Generalized @entity302 are underlied by specific circuits where GABAergic synapses are involved at different levels. The role of these synapses depends on (i) the type of @entity302 and (ii) their localization within the central nervous system. This dual complexity can be illustrated by two examples from animal experimentation. Clinical, as well as experimental data have shown that the neural mechanisms underlying generalized non- @entity410 (e.g., @entity2048 ) are distinct from those involved in @entity410 . Pharmacological reactivity to anti- @entity302 compounds is different between these two forms of @entity410 . Hippocampus and amygdala are key-structures in @entity410 whereas they are not involved in @entity2048 . A thalamo-cortical circuit generates the spike-and-wave discharges in @entity2048 . Global activation of GABAergic transmission by systemic administration generally suppresses @entity410 whereas it aggravates absence in both @entity1 and animals. Further investigations using a genetic model of @entity2048 in the @entity35 have suggested that this aggravation may be related to the role of post-synaptic @entity1246 -B receptors in slow hyperpolarization, in the relay nuclei of the thalamus. By "de-inactivating" low-threshold @entity460 currents, activation of these receptors facilitates rhythmic activity in the thalamo-cortical circuit. In addition, regulation of transmitter release by presynaptic @entity1246 -B receptors in the thalamus and the cortex may also contribute to the control of @entity2048 . A blockade of the @entity1246 -B receptors, either locally in the thalamus or systemically suppresses @entity2048 . The critical role of the substantia nigra in the control of different forms of @entity410 has been demonstrated recently in the @entity35 . This structure is one of the richest regions of the brain for GABAergic terminals, neurons and receptors. Local applications of @entity1246 mimetics resulting in the desinhibition of their target neurons in the superior colliculus were shown to suppress both @entity410 and non- @entity410 . This circuitry involving the basal ganglia may exert a "remote inhibitory control" over @entity6191 generated in other areas. In conclusion, the pharmacological manipulation of GABAergic transmission has different consequences on @entity302 depending on the form of @entity410 and the connections and functions of the GABAergic neurons in a given structure. The design of new therapeutical tools based on the manipulation of GABAergic mechanisms in the central nervous system requires to take into account this neuroanatomical dimension.

[GABAergic mechanisms in XXXX : the neuroanatomical dimension].

@entity1 :: ('9606', 'Species') :: ['humans'] @entity410 :: ('MESH:D012640', 'Disease') :: ['convulsive', 'seizures', 'convulsive generalized seizures', 'convulsive seizures'] @entity1246 :: ('MESH:D005680', 'Chemical') :: ['GABA'] @entity302 :: ('MESH:D004827', 'Disease') :: ['epileptic seizures', 'epileptic', 'epilepsy'] @entity2048 :: ('MESH:D004832', 'Disease') :: ['absence seizures', 'absence-epilepsy', 'absence epilepsy'] @entity460 :: ('MESH:D002118', 'Chemical') :: ['calcium'] @entity35 :: ('10116', 'Species') :: ['rat'] @entity6191 :: ('MESH:D004829', 'Disease') :: ['generalized epilepsies']
@entity6191 :: (MESH:D004829,Disease) :: ['generalized epilepsies']
