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Neuroscience_topics
Neuroscience: CNS disease, pain, brain research, ion channels, synaptic transmission, channelopathies, neuronal network
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Autaptic self-inhibition of cortical GABAergic neurons: Synaptic narcissism or useful introspection?

Autaptic self-inhibition of cortical GABAergic neurons: Synaptic narcissism or useful introspection? | Neuroscience_topics | Scoop.it
Highlights: 

-  Specific connectivity patterns between interneurons and excitatory cells.

- Cortical disinhibition is necessary for behavioral functions.

- Cortical disinhibition is provided by specific interneuron–interneuron connections.

- Autaptic self-inhibition of PV cells: a very efficient disinhibition stratagem.

- A dual role of autaptic inhibition in temporally coordinating PV basket cells. (...) - by Deleuze C et al., Current Opinion in Neurobiology, Volume 26, June 2014, Pages 64–71

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Inhibitory Plasticity Dictates the Sign of Plasticity at Excitatory Synapses

The broad connectivity of inhibitory interneurons and the capacity of inhibitory synapses to be plastic make them ideal regulators of the level of excitability of many neurons simultaneously. Whether inhibitory synaptic plasticity may also contribute to the selective regulation of single neurons and local microcircuits activity has not been investigated. Here we demonstrate that in rat primary visual cortex inhibitory synaptic plasticity is connection specific and depends on the activation of postsynaptic GABAB–Gi/o protein signaling. Through the activation of this intracellular signaling pathway, inhibitory plasticity can alter the state of a single postsynaptic neuron and directly affect the induction of plasticity at its glutamatergic inputs. This interaction is modulated by sensory experience. Our data demonstrate that in recurrent circuits, excitatory and inhibitory forms of synaptic plasticity are not integrated as independent events, but interact to cooperatively drive the activity-dependent rewiring of local microcircuits. (...) - by Wang L and Maffei A, The Journal of Neuroscience, 22 January 2014, 34(4): 1083-1093

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NMDA and GABAB (KIR) Conductances: The “Perfect Couple” for Bistability

[Abstract] Networks that produce persistent firing in response to novel input patterns are thought to be important in working memory and other information storage functions. One possible mechanism for maintaining persistent firing is dendritic voltage bistability in which the depolarized state depends on the voltage dependence of the NMDA conductance at recurrent synapses. In previous models, the hyperpolarized state is dependent on voltage-independent conductances, including GABAA. The interplay of these conductances leads to bistability, but its robustness is limited by the fact that the conductance ratio must be within a narrow range. The GABAB component of inhibitory transmission was not considered in previous analyses. Here, we show that the voltage dependence of the inwardly rectifying potassium (KIR) conductance activated by GABAB receptors adds substantial robustness to network simulations of bistability and the persistent firing that it underlies. The hyperpolarized state is robust because, at hyperpolarized potentials, the GABAB/KIR conductance is high and the NMDA conductance is low; the depolarized state is robust because, at depolarized potentials, the NMDA conductance is high and the GABAB/KIR conductance is low. Our results suggest that this complementary voltage dependence of GABAB/KIR and NMDA conductances makes them a “perfect couple” for producing voltage bistability. - Sanders H. et al., The Journal of Neuroscience, 9 January 2013, 33(2): 424-429

Julien Hering, PhD's insight:

The NMDA/GABAB receptor channels bipolar couple is perfect to generate bistability in a narrow window of voltage. 

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GABAergic excitation after febrile seizures induces ectopic granule cells and adult epilepsy

GABAergic excitation after febrile seizures induces ectopic granule cells and adult epilepsy | Neuroscience_topics | Scoop.it

