GABAA receptor-induced inhibition of neuronal burst firing is weak in rat somatosensory cortex

Ji, Oka; Kobayashi, Toshinori; Nagao, Takeki; Tp, Hicks; Fukuda, H

doi:10.1097/00001756-199306000-00033

Cited by 3 publications

(1 citation statement)

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“…Thus, an increase in the ratio of RS vs. IB cells could be interpreted as an increase in inhibition. (ii) Pharmacological experiments using the GABA A receptor agonist muscimol and the benzodiazepine receptor agonist flurazepam in combination with electrophysiological recordings from the somatosensory cortex of anesthetized rats (Oka et al, 1993) revealed two distinct firing patterns (regular spiking and bursting). Inhibition of cells characterized by bursting pattern of firing was significantly weaker than in cells displaying the regular spiking pattern.…”

Section: Lack Of Pv and Firing Pattern Of Cortical Pyramidal Neuronsmentioning

confidence: 99%

Parvalbumin deficiency affects network properties resulting in increased susceptibility to epileptic seizures

Schwaller

Tetko

Tandon

et al. 2004

Molecular and Cellular Neuroscience

154

131

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Networks of GABAergic interneurons are of utmost importance in generating and promoting synchronous activity and are involved in producing coherent oscillations. These neurons are characterized by their fast-spiking rate and by the expression of the Ca 2+ -binding protein parvalbumin (PV). Alteration of their inhibitory activity has been proposed as a major mechanism leading to epileptic seizures and thus the role of PV in maintaining the stability of neuronal networks was assessed in knockout (PVÀ/À) mice. Pentylenetetrazole induced generalized tonic -clonic seizures in all genotypes, but the severity of seizures was significantly greater in PVÀ/À than in PV+/+ animals. Extracellular single-unit activity recorded from over 1000 neurons in vivo in the temporal cortex revealed an increase of units firing regularly and a decrease of cells firing in bursts. In the hippocampus, PV deficiency facilitated the GABA A ergic current reversal induced by high-frequency stimulation, a mechanism implied in the generation of epileptic activity. We postulate that PV plays a key role in the regulation of local inhibitory effects exerted by GABAergic interneurons on pyramidal neurons. Through an increase in inhibition, the absence of PV facilitates synchronous activity in the cortex and facilitates hypersynchrony through the depolarizing action of GABA in the hippocampus.

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Section: Lack Of Pv and Firing Pattern Of Cortical Pyramidal Neuronsmentioning

confidence: 99%