The recovery cycle of bat duration-selective collicular neurons varies with hunting phase

Wang, Xin; Luo, Feng; Wu, Fei-Jian; Chen, Qi‐Cai; Jen, Philip H.‐S.

doi:10.1097/wnr.0b013e3282ffb574

Cited by 29 publications

(34 citation statements)

References 22 publications

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“…Sleep and circadian rhythm are known to be disrupted in MPTP-treated rodents (Laloux et al 2008), rotenone-treated rats (García-García et al 2005), and Thy1-αSyn mice and VMAT2-deficient mice (Taylor et al 2009). Gastrointestinal function has been shown to be abnormal in MPTP-treated mice (Anderson et al 2007), rotenone-treated rats (Drolet et al 2009), Thy1-αSyn mice (Wang et al 2008, 2012), SNCA PAC mice (which expresss mutant human α-synuclein from a P1 artificial chromosome containing its endogenous regulatory elements) (Kuo et al 2010), and VMAT2-deficient mice (Taylor et al 2009). These findings are of interest because they demonstrate that toxicant exposures and genetic manipulations used to induce motor signs of PD can also induce non-motor features.…”

Section: Implications For Parkinson’s Etiology and Experimental Researchmentioning

confidence: 99%

Research on the Premotor Symptoms of Parkinson’s Disease: Clinical and Etiological Implications

Chen

Burton

Ross

et al. 2013

Environ Health Perspect

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Background: The etiology and natural history of Parkinson’s disease (PD) are not well understood. Some non-motor symptoms such as hyposmia, rapid eye movement sleep behavior disorder, and constipation may develop during the prodromal stage of PD and precede PD diagnosis by years.Objectives: We examined the promise and pitfalls of research on premotor symptoms of PD and developed priorities and strategies to understand their clinical and etiological implications.Methods: This review was based on a workshop, Parkinson’s Disease Premotor Symptom Symposium, held 7–8 June 2012 at the National Institute of Environmental Health Sciences in Research Triangle Park, North Carolina.Discussion: Research on premotor symptoms of PD may offer an excellent opportunity to characterize high-risk populations and to better understand PD etiology. Such research may lead to evaluation of novel etiological hypotheses such as the possibility that environmental toxicants or viruses may initiate PD pathogenesis in the gastrointestinal tract or olfactory bulb. At present, our understanding of premotor symptoms of PD is in its infancy and faces many obstacles. These symptoms are often not specific to PD and have low positive predictive value for early PD diagnosis. Further, the pathological bases and biological mechanisms of these premotor symptoms and their relevance to PD pathogenesis are poorly understood.Conclusion: This is an emerging research area with important data gaps to be filled. Future research is needed to understand the prevalence of multiple premotor symptoms and their etiological relevance to PD. Animal experiments and mechanistic studies will further understanding of the biology of these premotor symptoms and test novel etiological hypothesis.Citation: Chen H, Burton EA, Ross GW, Huang X, Savica R, Abbott RD, Ascherio A, Caviness JN, Gao X, Gray KA, Hong JS, Kamel F, Jennings D, Kirshner A, Lawler C, Liu R, Miller GW, Nussbaum R, Peddada SD, Comstock Rick A, Ritz B, Siderowf AD, Tanner CM, Tröster AI, Zhang J. 2013. Research on the premotor symptoms of Parkinson’s Disease: clinical and etiological implications. Environ Health Perspect 121:1245–1252; http://dx.doi.org/10.1289/ehp.1306967

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Section: Implications For Parkinson’s Etiology and Experimental Researchmentioning

confidence: 99%

Research on the Premotor Symptoms of Parkinson’s Disease: Clinical and Etiological Implications

Chen

Burton

Ross

et al. 2013

Environ Health Perspect

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“…Proteinase K-resistant α-Syn inclusions also have been identified in many brain regions of these mice (Fernagut et al, 2007; Fleming et al, 2008), and the mice show progressive sensorimotor alterations, beginning as early as 2 months of age (Fleming et al, 2004, 2006). Because the mice have a full complement of nigral dopamine (DA) cell bodies and striatal DA terminals at the times when they exhibit such deficits (Fernagut et al, 2007), it has been proposed that, at these early ages, they represent a model of premanifest PD (Chesselet, 2008), a contention supported by the demonstration of early nonmotor olfactory deficits and autonomic changes in these mice characteristic of early stages of the disease (Fleming et al, 2008; Wang et al, 2008; Magen and Chesselet, 2010). …”

mentioning

confidence: 99%

Elevated tonic extracellular dopamine concentration and altered dopamine modulation of synaptic activity precede dopamine loss in the striatum of mice overexpressing human α‐synuclein