Temporal lobe epilepsy (TLE) is accompanied by an abnormal location of granule cells in the dentate gyrus. Using a rat model of complex febrile seizures, which are thought to be a precipitating insult of TLE later in life, we report that aberrant migration of neonatal-generated granule cells results in granule cell ectopia that persists into adulthood. Febrile seizures induced an upregulation of GABAA receptors (GABAA-Rs) in neonatally generated granule cells, and hyperactivation of excitatory GABAA-Rs caused a reversal in the direction of granule cell migration. This abnormal migration was prevented by RNAi-mediated knockdown of the Na+K+2Cl− co-transporter (NKCC1), which regulates the excitatory action of GABA. NKCC1 inhibition with bumetanide after febrile seizures rescued the granule cell ectopia, susceptibility to limbic seizures and development of epilepsy. Thus, this work identifies a previously unknown pathogenic role of excitatory GABAA-R signaling and highlights NKCC1 as a potential therapeutic target for preventing granule cell ectopia and the development of epilepsy after febrile seizures. - by Koyama R. et al., Nature Medicine 18, 1271–1278, 15 July 2012

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GABA actions and ionic plasticity in epilepsy

GABA actions and ionic plasticity in epilepsy | Neuroscience_topics | Scoop.it
[Review] Highlights:- Ionic plasticity of GABA signaling relies on short-term and long term changes in EGABA-  Cl− transport and carboanhydrases play a key role in ionic plasticity and epilepsy.

- GABAergic transmission has both seizure-suppressing and seizure-promoting effects.

- TrkB and calpain act on GABA signaling to coordinate the process of epileptogenesis.

- GABA signaling has context-specific and age-specific effects in health and disease.

- by Kaila Kai et al., Current Opinion in Neurobiology, Volume 26, June 2014, Pages 34–41

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Ion channels in genetic and acquired forms of epilepsy

Ion channels in genetic and acquired forms of epilepsy | Neuroscience_topics | Scoop.it

Genetic mutations causing dysfunction of both voltage- and ligand-gated ion channels make a major contribution to the cause of many different types of familial epilepsy. Key mechanisms comprise defective Na+ channels of inhibitory neurons, or GABAA receptors affecting pre- or postsynaptic GABAergic inhibition, or a dysfunction of different types of channels at axon initial segments. Many of these ion channel mutations have been modelled in mice, which has largely contributed to the understanding of where and how the ion channel defects lead to neuronal hyperexcitability. Animal models of febrile seizures or mesial temporal epilepsy have shown that dendritic K+ channels, hyperpolarization-activated cation channels and T-type Ca2+ channels play important roles in the generation of seizures. For the latter, it has been shown that suppression of their function by pharmacological mechanisms or in knock-out mice can antagonize epileptogenesis. Defects of ion channel function are also associated with forms of acquired epilepsy. Autoantibodies directed against ion channels or associated proteins, such as K+ channels, LGI1 or NMDA receptors, have been identified in epileptic disorders that can largely be included under the term limbic encephalitis which includes limbic seizures, status epilepticus and psychiatric symptoms. We conclude that ion channels and associated proteins are important players in different types of genetic and acquired epilepsies. Nevertheless, the molecular bases for most common forms of epilepsy are not yet clear, and evidence to be discussed indicates just how much more we need to understand about the complex mechanisms that underlie epileptogenesis. - Lerche H et al.The Journal of Physiology, 591, 753-764., February 15, 2013

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Janys Venne's curator insight, October 26, 2013 2:02 AM


I'll appreciate your time & help to visit my website on #seizures #epilepsy at http://seizures.dolyan.com/. Thank you :)

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Plasticity of Inhibition

Plasticity of Inhibition | Neuroscience_topics | Scoop.it

[Review] Until recently, the study of plasticity of neural circuits focused almost exclusively on potentiation and depression at excitatory synapses on principal cells. Other elements in the neural circuitry, such as inhibitory synapses on principal cells and the synapses recruiting interneurons, were assumed to be relatively inflexible, as befits a role of inhibition in maintaining stable levels and accurate timing of neuronal activity. It is now evident that inhibition is highly plastic, with multiple underlying cellular mechanisms. This Review considers these recent developments, focusing mainly on functional and structural changes in GABAergic inhibition of principal cells and long-term plasticity of glutamateric recruitment of inhibitory interneurons in the mammalian forebrain. A major challenge is to identify the adaptive roles of these different forms of plasticity, taking into account the roles of inhibition in the regulation of excitability, generation of population oscillations, and precise timing of neuronal firing. - by Kullmann DM et al., Neuron, Volume 75, Issue 6, 951-962, 20 September 2012

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