Changing the strength of connections between neurons is widely assumed to be the mechanism by which memory traces are encoded and stored in the central nervous system. In its most general form, the synaptic plasticity and memory hypothesis states that "activity-dependent synaptic plasticity is induced at appropriate synapses during memory formation and is both necessary and sufficient for the infor- mation storage underlying the type of memory mediated by the brain area in which that plasticity is observed." We outline a set of criteria by which this hypothesis can be judged and describe a range of experimental strategies used to investigate it. We review both classical and newly discovered properties of synaptic plasticity and stress the importance of the neural architecture and synaptic learning rules of the network in which it is embedded. The greater part of the article focuses on types of memory mediated by the hippocampus, amygdala, and cortex. We conclude that a wealth of data supports the notion that synaptic plasticity is necessary for learning and memory, but that little data currently supports the notion of sufficiency.

Synaptic plasticity and memory: an evaluation of the hypothesis

The basal ganglia: focused selection and inhibition of competing motor programs.

Addiction is a state of compulsive drug use; despite treatment and other attempts to control drug taking, addiction tends to persist. Clinical and laboratory observations have converged on the hypothesis that addiction represents the pathological usurpation of neural processes that normally serve reward-related learning. The major substrates of persistent compulsive drug use are hypothesized to be molecular and cellular mechanisms that underlie long-term associative memories in several forebrain circuits (involving the ventral and dorsal striatum and prefrontal cortex) that receive input from midbrain dopamine neurons. Here we review progress in identifying candidate mechanisms of addiction.

https://www.ausl.fe.it/azienda/dipartimenti/daismdp/staff/osservatorio-epidemiologico/documenti-scaricabili/convegni/corso-di-formazione-aggiornamento-di-farmacoterapia-in-uso-al-sert/3-himan-mecc-dipendenza/at_download/file

NEURAL MECHANISMS OF ADDICTION: The Role of Reward-Related Learning and Memory

What makes organizations so similar? We contend that the engine of rationalization and bureaucratization has moved from the competitive marketplace to the state and the professions. Once a set of organizations emerges as a field, a paradox arises: rational actors make their organizations increasingly similar as they try to change them. We describe three isomorphic processes-coercive, mimetic, and normative—leading to this outcome. We then specify hypotheses about the impact of resource centralization and dependency, goal ambiguity and technical uncertainty, and professionalization and structuration on isomorphic change. Finally, we suggest implications for theories of organizations and social change.

The iron cage revisited: Institutional isomorphism and collective rationality in organizational fields (Chinese Translation)

Applications of the Morris water maze in the study of learning and memory.

Rotenone destroys dopaminergic neurons and induces parkinsonian symptoms in rats.

Aminoadamantanes as NMDA receptor antagonists and antiparkinsonian agents : Preclinical studies

6-Hydroxydopamine lesion of the rat prefrontal cortex increases locomotor activity, impairs acquisition of delayed alternation tasks, but does not affect uninterrupted tasks in the radial maze.

Prominent projections of the medial prefrontal cortex (mPFC) to the nucleus accumbens (NAS) and the ventral tegmental area (VTA) exist, but it has been difficult to assign a clear functional role to either of these projections. With some exceptions to be discussed in some detail, only a few neurochemical and behavioral effects of manipulating the mPFC can be explained by invoking the mPFC-NAS projection, while most effects are compatible with an involvement of the mPFC-VTA-NAS or mPFC-pedunculopontine tegmental nucleus (PPTg)-VTA-NAS circuits. What is known about the organization and function of these loops is generally consistent with the results obtained by stimulating or lesioning or injecting drugs into the mPFC, yet these findings are largely inconsistent with the functional organization of the mPFC-NAS projection. This review briefly summarizes some of the most important aspects of what is known about the functional interactions of the mPFC. NAS, VTA, and associated areas, and focuses on functional differences between the mesocortical and the mesoaccumbal dopaminergic projections, and between the corticomesencephalic and the corticoaccumbal glutamatergic projections.

Werner J. Schmidt

Papers

Rotenone destroys dopaminergic neurons and induces parkinsonian symptoms in rats.

Aminoadamantanes as NMDA receptor antagonists and antiparkinsonian agents : Preclinical studies

6-Hydroxydopamine lesion of the rat prefrontal cortex increases locomotor activity, impairs acquisition of delayed alternation tasks, but does not affect uninterrupted tasks in the radial maze.

Functional relationship among medial prefrontal cortex, nucleus accumbens, and ventral tegmental area in locomotion and reward.

N-Methyl-d-aspartic acid-receptor antagonists block morphine-induced conditioned place preference in rats