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At least 379 records · Page 21Linked to original sources
PubMed1990

Amygdalar interaction with the mediodorsal nucleus of the thalamus and the ventromedial prefrontal cortex in stimulus-reward associative learning in the monkey.

Cynomolgus monkeys (Macaca fascicularis) were assessed for their ability to associate visual stimuli with food reward. They learned a series of new 2-choice visual discriminations between colored patterns displayed on a monitor screen. The feedback for correct choice was the delivery of food. In order to promote associative learning between the visual stimuli and the incentive value of the food reward, reward delivery was not accompanied by any distinctive visual feedback on the display screen. The rate of learning new problems was assessed before and after surgery in a total of 16 monkeys. Three groups of 3 monkeys received bilaterally symmetrical ablations in either the amygdala, the mediodorsal nucleus of the thalamus, or the ventromedial prefrontal cortex. All these groups showed a severe postoperative learning impairment. Seven other animals were given a unilateral ablation in 1 of those 3 structures and a second unilateral ablation, in each case contralateral to and different from the first, in order to produce 2 groups in which a putative amygdalo-thalamo-prefrontal pathway had been disconnected by crossed unilateral lesions. One disconnection group had lesions in the amygdala and ventromedial prefrontal cortex; the other had lesions in the amygdala and the mediodorsal nucleus of the thalamus. The disconnection groups showed a significant impairment, but the effect of the disconnection surgeries was significantly milder than the effect of any of the 3 bilaterally symmetrical lesions. Therefore, symmetrical bilateral lesions in either the amygdala, the mediodorsal nucleus, or the ventromedial prefrontal cortex produce similar impairments in the present task, implying that these structures are functionally related to each other; but the relatively mild effect of disconnecting these structures from each other argues against the hypothesis that they are serial stages in a single, tightly linked functional pathway.

Amygdala↗
PubMed2004

The alpha(2A)-adrenergic agonist guanfacine improves visuomotor associative learning in monkeys.

Two monkeys were trained on two-problem visuomotor associations: if the cue was a circle pattern, move a handle to the left ('go-left'), and if it was a triangle pattern, move the handle to the right ('go-right'). These two visuomotor associations were unchanged throughout all the experiments and therefore were very familiar to the monkeys. For learning of new visuomotor associations, each monkey was presented with a new set of four novel patterns in each and every daily session, two of which instructed 'go-left' response and the other two 'go-right' response. Systemically administered guanfacine, a selective alpha(2A)-adrenergic agonist, improved the monkeys' learning ability: trials and errors to the learning criterion of 90% correct decreased significantly. The monkeys showed an enhanced capability of using at least three response strategies: win-stay on 'repeat trial', change-stay and change-shift on 'change trial'. The beneficial effect could be reversed by the coadministered idaxozan, an alpha(2)-adrenergic antagonist, which had no effect when administered alone. Similar treatment with guanfacine had no beneficial effect on visual discriminative learning, a task that involves the inferotemporal cortex. The present results indicate that stimulation by guanfacine of alpha(2A)-adrenoceptors improves visuomotor associative learning, probably through actions at alpha(2A)-adrenoceptors in the prefrontal cortex.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1979

Associative learning, habit, and health behavior.

Habit is defined as a firmly established behavior pattern marked by increasing automaticity, decreasing awareness, and partial independence from reinforcement. Reinforcement is viewed as of primary importance in the acquisition of behavior, whereas principles of associative learning enter to complement reinforcement in the maintenance of behavior. Habit is seen as a mechanism for short-circuiting the reinforcement process to avoid its overload and for providing the organism with speed and stability of response instead of the variability offered by reinforcement. The implications of this definition of habit for acquisition and alteration of health behavior are discussed; examples include smoking, obesity, alcoholism, and coronary-prone (type A) behavior.

Alcoholism↗
PubMed1961

Repetition and paired associates learning.

