Anatomical imaging of the piriform cortex in epilepsy

Young, James C; Vaughan, David N.; Nasser, Helen M.; Jackson, Graeme D.

doi:10.1016/j.expneurol.2019.113013

Cited by 28 publications

(33 citation statements)

References 78 publications

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“…The regions analyzed in this manuscript are well studied and play specific roles in biological processes. The PC is a structure, consisting of several layers, primarily involved in olfactory processing and is also known to have some function in memory (Haberly, 1985;Linster and Hasselmo, 2001;Young et al, 2019). The amygdala is a structure consisting of several interconnected nuclei which are most classically known to play a role in emotion, particularly fear and anxiety but also cognition (Davis and Whalen, 2000;Rasia-Filho et al, 2000;Schaefer and Gray, 2007).…”

Section: Discussionmentioning

confidence: 99%

Differential Impact of Severity and Duration of Status Epilepticus, Medical Countermeasures, and a Disease-Modifier, Saracatinib, on Brain Regions in the Rat Diisopropylfluorophosphate Model

Gage

Putra

Gomez-Estrada

et al. 2021

Front. Cell. Neurosci.

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Acute organophosphate (OP) toxicity poses a significant threat to both military and civilian personnel as it can lead to a variety of cholinergic symptoms including the development of status epilepticus (SE). Depending on its severity, SE can lead to a spectrum of neurological changes including neuroinflammation and neurodegeneration. In this study, we determined the impact of SE severity and duration on disease promoting parameters such as gliosis and neurodegeneration and the efficacy of a disease modifier, saracatinib (AZD0530), a Src/Fyn tyrosine kinase inhibitor. Animals were exposed to 4 mg/kg diisopropylfluorophosphate (DFP, s.c.) followed by medical countermeasures. We had five experimental groups: controls (no DFP), animals with no continuous convulsive seizures (CS), animals with ∼20-min continuous CS, 31-60-min continuous CS, and > 60-min continuous CS. These groups were then assessed for astrogliosis, microgliosis, and neurodegeneration 8 days after DFP exposure. The 31-60-min and > 60-min groups, but not ∼20-min group, had significantly upregulated gliosis and neurodegeneration in the hippocampus compared to controls. In the piriform cortex and amygdala, however, all three continuous CS groups had significant upregulation in both gliosis and neurodegeneration. In a separate cohort of animals that had ∼20 and > 60-min of continuous CS, we administered saracatinib for 7 days beginning three hours after DFP. There was bodyweight loss and mortality irrespective of the initial SE severity and duration. However, in survived animals, saracatinib prevented spontaneous recurrent seizures (SRS) during the first week in both severity groups. In the ∼20-min CS group, compared to the vehicle, saracatinib significantly reduced neurodegeneration in the piriform cortex and amygdala. There were no significant differences in the measured parameters between the naïve control and saracatinib on its own (without DFP) groups. Overall, this study demonstrates the differential effects of the initial SE severity and duration on the localization of gliosis and neurodegeneration. We have also demonstrated the disease-modifying potential of saracatinib. However, its’ dosing regimen should be optimized based on initial severity and duration of CS during SE to maximize therapeutic effects and minimize toxicity in the DFP model as well as in other OP models such as soman.

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Section: Discussionmentioning

confidence: 99%

Differential Impact of Severity and Duration of Status Epilepticus, Medical Countermeasures, and a Disease-Modifier, Saracatinib, on Brain Regions in the Rat Diisopropylfluorophosphate Model

Gage

Putra

Gomez-Estrada

et al. 2021

Front. Cell. Neurosci.

