Dear fellow neuroscientists,
We would like to invite you to join us on Tuesday,
October 11 at 1:00 pm EDT (UTC-4) for the next edition of E.A.R.S. (Electronic Auditory Research Seminars),
a monthly auditory seminar series focused on central auditory processing and circuits.
IMPORTANT: Please note that we have migrated the seminars to Zoom. You
can access the seminars here: https://pennmedicine.zoom.us/j/95396120820.
This link is also posted on our website https://sites.google.com/view/ears2020/home.
The E.A.R.S. subscriber list will migrate from Crowdcast to the ears-seminar google group, which you can join by emailing: ears2022+subscribe@xxxxxxxxxxxxxxxx or
visiting the following the link: https://groups.google.com/g/ears2022.
If you want to stay subscribed, there is no need to do anything, your email address will be automatically transferred.
Speakers:
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Karine Fenelon (University of Massachusetts Amherst): Brainstem
mechanisms modulating prepulse inhibition of the startle reflex
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Governed by central inhibitory mechanisms, sensorimotor gating is a fundamental pre-attentive process that, if reduced, is associated with cognitive and motor symptoms. The PrePulse Inhibition
(PPI) of the auditory startle response task is the gold standard operational measure of sensorimotor gating, used in humans and translational models. PPI occurs when a weak stimulus presented prior to a startle stimulus inhibits the startle response. PPI is
impaired in various neurological and neuropsychiatric disorders where it is often predictive of psychosis, obsessions, compulsions, and motor/speech dysfunctions. The reversal of PPI deficits is routinely tested in disease experimental systems as pre-clinical
trials of neurological drug screening. Yet, the cellular and circuit-level mechanisms remain largely unclear, even under non-pathological conditions, limiting therapeutic advances. Recent evidence ruled out the longstanding hypothesis that PPI is mediated
by midbrain cholinergic inputs to the caudal pontine reticular nucleus (PnC). Instead, glutamatergic, glycinergic, and GABAergic inhibitory mechanisms are now suggested to be crucial for PPI, at the PnC level. Since dysfunctions of the amygdala are common
to pathologies displaying sensorimotor gating deficits, we tested how direct projections to the PnC originating from the amygdala contribute to PPI. Using mice, we employed tract-tracing, immunohistochemical analyses and in vitro electrophysiological recordings
to demonstrate that the central nucleus of the amygdala (CeA) sends glutamatergic inputs to PnC neurons, including PnC glycinergic neurons. Then we used an in vivo Ca2+-dependent photo-sensitive approach (i.e., “Cal-Light”) to tag CeA and PnC neurons active
during PPI, with high spatio-temporal precision. Finally, we were able to restore PPI-deficits in a schizophrenia-relevant mouse model, by photo-stimulating CeA-PnC glutamatergic synapses. Our results show that an amygdala-dependent mechanism within the brainstem
startle circuit contributes to PPI. We therefore provide new insights to the clinically relevant theoretical construct of PPI, which is disrupted in various psychiatric and neurological diseases.
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Malte Wöstmann (Universität zu Lübeck): Behavioural
and electrophysiological signatures of auditory distraction in time and space
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Acoustic events in our environment are often relevant for behaviour, but irrelevant sounds can be powerful sources of distraction. Auditory attention is thought to enhance target sounds and to suppress distraction. I will present
evidence from behavioural and electroencephalography (EEG) studies in humans that elucidate the spatial and temporal dynamics of processing distracting sounds. First, when we decouple auditory target enhancement from distractor suppression in spatial attention,
we find two respective lateralized alpha oscillatory responses in the EEG (~10 Hz), which are uncorrelated. This demonstrates that the neurobiological foundation of auditory spatial attention implies a selection-independent neural mechanism related to processing
distraction. Second, when we vary the onset time of auditory distractors, we find that distractor onset co-modulates distractor-evoked behavioural detriments in memory performance and EEG responses in ~2–5 cycles per second. This suggests that auditory distractibility
is not uniformly distributed across time but exhibits spontaneous fluctuations on a sub-second time scale.
Additional upcoming E.A.R.S seminars (1:00 pm ET):
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11/01/2022: Professional Development session
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12/13/2022: Trainee Talks
With kind wishes,
Maria Geffen
Yale Cohen
Steve Eliades
Stephen David
Alexandria Lesicko
Nathan Vogler
Jean-Hugues Lestang
Huaizhen Cai
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