle pathway

Simons-Weidenmaier, Nadine S; Weber, M.; Plappert, Claudia F.; Pilz, P.; Schmid, Susanne

doi:10.1186/1471-2202-7-38

Cited by 78 publications

(43 citation statements)

References 34 publications

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“…An overall sensitization is often found in the first 2–4 trials of a block of startle-eliciting stimuli, followed by a gradual decline in responses (habituation) to the remainder of presented trials (Aggernaes et al, 2010; Meincke et al, 2004). Habituation (short-term) is assumed to be caused by synaptic mechanisms intrinsic to sensory pathways (Davis et al, 1982; Leaton et al, 1985; Simons-Weidenmaier et al, 2006). Specifically, short-term habituation of startle has been proposed to be caused by activity-induced synaptic depression at the sensorimotor synapses in the pontine reticular formation, mediated by the activation of voltage- and calcium dependent large conductance potassium channels, called Maxi K, KCa1.1, or BK channels (Simons-Weidenmaier et al, 2006; Typlt et al, 2013b; Weber et al, 2002).…”

Section: Objective Measurement Of Sensory Processingmentioning

confidence: 99%

“…Habituation (short-term) is assumed to be caused by synaptic mechanisms intrinsic to sensory pathways (Davis et al, 1982; Leaton et al, 1985; Simons-Weidenmaier et al, 2006). Specifically, short-term habituation of startle has been proposed to be caused by activity-induced synaptic depression at the sensorimotor synapses in the pontine reticular formation, mediated by the activation of voltage- and calcium dependent large conductance potassium channels, called Maxi K, KCa1.1, or BK channels (Simons-Weidenmaier et al, 2006; Typlt et al, 2013b; Weber et al, 2002). Sensitization and long-term habituation are caused through an extrinsic modulation of the startle pathway by structures including the pedunculopontine tegmentum, the cerebellar vermis, the amygdala and the bed nucleus of the stria terminalis (Davis et al, 1997; Gonzalez-Lima et al, 1989; Koch, 1999; Leaton and Supple, 1986, 1991).…”

Section: Objective Measurement Of Sensory Processingmentioning

confidence: 99%

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Sensory processing in autism spectrum disorders and Fragile X syndrome—From the clinic to animal models

Sinclair

Oranje

Razak

et al. 2017

Neuroscience & Biobehavioral Reviews

159

148

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Brains are constantly flooded with sensory information that needs to be filtered at the pre-attentional level and integrated into endogenous activity in order to allow for detection of salient information and an appropriate behavioral response. People with Autism Spectrum Disorder (ASD) or Fragile X Syndrome (FXS) are often over- or under-reactive to stimulation, leading to a wide range of behavioral symptoms. This altered sensitivity may be caused by disrupted sensory processing, signal integration and/or gating, and is often being neglected. Here, we review translational experimental approaches that are used to investigate sensory processing in humans with ASD and FXS, and in relevant rodent models. This includes electroencephalographic measurement of event related potentials, neural oscillations and mismatch negativity, as well as habituation and pre-pulse inhibition of startle. We outline robust evidence of disrupted sensory processing in individuals with ASD and FXS, and in respective animal models, focusing on the auditory sensory domain. Animal models provide an excellent opportunity to examine common mechanisms of sensory pathophysiology in order to develop therapeutics.

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Section: Objective Measurement Of Sensory Processingmentioning

confidence: 99%

Section: Objective Measurement Of Sensory Processingmentioning

confidence: 99%

Sensory processing in autism spectrum disorders and Fragile X syndrome—From the clinic to animal models

Sinclair

Oranje

Razak

et al. 2017

Neuroscience & Biobehavioral Reviews

159

148

View full text Add to dashboard Cite

show abstract

“…Interestingly, Castelluci et al (1978) analyzed the habituation behavior in Aplysia and showed that both, short-and long-term habituation produce a profound depression in the efficacy of synaptic transmission. More recently, Simons-Weidenmaier et al (2006) proposed that the habituation of the startle response in rats is mediated by synaptic depression of the sensory pathway. In sum, it is widely accepted that habituation is mediated by a synaptic depression of the neuronal circuitry.…”

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confidence: 99%

PKMζ inactivation induces spatial familiarity

Moncada¹,

Viola²

2008

Learn. Mem.