Recent experiments have suggested that paired-associate items which are practiced and missed are equivalent to new items on future trials, supporting an all-or-none interpretation of the formation of associative bonds. Experiments reported here show that if correct items are discarded after each trial the probability of getting a missed item correct on the next trial is higher than the probability of getting a new item correct.

Humans↗
PubMed2006

Motor-skill learning-associated gene regulation in the striatum: effects of cocaine.

Psychostimulant-induced molecular changes in cortico-basal ganglia-cortical circuits play a critical role in addiction and dependence. These changes include alterations in gene regulation particularly in projection neurons of the sensorimotor striatum. We previously showed that cocaine-induced gene regulation in such neurons is dependent on the behavior performed during drug action. Rats trained on a running wheel under the influence of cocaine for 4 days subsequently displayed greater c-fos induction by cocaine than untrained controls. This effect was selective for the sensorimotor striatum, which is known to mediate forms of motor learning. In the present study, we investigated whether this enhanced cellular responsiveness was associated with learning of wheel running or with prolonged running (exercising), by assessing c-fos inducibility after 1, 2, or 8 days of training. Wheel training was performed after injection of cocaine (25 mg/kg) or vehicle, and c-fos induction by a cocaine challenge was measured 24 h later. Rats that trained under cocaine (but not vehicle) showed a greater c-fos response in the striatum compared to locked-wheel controls. This effect was present after the 1-day training, peaked after 2 days, and dissipated by 8 days of training. Similar effects were found for substance P, but not enkephalin, expression. These changes in striatal gene regulation paralleled improvement in wheel running, which was facilitated by cocaine. Thus, these training-induced molecular changes do not appear to represent exercising effects, but may reflect motor learning-associated neuronal changes altered by cocaine. Such cocaine effects may contribute to aberrant motor learning implicated in psychostimulant addiction.

Animals↗
PubMed1979

Imagery in the associative learning of schizophrenics.

The present experiment is similar to Bower's (1970) study on imagery as a relational organizer in paired-associate (PA) learning with normals. Three groups of 20 schizophrenic patients learned three different lists of 30 word-word paired-associates, which used either interactive imagery, separation imagery, or rote repetition encoding. Ss were tested on stimulus recognition and paired-associate recall, given recognition. Differences in stimulus recognition and paired-associate recall were not significant across the three encoding methods. Results suggest that schizophrenics are unable to benefit from imaginal cues to facilitate learning in a manner similar to normals. These results are interpreted as providing additional support for the notion that the schizophrenics' cognitive deficit is associated with the relational organizing process of learning.

Adult↗
PubMedDate not supplied

Protein kinase C activation induces conductance changes in Hermissenda photoreceptors like those seen in associative learning.

Phosphorylation of ion channels has been suggested as one molecular mechanism responsible for learning-produced long-term changes in neuronal excitability. Persistent training-produced changes in two distinct K+ currents (IA (ref. 2), IK-Ca (refs 3,4)) and a voltage-dependent calcium current (ICa; refs 3,4) have previously been shown to occur in type B photoreceptors of Hermissenda, as a result of associative learning. But the identity of the phosphorylation pathway(s) responsible for these changes has not as yet been determined. Injections of cyclic AMP-dependent protein kinase reduce a K+ current (IK) in B cells which is different from those changed by training, but fails to reduce IA and IK-Ca. Phosphorylase b kinase (an exogenous calcium/calmodulin-dependent kinase) reduces IA, but whether IK-Ca and ICa are changed in the manner of associative training is not yet known. Another protein kinase present in high concentrations in both mammalian brain and molluscan nervous systems is protein kinase C, which is both calcium- and phospholipid-sensitive. We now present evidence that activation of protein kinase C by the tumour promoter phorbol ester (PDB) and intracellular injection of the enzyme induce conductance changes similar to those caused by associative training in Hermissenda B cells (that is a reduction of IA and IK-Ca, and enhancement of ICa). These results represent the first direct demonstration that protein kinase C affects membrane K+ ion conductance mechanisms.

Animals↗