Epilepsy, a neurological disorder characterized by recurrent unprovoked seizures, significantly impacts patient quality of life. Current classification methods focus primarily on clinical observations and electroencephalography (EEG) analysis, often overlooking the underlying dynamics driving seizures. This study uses surface EEG data to identify seizure transitions using a dynamical systems–based framework—the taxonomy of seizure dynamotypes—previously examined only in invasive data. We applied principal component and independent component analysis to surface EEG recordings from 1,177 seizures in 158 patients with focal epilepsy, decomposing the signals into independent components (ICs). The ICs were visually labeled for clear seizure transitions and bifurcation morphologies, which were then examined using Bayesian multilevel modeling in the context of clinical factors. Our analysis reveals that certain onset bifurcations (SNIC and SupH) are more prevalent during wakefulness compared to their reduced rat...

Psychiatric disorders, including anxiety and depression, are highly comorbid in people with epilepsy. However, the mechanisms mediating the shared pathophysiology are currently unknown. There is considerable evidence implicating the basolateral amygdala (BLA) in the network communication of anxiety and fear, a process demonstrated to involve parvalbumin-positive (PV) interneurons. The loss of PV interneurons has been well described in the hippocampus of chronically epileptic mice and in postmortem human tissue of patients with temporal lobe epilepsy (TLE). We hypothesize that a loss of PV interneurons in the BLA may contribute to comorbid mood disorders in epilepsy. To test this hypothesis, we employed a ventral intrahippocampal kainic acid (vIHKA) model of temporal lobe epilepsy in mice, which exhibits profound behavioral deficits associated with chronic epilepsy. We demonstrate a loss of PV interneurons and dysfunction of remaining PV interneurons in the BLA of chronically epileptic mice. Further, we dem...

Are you considering graduate school? Four neuroscience program faculty members explain the type of experience and considerations that may be beneficial before you apply.

How does the brain form new memories? Converging evidence shows that the key brain structures crucial for the formation of new memories are located in the medial temporal lobes (MTL).

Literature focused on scientific rigor is ever-growing. In addition to the resources found in the Promoting Awareness and Knowledge to Enhance Scientific Rigor in Neuroscience collection, the articles below can help you explore various issues, solutions, and approaches to implement high standards of scientific rigor in your research.

Do you have questions about how to thoughtfully respond to reviews you may not agree with, making recommendations to editors as a reviewer, and other topics related to the peer review process?

Halfway through my second year in a neuroscience graduate program this winter, I encountered a new challenge in the lab.

Epilepsy–aphasia syndrome (EAS) is a spectrum of childhood disorders that exhibit complex comorbidities that include epilepsy and the emergence of cognitive and language disorders. CNKSR2 is an X-linked gene in which mutations are linked to EAS. We previously demonstrated Cnksr2 knock-out (KO) mice model key phenotypes of EAS analogous to those present in clinical patients with mutations in the gene. Cnksr2 KO mice have increased seizures, impaired learning and memory, increased levels of anxiety, and loss of ultrasonic vocalizations (USVs). The intricate interplay between these diverse phenotypes at the brain regional and cell-type level remains unknown. Here, we leverage conditional deletion of the X-linked Cnksr2 in a neuronal cell-type manner in male mice to demonstrate that anxiety and impaired USVs track with its loss from excitatory neurons. Finally, we further narrow the essential role of Cnksr2 loss in USV deficits to excitatory neurons of the ACC, a region in mice recently implicated in USV produ...

Hydroxychloroquine (HCQ), a well-known antimalarial and anti-inflammatory drug, has demonstrated potential neuroprotective effects in ischemic stroke by inhibiting pyroptosis, a programmed cell death associated with inflammation. This study investigates the impact of HCQ on ischemic stroke pathology using both in vivo and in vitro models. In vivo, C57BL/6 mice subjected to middle cerebral artery occlusion (MCAO) were treated with HCQ. Neurological deficits, infarct volume, and the expression of pyroptosis markers were evaluated. The results demonstrated that HCQ significantly improved motor function and reduced infarct volume in the MCAO mouse model. In vitro, BV2 microglial cells exposed to lipopolysaccharide (LPS) and oxygen–glucose deprivation (OGD) were treated with HCQ. Western blot and immunofluorescence analyses revealed that HCQ effectively suppressed the expression of pyroptosis markers GSDMD and NLRP3 in both in vivo and in vitro models. These findings suggest that HCQ mitigates ischemic stroke d...

It is widely believed that axons in the central nervous system of adult mammals do not regrow following injury. This failure is thought, at least in part, to underlie the limited recovery of function following injury to the brain or spinal cord. Some studies of fixed tissue have suggested that, counter to dogma, norepinephrine (NE) axons regrow following brain injury. Here, we have used in vivo two-photon microscopy in layer 1 of the primary somatosensory cortex in transgenic mice harboring a fluorophore selectively expressed in NE neurons. This protocol allowed us to explore the dynamic nature of NE axons following injury with the selective NE axon toxin N -(2-chloroethyl)- N -ethyl-2-bromobenzylamine (DSP4). Following DSP4, NE axons were massively depleted and then slowly and partially recovered their density over a period of weeks. This regrowth was dominated by new axons entering the imaged volume. There was almost no contribution from local sprouting from spared NE axons. Regrown axons did not appear ...