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“…As one of the primary olfactory cortex, the PC is involved in encoding odor identification (Gottfried et al, 2006;Howard et al, 2009;Wilson and Sullivan, 2011;Bekkers and Suzuki, 2013;Courtiol and Wilson, 2017), odor associated values or contexts (Gottfried and Dolan, 2003;Calu et al, 2007;Roesch et al, 2007), and odor memory (Zelano et al, 2011;Strauch and Manahan-Vaughan, 2018). Besides, the PC is also implicated in various neurological disorders, such as epilepsy (Loscher and Ebert, 1996;Vismer et al, 2015;Young et al, 2019), Alzheimer's disease (Samudralwar et al, 1995;Saiz-Sanchez et al, 2015), autism spectrum disorder (Menassa et al, 2017;Koehler et al, 2018) and Parkinson's disease (Wu et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Cell-Type-Specific Whole-Brain Direct Inputs to the Anterior and Posterior Piriform Cortex

Wang

Zhang

Chen

et al. 2020

Front. Neural Circuits

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The piriform cortex (PC) is a key brain area involved in both processing and coding of olfactory information. It is implicated in various brain disorders, such as epilepsy, Alzheimer's disease, and autism. The PC consists of the anterior (APC) and posterior (PPC) parts, which are different anatomically and functionally. However, the direct input networks to specific neuronal populations within the APC and PPC remain poorly understood. Here, we mapped the whole-brain direct inputs to the two major neuronal populations, the excitatory glutamatergic principal neurons and inhibitory γ-aminobutyric acid (GABA)-ergic interneurons within the APC and PPC using the rabies virus (RV)mediated retrograde trans-synaptic tracing system. We found that for both types of neurons, APC and PPC share some similarities in input networks, with dominant inputs originating from the olfactory region (OLF), followed by the cortical subplate (CTXsp), isocortex, cerebral nuclei (CNU), hippocampal formation (HPF) and interbrain (IB), whereas the midbrain (MB) and hindbrain (HB) were rarely labeled. However, APC and PPC also show distinct features in their input distribution patterns. For both types of neurons, the input proportion from the OLF to the APC was higher than that to the PPC; while the PPC received higher proportions of inputs from the HPF and CNU than the APC did. Overall, our results revealed the direct input networks of both excitatory and inhibitory neuronal populations of different PC subareas, providing a structural basis to analyze the diverse PC functions.

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“…Recent metaanalysis of patients with epilepsy revealed that, of all forms of epilepsy, TLE and mixed frontal epilepsy had the strongest association with olfactory deficits [1]. The olfactory bulb transmits olfactory information as afferent input to the primary olfactory cortex, which includes the piriform cortex, periamygdaloid cortex, entorhinal cortex, and amygdala [10]. The primary olfactory cortex projects the olfactory information to secondary structures such as the hippocampus, thalamus, orbitofrontal cortex, and insular cortex for higher cortical processing [10].…”

Section: Tle and Olfactory Dysfunctionmentioning

confidence: 99%

“…The olfactory bulb transmits olfactory information as afferent input to the primary olfactory cortex, which includes the piriform cortex, periamygdaloid cortex, entorhinal cortex, and amygdala [10]. The primary olfactory cortex projects the olfactory information to secondary structures such as the hippocampus, thalamus, orbitofrontal cortex, and insular cortex for higher cortical processing [10]. The epileptogenic network may be variable in patients; however, in patients with TLE, it mainly consists of the temporal cortex, amygdala, hippocampus, and insular cortex.…”

Section: Tle and Olfactory Dysfunctionmentioning

confidence: 99%

Characteristics of olfactory dysfunction in patients with temporal lobe epilepsy

Motoki

Akamatsu

Fumuro

et al. 2021

Epilepsy & Behavior

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Anatomical imaging of the piriform cortex in epilepsy

Cited by 28 publications

References 78 publications

Differential Impact of Severity and Duration of Status Epilepticus, Medical Countermeasures, and a Disease-Modifier, Saracatinib, on Brain Regions in the Rat Diisopropylfluorophosphate Model

Differential Impact of Severity and Duration of Status Epilepticus, Medical Countermeasures, and a Disease-Modifier, Saracatinib, on Brain Regions in the Rat Diisopropylfluorophosphate Model

Cell-Type-Specific Whole-Brain Direct Inputs to the Anterior and Posterior Piriform Cortex

Characteristics of olfactory dysfunction in patients with temporal lobe epilepsy

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