Lesions producing REM sleep without atonia disinhibit the acoustic startle reflex without affecting prepulse inhibition

Wu, Ming-Fung; Siegel, Jerome M.; Shouse, Margarate N.; Schenkel, Elizabeth

doi:10.1016/0006-8993(90)91677-9

Cited by 14 publications

(4 citation statements)

References 30 publications

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“…Recent evidence seems to suggest that the PPN, but not the NCF, is the primary structure to mediate prepulse inhibition. Neurotoxic lesions of the NCF, which spared the cholinergic PPN neurons, or electrolytic lesions of a cholinoceptive area just medial to the PPN, produced no effect on prepulse inhibition (Wu & Siegel, 1991; Wu et al, 1990). On the other hand, lesions of PPN alone greatly attenuated prepulse inhibition (Wu & Siegel, 1991).…”

Section: Discussionmentioning

confidence: 99%

“…It is not known whether one form of startle modulation, the suppression of startle by a preceding stimulus ( prepulse inhibition ), is also affected by this procedure. It has been hypothesized that the dorsolateral pons, which contains one major source of cholinergic neurons in the brainstem, may mediate prepulse inhibition (Wu, Siegel, Shouse, & Schenkel, 1990). To test this hypothesis we examined prepulse inhibition in choline-deficient, NADe-treated rats by using the dietary protocol developed by Jenden and his colleagues (e.g., Newton et al, 1986).…”

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confidence: 99%

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Cholinergic mechanisms in startle and prepulse inhibition: Effects of the false cholinergic precursor N-aminodeanol.

Wu¹,

Jenden²,

Fairchild³

et al. 1993

Behavioral Neuroscience

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We examined the effects of cholinergic deficiency on prepulse inhibition (PPI) of the acoustic startle. Rats treated with a choline-free diet that contained the false cholinergic precursor N-aminodeanol showed great deficit in PPI. This deficit does not appear to be secondary to an increase of stereotyped behaviors. Startle threshold was also greatly reduced, as these rats startled to the 70-dB prepulse and the baseline startle amplitude was increased by 60% over the control rats. Arecoline (4 mg/kg) partially reversed the deficit in PPI. This improvement persisted beyond the period of drug treatment. On the other hand, scopolamine (1 mg/kg) reduced PPI in the control rats. These results suggest that cholinergic systems play a major role in both the elicitation and prepulse inhibition of startle.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Cholinergic mechanisms in startle and prepulse inhibition: Effects of the false cholinergic precursor N-aminodeanol.

Wu¹,

Jenden²,

Fairchild³

et al. 1993

Behavioral Neuroscience

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“…Although PPI is not affected by either brainstem lesions producing REM sleep (Wu et al, 1990) sensory gating is abnormal during this stage (van Luijtelaar et al, 1998). An intriguing possibility is that intrusion or leakage of REM sleep events into waking may contribute to the gating impairments following prolonged SD.…”

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confidence: 97%

Sleep deprivation disrupts prepulse inhibition of the startle reflex: reversal by antipsychotic drugs

Frau

Orrù

Puligheddu

et al. 2008

Int. J. Neuropsychopharm.

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Sleep deprivation (SD) is known to induce perceptual impairments, ranging from perceptual distortion to hallucinatory states. Although this phenomenon has been extensively described in the literature, its neurobiological underpinnings remain elusive. In rodents, SD induces a series of behavioural patterns that might be reflective of psychosis and mania, such as hyperlocomotion and sensitization to psychotogenic drugs. Notably, such changes are accompanied by transitory alterations of dopaminergic signalling. Based on the hypothesis that both psychotic and manic disorders reflect gating impairments, the present study was aimed at the assessment of the impact of SD on the behavioural model of prepulse inhibition (PPI) of the startle reflex, a reliable paradigm for the study of informational filtering. Rats subjected to SD (24 h, 48 h, 72 h) exhibited a time-dependent increase in startle reflex and a dramatic deficit in PPI. Both alterations were reversed 24 h after termination of the SD period. Interestingly, PPI disruption was efficiently prevented by haloperidol (0.1 mg/kg i.p.) clozapine (5 mg/kg i.p.) and risperidone (1 mg/kg i.p.). Conversely, neither the anxiolytic diazepam (5 mg/kg i.p.) nor the antidepressant citalopram (5 mg/kg i.p) affected the PPI disruption mediated by SD, although diazepam reversed the enhancement in startle reflex magnitude induced by this manipulation. Our data suggest that SD induces gating deficits that might be relevant to the hallucinatory phenomena observed in humans, and provide a novel reliable animal model where such relationship can be studied.