Lam

Cely

et al. 2011

J of Neuroscience Research

157

191

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Overexpression or mutation of α-synuclein (α-Syn), a protein associated with presynaptic vesicles, causes familial forms of Parkinson’s disease in humans and is also associated with sporadic forms of the disease. We used in vivo microdialysis, tissue content analysis, behavioral assessment, and whole-cell patch clamp recordings from striatal medium-sized spiny neurons (MSSNs) in slices to examine dopamine transmission and dopaminergic modulation of corticostriatal synaptic function in mice overexpressing human wild-type α-Syn under the Thy1 promoter (α-Syn mice). Tonic striatal extracellular dopamine and 3-methoxytyramine levels were elevated in α-Syn mice at 6 months of age, prior to any reduction in total striatal tissue content, and were accompanied by an increase in open-field activity. Dopamine clearance and amphetamine-induced dopamine efflux were unchanged. The frequency of MSSN spontaneous excitatory postsynaptic currents (sEPSCs) was lower in α-Syn mice. Amphetamine reduced sEPSC frequency in wild types (WTs) but produced no effect in α-Syn mice. Furthermore, whereas quinpirole reduced and sulpiride increased sEPSC frequency in WT mice, they produced the opposite effects in α-Syn mice. These observations indicate that overexpression of α-Syn alters dopamine efflux and D2 receptor modulation of corticostriatal glutamate release at a young age. At 14 months of age, the α-Syn mice presented with significantly lower striatal tissue dopamine and tyrosine hydroxylase content relative to WT littermates, accompanied by an L-DOPA-reversible sensory motor deficit. Together, these data further validate this transgenic mouse line as a slowly progressing model of Parkinson’s disease and provide evidence for early dopamine synaptic dysfunction prior to loss of striatal dopamine.

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“…Indeed, we have shown previously that the echo frequency and amplitude sensitivity of duration-sensitive collicular neurons are better for expected than for unexpected echo durations [8,9,25]. We have also shown that collicular neurons with a short best duration recover rapidly when stimulated with P-E pairs with short durations and small P-E amplitude differences, whereas neurons with a long best duration recover rapidly when stimulated with P-E pairs with long durations and large P-E amplitude differences [26]. Furthermore, echo duration and frequency sensitivity of collicular neurons improve with decreasing P-E duration, P-E gap, and P-E amplitude difference [7,9,27].…”

Section: Discussionmentioning

confidence: 68%

Echo amplitude sensitivity of bat auditory neurons improves with decreasing pulse–echo gap

Jen

Wu²

2015

NeuroReport

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During hunting, insectivorous bats systematically vary the parameters of emitted pulses and analyze the returning echoes to extract prey features. As such, the duration of the pulse (P) and echo (E), the P-E gap, and the P-E amplitude difference progressively decrease throughout the prey-approach sequence. Our previous studies have shown that most inferior collicular neurons of bats discharge maximally to a best duration, and they have the sharpest echo frequency and amplitude sensitivity when stimulated with P-E pairs with duration the same as the best duration. Furthermore, their echo duration and frequency sensitivity improves with decreasing P-E duration and P-E gap. The present study shows that this is also true in the amplitude domain. Thus, all these data indicate that bats can better extract multiple parameters of expected rather than unexpected echo after pulse emission. They also support the hypothesis that a bat's inferior collicular neurons improve the response sensitivity in multiple parametric domains as the prey is approached to increase the success of hunting.

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The recovery cycle of bat duration-selective collicular neurons varies with hunting phase

Cited by 29 publications

References 22 publications

Research on the Premotor Symptoms of Parkinson’s Disease: Clinical and Etiological Implications

Research on the Premotor Symptoms of Parkinson’s Disease: Clinical and Etiological Implications

Elevated tonic extracellular dopamine concentration and altered dopamine modulation of synaptic activity precede dopamine loss in the striatum of mice overexpressing human α‐synuclein

Echo amplitude sensitivity of bat auditory neurons improves with decreasing pulse–echo gap

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