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Spatial familiarization consists of a decrease in the exploratory activity over time after exposure to a place. Here, we show that a 30-min exposure to an open field led to a pronounced decrease in the exploratory behavior of rats, generating context familiarity. This behavioral output is associated with a selective decrease in hippocampal PKM levels. A short 5-min exposure did not induce spatial familiarity or a decrease in PKM, while inactivation of hippocampal PKM by the specific inhibitor ZIP was sufficient to induce spatial familiarity, suggesting that the decrease in PKM is involved in setting a given context as a familiar place.Rodents have an innate and spontaneous exploratory behavior. When rats face a novel environment, they actively explore it in order to gather information about the place, and then, in subsequent exposures, their exploratory behavior begins to decrease. With persistent exposure, not accompanied by any biologically relevant consequence, the environment becomes familiar, and exploration wanes.When animals go over a place, they realize whether that place is novel or was previously explored by comparing it with stored memories. In parallel, rats recollect information about specific environmental details such as remembering particular characteristics about the place, when it was visited, or what happened there. The efficiency and speed of novelty detection confer an evolutionary advantage that provide a reason for the existence of a familiarity discrimination network in addition to those networks used for recollection (Brown and Aggleton 2001;Bogacz and Brown 2003). In a recent review, it was emphasized that recollection and familiarity signals are evident in both perirhinal cortex and the hippocampus, suggesting that these two components of memory could be interpreted in terms of strong and weak memories (Squire et al. 2007).The hippocampal region is critically involved in the processing of spatial and associative learning tasks. Particularly, surgical or pharmacological interventions in the dorsal hippocampus prevent the formation of these memories (Broadbent et al. 2004;Izquierdo et al. 2006). However, a recent study reported that, in rats with a selective damage to the hippocampus involving its dorsal region, an increased familiarity of an odor paradigm was found (Sauvage et al. 2008). This result suggests that the inactivation of the hippocampus improves familiarity processes.We have previously studied the molecular changes in the hippocampus of rats submitted to a novel or familiar environment. We found that a short exposure to a novel arena, in this case a 5-min open field (OF) session, led to an active exploration associated with a sequential rise in protein kinase A (PKA) activity and activation of the extracellular regulated kinases (ERKs) 1/2 and the ␣-subunit of calcium calmodulin-dependent protein kinase (CAMKII␣) in the hippocampus of rats (Vianna et al. 2000). Indeed, we reported an increment in phosphorylated cAMP response element-binding protein (pCREB) levels, specifical...

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“…This reflex is a protective response to a sudden acoustic, tactile or vestibular stimulus and is initiated by mechanoreceptors that detect mechanical forces applied to the body 11 . Stimulation of these sensory receptors elicits the activation of small clusters of giant neurons located in the pontine reticular nucleus (PnC) that project directly and indirectly to motor neurons in the facial motor nucleus and the spinal cord, leading to a fast activation of a number of facial and peripheral muscles, as well as a positive autonomic activation 13–18 . The hypothesis underlying this proof-of-concept study is that bursts of kinesthetic stimulation delivered during the early phase of apneas or hypopneas may elicit a cotrolled startle response that can activate sub-cortical centers controlling upper airways muscles and the autonomic nervous system, stopping respiratory events without generating a cortical arousal.…”

Section: Introductionmentioning

confidence: 99%

Kinesthetic stimulation for obstructive sleep apnea syndrome: An “on-off” proof of concept trial

Hernández

Romero

Feuerstein

et al. 2018

Sci Rep

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Obstructive sleep apnea (OSA) occurs when the upper airway narrows or collapses due to the loss of upper airway muscle activation at sleep onset. This study investigated the effectiveness of triggered kinesthetic stimulation in patients with OSA. This proof-of-concept, open-label, multicenter prospective study was conducted on 24 patients with severe OSA. During a one night evaluation, kinesthetic stimulation was intermittently delivered in 30 minute periods. The duration of apneas and hypopneas during Stimon and Stimoff periods were compared. Five hospital-based university centers in France participated. Sleep studies were evaluated by a single scorer at a core laboratory (CHU Grenoble). Results show that during the Stimon phases, statistically significant decreases in durations of apneas and hypopneas were observed in 56% and 46% of patients, respectively. Overall, 75% of patients showed an improvement in apneas or hypopneas durations. The mean reduction in durations for patients with a significant decrease was 4.86 seconds for apneas and 6.00 seconds for hypopneas. This proof of concept study is the first to identify kinesthetic stimulation as a potentially effective therapy for OSA. These data justify evaluation in a controlled study.

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Synaptic depression and short-term habituation are located in the sensory part of the mammalian startle pathway

Cited by 78 publications

References 34 publications

Sensory processing in autism spectrum disorders and Fragile X syndrome—From the clinic to animal models

Sensory processing in autism spectrum disorders and Fragile X syndrome—From the clinic to animal models

PKMζ inactivation induces spatial familiarity

Kinesthetic stimulation for obstructive sleep apnea syndrome: An “on-off” proof of concept trial

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