The explore-exploit dilemma occurs anytime we must choose between exploring unknown options for information and exploiting known resources for reward. Previous work suggests that people use two different strategies to solve the explore-exploit dilemma: directed exploration, driven by information seeking, and random exploration, driven by decision noise. Here, we show that these two strategies rely on different neural systems. Using transcranial magnetic stimulation to inhibit the right frontopolar cortex, we were able to selectively inhibit directed exploration while leaving random exploration intact. This suggests a causal role for right frontopolar cortex in directed, but not random, exploration and that directed and random exploration rely on (at least partially) dissociable neural systems.

Since its discovery over four decades ago, somatostatin receives growing scientific and clinical interest. Being localized in the nervous system in a subset of interneurons somatostatin acts as a neurotransmitter or neuromodulator and its role in the fine-tuning of neuronal activity and involvement in synaptic plasticity and memory formation are widely recognized in the recent literature. Combining transgenic animals with electrophysiological, anatomical and molecular methods allowed to characterize several subpopulations of somatostatin-containing interneurons possessing specific anatomical and physiological features engaged in controlling the output of cortical excitatory neurons. Special characteristic and connectivity of somatostatin-containing neurons set them up as significant players in shaping activity and plasticity of the nervous system. However, somatostatin is not just a marker of particular interneuronal subpopulation. Somatostatin itself acts pre- and postsynaptically, modulating excitability and neuronal responses. In the present review we combine the knowledge regarding somatostatin and somatostatin-containing interneurons, trying to incorporate it into the current view concerning the role of the somatostatinergic system in cortical plasticity.

1. A quantitative 2-[14C]deoxy-D-glucose (2DG) autoradiographic study was undertaken to determine the functional (metabolic) organization of an individual column in the first somatosensory cortex (SI) of the awake restrained rat. Manual or mechanically controlled brush stroking of a single vibrissa (typically C3) was used in order to evoke neural activity and increase glucose utilization in a single cortical barrel in lamina IV and in adjacent supra- and infragranular layers in register with the single cortical barrel labeling in lamina IV. 2. The single activated vibrissal column was found to extend from layer I to the superficial half of layer VI of the contralateral SI cortex and was fusiform in shape, being of largest diameter (650-micron) in layer IV and smallest diameter (200 micron) in layer VI. 3. This single metabolic column was not uniform in its density of labeling. The greatest local cerebral metabolic rate of glucose (LCMRG) was found in layer IV (170 mumol.100 g-1.min-1), layers II-III, and V had, on the average, similar LCMRG values (115 mumol.100 g-1.min-1), which decreased with distance from layer IV. 4. The functional (metabolic) columnar activity center situated in layer IV corresponded in size to the appropriate anatomical barrel as determined from thionin-stained sections. Increased metabolic activity was not strictly confined to the candle-pin-shaped column but extended tangentially as radiating fingerlike projections toward the neighboring barrels. 5. In cortical layers other than IV, the metabolic column was less prominently labeled, and the metabolic activity also branched in the tangential plane. The labeling pattern profile in upper layers was characterized by numerous lateral spreading fingerlike projections of increased glucose metabolism. 6. Neonatal follicle lesions sparing only C3 vibrissa caused a great increase (125%) in cortical territory driven by the spared whisker with a concomitant loss of columnar shape and decrease in intensity of metabolic activity in response to its stimulation. 7. Similar lesions in adult rats produced a significant increase (40%) in dimensions of the spared C3 cortical column, which was, however, smaller than that produced after neonatal lesions. The metabolic activation of layer Vb in the spared C3 column was increased (17%) compared with that of the control column.(ABSTRACT TRUNCATED AT 400 WORDS)

It has been known for several years that receptive field properties of sensory cortical neurons can be altered by learning experiences. We attempted to visualize a global change of the cortical body map induced by learning. In order to do this a short-duration classical conditioning involving stimulation of a row of mystacial vibrissae in mice was followed with 2-deoxyglucose (2DG) mapping of functional activity. Three conditioning sessions that paired stimulation of a row of whiskers with a tail shock produced an increase of the functional representation in somatosensory cortex (SI) of a row of the whiskers stimulated during the training. This plastic change of vibrissal representation in SI was visualized with 2DG autoradiography a day after completion of training. The expansion of representation was the most pronounced in cortical layer IV, and to a lesser extent, in layer IIIb. The expansion was observed in conditioned but not in pseudoconditioned mice or in animals that received only the conditioned stimulus. If training was discontinued, the enlargement of vibrissal representation progressively faded. The reversal could be accelerated by a behavioral extinction procedure. This study gives the pictorial demonstration of rapid, transient, and extinguishable learning-dependent changes in SI cortical maps.

Huntington's disease (HD) is one of a group of neurodegenerative diseases caused by an expanded trinucleotide (CAG) repeat coding for an extended polyglutamine tract. The disease is inherited in an autosomal dominant manner, with onset of motor, cognitive, and psychiatric symptoms typically occurring in midlife, followed by unremitting progression and eventual death. We report here that motor presymptomatic R6/1 HD mice show a severe impairment of somatosensory-discrimination learning ability in a behavioral task that depends heavily on the barrel cortex. In parallel, there are deficits in barrel-cortex plasticity after a somatosensory whisker-deprivation paradigm. The present study demonstrates deficits in neocortical plasticity correlated with a specific learning impairment involving the same neocortical area, a finding that provides new insight into the cellular basis of early cognitive deficits in HD.

Modifications of properties of the adult sensory cortex by elimination of sensory input (deprivation) serves as a model for studying plasticity in the adult brain. We studied the effects of short- and long-term deprivation (sparing one row of vibrissae) upon the barrel cortex. The response to stimulation (exploration of a new environment) of the spared row was examined with [14C]-2-deoxyglucose autoradiography and c-Fos immunohistochemistry. Both methods found large increases of the functional cortical representation of the spared row of vibrissae, extending into parts of the barrel cortex previously activated by the deprived vibrissae. With both methods, the greatest expansion of spared input was observed in cortical layer IV. In this way, we established a model, which was applied for examining involvement of matrix metalloproteinase 9 (MMP-9), upon experience-dependent cortical plasticity. MMP-9 is an enzyme implicated in plastic modification of the neuronal connections. We found that MMP-9 activity was increased in response to stimulation, and furthermore, MMP-9 knockout mice showed a modest but significant decrease of plasticity in layer IV with 2-DG mapping and in layers II/III with c-Fos mapping. Thus, in adult mouse brain experience-dependent plasticity is in part supported by the activity of MMP-9.