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“…Sensorimotor gating-the ability to shift attentional resources to salient stimuli-is often operationalized and studied by assessing pre-pulse inhibition (PPI) of the acoustic startle response (ASR). In mammals the ASR is a rapid, reflexive contraction of skeletal, facial, and body muscles in response to a sudden, intense auditory stimulus (Davis et al, 1982;Koch and Schnitzler, 1997) and is conserved across many species, including rats, mice, guinea pigs, cats, dolphins, non-human primates, and humans (Saitoh et al, 1987;Wu et al, 1990;Geyer, 1999;Dawson et al, 2008;Dehmel et al, 2012;Saletti et al, 2014;Götz et al, 2020). PPI refers to the attenuation of the ASR when a subject is exposed to a lowintensity auditory "prepulse" prior to a startle-inducing auditory "pulse" (Geyer et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of the Deep and Intermediate Layers of the Superior Colliculus Disrupts Sensorimotor Gating in Monkeys

Waguespack

Aguilar

Málková

et al. 2020

Front. Behav. Neurosci.

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The deep and intermediate layers of the superior colliculus (DLSC) respond to visual, auditory, and tactile inputs and act as a multimodal sensory association area. In turn, activity in the DLSC can drive orienting and avoidance responses—such as saccades and head and body movements—across species, including in rats, cats, and non-human primates. As shown in rodents, DLSC also plays a role in regulating pre-pulse inhibition (PPI) of the acoustic startle response (ASR), a form of sensorimotor gating. DLSC lesions attenuate PPI and electrical stimulation of DLSC inhibits the startle response. While the circuitry mediating PPI is well-characterized in rodents, less is known about PPI regulation in primates. Two recent studies from our labs reported a species difference in the effects of pharmacological inhibition of the basolateral amygdala and substantia nigra pars reticulata (SNpr) on PPI between rats and macaques: in rats, inhibition of these structures decreased PPI, while in macaques, it increased PPI. Given that the SNpr sends direct inhibitory projections to DLSC, we next sought to determine if this species difference was similarly evident at the level of DLSC. Here, we transiently inactivated DLSC in four rhesus macaques by focal microinfusion of the GABAA receptor agonist muscimol. Similar to findings reported in rodents, we observed that bilateral inhibition of the DLSC in macaques significantly disrupted PPI. The impairment was specific to the PPI as the ASR itself was not affected. These results indicate that our previously reported species divergence at the level of the SNpr is not due to downstream differences at the level of the DLSC. Species differences at the level of the SNpr and basolateral amygdala emphasize the importance of studying the underlying circuitry in non-human primates, as impairment in PPI has been reported in several disorders in humans, including schizophrenia, autism, and PTSD.

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Lesions producing REM sleep without atonia disinhibit the acoustic startle reflex without affecting prepulse inhibition

Cited by 14 publications

References 30 publications

Cholinergic mechanisms in startle and prepulse inhibition: Effects of the false cholinergic precursor N-aminodeanol.

Cholinergic mechanisms in startle and prepulse inhibition: Effects of the false cholinergic precursor N-aminodeanol.

Sleep deprivation disrupts prepulse inhibition of the startle reflex: reversal by antipsychotic drugs

Inhibition of the Deep and Intermediate Layers of the Superior Colliculus Disrupts Sensorimotor Gating in Monkeys

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