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Thalamocortical circuit - disruption causes epilepsy (related to GABAb) oscillations between thalamus and cortex determine the level of consciousness and perception: Burst mode (sleep, low-f, synchronised); Tonic mode (awake, high-f, asynchronous)
Corticothalamic network and spike-wave generation 1 (EEG) 1)the thalamocortical relay neurons receive afferent sensory excitatory input and subsequently activate the cortical pyramidal neurons and adjacent GABA interneurons
Corticothalamic network and spike-wave generation 2 2)this is further spread to adjacent cortical neurons, generating a burst of activity and propagate back to the thalamus, acitivating nucleus reticularis thalami GABAergic neurons and local thalamic GABAerigc interneurons
Corticothalamic network and spike-wave generation 3 3)The hyperpolerising effects may activate low-threshold ch., generating slow waves which will then trigger the activation of the circuit
Systems involved 1)Glutamatergic transmission 2)GABAerigc transmission 3)Voltage-gated channels (Na, Ca and KCNQ)
Causes of epilepsy Dysfunction to ion channel and receptor trafficking Mutation of transmembrane channels (V and L-gated) are the underlying cause of many forms of human epilepsy Loss of function in inhibitory neurotransmission or gain """, leading to disinhibition
Definition of epilepsy long-term neurological disorder characterised by epileptic seizures
Neuronal excitability depends on the movement of ions ion channels are heterooligmeric proteins specially adapted to regulate trans membrane ion fluxes that respond to ligand binding/ voltage changes
Ca channels membrane excitability due to voltage-activated Ca currents P/Q type plays a dominant role in synaptic transmission *T currents can sustain rhythmic burst of firing in thalamocortical relay neurons, essential for synchronisation during absense seizures
Absence seizure Large part of T-C circuit becomes synchronised due to prolonged GABAB-R activation
Mutation of GABAa-R have been linked to three types of idiopathic epilepsies 1)childhood absence epilepsy 2)abnormal dominant epilepsy with febrile seizures plus (ADEFS+) 3)juvenile myoclonic epilepsy
Mutation in GABAa-R subunit gens have been associated with idiopathic generalised epilepsy syndromes mutation include mis-sense, nonsense, and frameshift mutations in coding or non-coding genes
Mis-sense in general, cause trafficking and/or gating defects
Premature translation-termination codon (PTC) generated by nonsense, deletion or frameshift mutation produce truncated protein, often causes server disease than mis-sense
Nonsense mediated decay PTC-generating mutant subunits are subject to NMD
ERAD mutants that escape NMD often are trafficking, misfold and misrouted - endoplasmic reticulum associated degradation
Gamma2 Q351X Mis-sense, produce no functional Cl ch. due to intracellular retention
Gamma2 K289M Mis-sense at linker of M2 and M3, tonic-chronic and febrile seizures, causes significant reduction in the amplitude of GABAa current and shortening of the receptor open time
Delta E177A Mis-sense, activated of the peak current under saturated doses of GABA without changing the binding affinity, decreased open time and reduced cellular expression
Anticonvulsants Carbamazepine (Na Ca) Valproate (Ca and GABA-T) Lamotrigine (Glu) Vigabatrin (GABA-T) Benzodiazepines and Barbiturates
Created by: JonLai