Increased GABAergic inhibition in the midline thalamus affects signaling and seizure spread in the hippocampus-prefrontal cortex pathway

Sloan, David M.; Zhang, DeXing; Bertram, Edward H.

doi:10.1111/j.1528-1167.2010.02919.x

Cited by 37 publications

(40 citation statements)

References 33 publications

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“…Electrophysiological studies in rodents have also shown that changes in PFC responses mediated by MD stimulation are involved in the modulation of hippocampus-evoked activity in the PFC [21], fear extinction [22], [23], and propagation of limbic seizures [24]–[27].…”

Section: Introductionmentioning

confidence: 99%

Muscarinic and Nicotinic Modulation of Thalamo-Prefrontal Cortex Synaptic Pasticity In Vivo

et al. 2012

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The mediodorsal nucleus of the thalamus (MD) is a rich source of afferents to the medial prefrontal cortex (mPFC). Dysfunctions in the thalamo-prefrontal connections can impair networks implicated in working memory, some of which are affected in Alzheimer disease and schizophrenia. Considering the importance of the cholinergic system to cortical functioning, our study aimed to investigate the effects of global cholinergic activation of the brain on MD-mPFC synaptic plasticity by measuring the dynamics of long-term potentiation (LTP) and depression (LTD) in vivo. Therefore, rats received intraventricular injections either of the muscarinic agonist pilocarpine (PILO; 40 nmol/µL), the nicotinic agonist nicotine (NIC; 320 nmol/µL), or vehicle. The injections were administered prior to either thalamic high-frequency (HFS) or low-frequency stimulation (LFS). Test pulses were applied to MD for 30 min during baseline and 240 min after HFS or LFS, while field postsynaptic potentials were recorded in the mPFC. The transient oscillatory effects of PILO and NIC were monitored through recording of thalamic and cortical local field potentials. Our results show that HFS did not affect mPFC responses in vehicle-injected rats, but induced a delayed-onset LTP with distinct effects when applied following PILO or NIC. Conversely, LFS induced a stable LTD in control subjects, but was unable to induce LTD when applied after PILO or NIC. Taken together, our findings show distinct modulatory effects of each cholinergic brain activation on MD-mPFC plasticity following HFS and LFS. The LTP-inducing action and long-lasting suppression of cortical LTD induced by PILO and NIC might implicate differential modulation of thalamo-prefrontal functions under low and high input drive.

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Section: Introductionmentioning

confidence: 99%

Muscarinic and Nicotinic Modulation of Thalamo-Prefrontal Cortex Synaptic Pasticity In Vivo

et al. 2012

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“…It is induced in specific brain regions, resembling complex partial seizures if applied into limbic structures and myoclonic seizures if applied into the sensorimotor cortex. AD is useful for investigating electrophysiological and behavioral correlates of focally generated seizure-like patterns that often spread to nonstimulated networks 53,54. Electrographic properties of AD largely depend on the brain region stimulated.…”

Section: Electrical Stimulationmentioning

confidence: 99%

Animal models of epilepsy: use and limitations

Kandratavicius¹,

Balista²,

Lopes-Aguiar³

et al. 2014

NDT

392

241

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Epilepsy is a chronic neurological condition characterized by recurrent seizures that affects millions of people worldwide. Comprehension of the complex mechanisms underlying epileptogenesis and seizure generation in temporal lobe epilepsy and other forms of epilepsy cannot be fully acquired in clinical studies with humans. As a result, the use of appropriate animal models is essential. Some of these models replicate the natural history of symptomatic focal epilepsy with an initial epileptogenic insult, which is followed by an apparent latent period and by a subsequent period of chronic spontaneous seizures. Seizures are a combination of electrical and behavioral events that are able to induce chemical, molecular, and anatomic alterations. In this review, we summarize the most frequently used models of chronic epilepsy and models of acute seizures induced by chemoconvulsants, traumatic brain injury, and electrical or sound stimuli. Genetic models of absence seizures and models of seizures and status epilepticus in the immature brain were also examined. Major uses and limitations were highlighted, and neuropathological, behavioral, and neurophysiological similarities and differences between the model and the human equivalent were considered. The quest for seizure mechanisms can provide insights into overall brain functions and consciousness, and animal models of epilepsy will continue to promote the progress of both epilepsy and neurophysiology research.

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“…DTI shows increased connectivity between hippocampus and thalamus in patients with TLE (Dinkelacker et al, 2015). This changed connectivity could certainly be important given that limbic seizures are known to propagate through the thalamus in both human and animal models (Blumenfeld et al, 2004; Guye et al, 2006; Patel et al, 1988; Sloan et al, 2011). Additionally, MEG analysis was able to demonstrate the presence of hub-like regions in both temporal cortex and hippocampus of patients with TLE that do not exist in control subjects, and the importance of hubs to excitability was discussed earlier (Jin et al, 2015).…”

Section: Network Organization At the Macrocircuit Level: Applicatiomentioning

confidence: 99%

Organization and control of epileptic circuits in temporal lobe epilepsy

Alexander¹,

Maroso²,

Soltész³

2016

Progress in Brain Research

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When studying the pathological mechanisms of epilepsy, there are a seemingly endless number of approaches from the ultrastructural level—receptor expression by EM—to the behavioral level—comorbid depression in behaving animals. Epilepsy is characterized as a disorder of recurrent seizures, which are defined as “a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain” (Fisher et al., 2005). Such abnormal activity typically does not occur in a single isolated neuron; rather, it results from pathological activity in large groups—or circuits—of neurons. Here we choose to focus on two aspects of aberrant circuits in temporal lobe epilepsy: their organization and potential mechanisms to control these pathological circuits. We also look at two scales: microcircuits, ie, the relationship between individual neurons or small groups of similar neurons, and macrocircuits, ie, the organization of large-scale brain regions. We begin by summarizing the large body of literature that describes the stereotypical anatomical changes in the temporal lobe—ie, the anatomical basis of alterations in microcircuitry. We then offer a brief introduction to graph theory and describe how this type of mathematical analysis, in combination with computational neuroscience techniques and using parameters obtained from experimental data, can be used to postulate how microcircuit alterations may lead to seizures. We then zoom out and look at the changes which are seen over large whole-brain networks in patients and animal models, and finally we look to the future.

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Increased GABAergic inhibition in the midline thalamus affects signaling and seizure spread in the hippocampus-prefrontal cortex pathway

Cited by 37 publications

References 33 publications

Muscarinic and Nicotinic Modulation of Thalamo-Prefrontal Cortex Synaptic Pasticity In Vivo

Muscarinic and Nicotinic Modulation of Thalamo-Prefrontal Cortex Synaptic Pasticity In Vivo

Animal models of epilepsy: use and limitations

Organization and control of epileptic circuits in temporal lobe epilepsy

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