Γ-Aminobutyric acid in adult brain: an update.

This review assesses the parallel literature on the role of gamma - aminobutyric acid (GABA) in brain plasticity and GABA elements dysfunction related disorders. I review historical and new data from both animal and human sources which have helped define the key role for this transmitter synthesis, release and reuptake, GABA receptors subtype regulation, and GABAergic neurons function in the adult brain. The role of GABAergic elements in neurological and psychiatric disorders is briefly discussed.

CB1 Cannabinoid Receptor Expression in the Barrel Field Region Is Associated with Mouse Learning.

We found previously that fear conditioning by combined stimulation of a row B facial vibrissae (conditioned stimulus, CS) with a tail shock (unconditioned stimulus, UCS) leads to expansion of the cortical representation of the "trained" row, labeled with 2-deoxyglucose (2DG), in the layer IIIb/IV of the adult mouse the primary somatosensory cortex (S1) 24 h later. We have observed that these learning-dependent plastic changes are manifested by increased expression of somatostatin, cholecystokinin (SST+, CCK+) but not parvalbumin (PV+) immunopositive interneurons We have expanded this research and quantified a numerical value of CB1-expressing and PV-expressing GABAergic axon terminals (CB1+ and PV+ immunopositive puncta) that innervate different segments of postsynaptic cells in the barrel hollows of S1 cortex. We used 3D microscopy to identify the CB+ and PV+ puncta in the barrel cortex "trained" and the control hemispheres CS+UCS group and in controls: Pseudoconditioned, CS-only, UCS-only, and naive animals.

Neurochemical correlates of functional plasticity in the mature cortex of the brain of rodents.

It is commonly accepted that increase of input to sensory structures in mammals is known to produce marked changes in cortical recipient areas. This paper reviews the data concerning manifestations of changes in primary somatosensory cortex of adult animals caused by classical conditioning with reinforcement: aversive (whisker-shock) and appetitive (whisker-water) trainings. These include: anatomical, electrophysiological responses, receptor autoradiography, expression of GABA, GAD at mRNA and protein levels, expression of neuronal and astroglial GAT-1 puncta and inhibitory synaptogenesis in the hollows of "trained" barrels of the adult mouse.

Effect of Associative Learning on Memory Spine Formation in Mouse Barrel Cortex.

Associative fear learning, in which stimulation of whiskers is paired with mild electric shock to the tail, modifies the barrel cortex, the functional representation of sensory receptors involved in the conditioning, by inducing formation of new inhibitory synapses on single-synapse spines of the cognate barrel hollows and thus producing double-synapse spines. In the barrel cortex of conditioned, pseudoconditioned, and untreated mice, we analyzed the number and morphological features of dendritic spines at various maturation and stability levels: sER-free spines, spines containing smooth endoplasmic reticulum (sER), and spines containing spine apparatus. Using stereological analysis of serial sections examined by transmission electron microscopy, we found that the density of double-synapse spines containing spine apparatus was significantly increased in the conditioned mice.

Increases in the numerical density of GAT-1 positive puncta in the barrel cortex of adult mice after fear conditioning.

Three days of fear conditioning that combines tactile stimulation of a row of facial vibrissae (conditioned stimulus, CS) with a tail shock (unconditioned stimulus, UCS) expands the representation of "trained" vibrissae, which can be demonstrated by labeling with 2-deoxyglucose in layer IV of the barrel cortex. We have also shown that functional reorganization of the primary somatosensory cortex (S1) increases GABAergic markers in the hollows of "trained" barrels of the adult mouse. This study investigated how whisker-shock conditioning (CS+UCS) affected the expression of puncta of a high-affinity GABA plasma membrane transporter GAT-1 in the barrel cortex of mice 24 h after associative learning paradigm.