Consolidation Hypothesis

The consolidation hypothesis describes the concept of memory consolidation Opens in new window as the stabilization of a new memory over time by neural processes activated by recently learned information, and offers that recent memories are selectively lost after head injury because they were not consolidated prior to the injury, and as a result were not stored.

Early History: The Perseveration–Consolidation Hypothesis of Müller and Pilzecker

The perseveration–consolidation hypothesis was originally proposed by George E Müller and Alfons Pilzecker in 1900. In a series of studies with human subjects conducted between 1892 and 1900 at the University of Göttingen, Germany, Müller and Pilzecker showed that the retention of recently learned information was disrupted by the presentation of novel information shortly after the original learning.

The consolidation hypothesis offered an explanation for Théodule Ribot’s observation (1890) that with brain injury or disease, more recent memories are lost, whereas remote memories are preserved.

Although the consolidation hypothesis provided a conceptual framework for explaining retrograde amnesia Opens in new window seen after head injury, as noted by William McDougall as early as 1901, about half a century passed before it became a major influence on experimental studies of learning and memory.

In 1946, Russell and Nathan published a study summarizing a large number of cases of retrograde amnesia induced by head injury. The patients could not recall events occurring minutes, hours, or days prior to the injury.

According to the consolidation hypothesis, recent memories are selectively lost after head injury because they were not consolidated prior to the injury, and were thus not stored.

Experimental Manipulation of Memory Consolidation

The first evidence of experimentally induced retrograde amnesia was provided by the independent studies of both Duncan and Gerard in 1949, showing that the amount of memory impairment induced by electroconvulsive shock (ECS) after training varied inversely with the interval between training and ECS administration.

In the 1960s, a number of findings were instrumental in increasing our understanding of the neural mechanisms involved in experimental retrograde amnesia.

The demonstration that electrical stimulation of the amygdala after training induced retrograde memory loss stimulated the investigation of brain systems mediating consolidation.

Studies showing that the administration of protein synthesis inhibitors after training blocks memory consolidation in animals provided a stepping stone for the investigation of molecular mechanisms mediating memory formation.

Importantly, the finding that protein synsthesis inhibitors impaired long-term memory Opens in new window without blocking short-term memory Opens in new window provided strong support for the view that recent and remote memories are based on different neural processes.

The application of protein synthesis inhibitors continues to this day as a widely used tool for the investigation of the molecular basis of memory, despite increasing evidence that protein synthesis inhibitors can induce nonspecific effects, such as stimulation of neuro-transmitter release, which might confound the interpretation of the findings.

Finally, the finding by McGaugh that memory retention in rats is enhanced by the posttraining administration of stimulant drugs showed that memory consolidation can be experimentally enhanced as well as impaired, strongly indicating that memory consolidation is sensitive to different types of postraining manipulations. Together, these early studies provided the basic framework upon which subsequent experimental work on memory consolidation has relied up to the present day.

The introduction of posttraining manipulations contributed a powerful approach for the experimental investigation of memory consolidation Opens in new window.

When an animal is given a treatment (e.g., a brain lesion or an injection of an inhibitory or stimulant drug) before being trained in a memory task, or prior to memory retention testing, any resulting alteration in behavioral performance might be due to the treatment’s effects on sensory and motor functioning in place of or in addition to effects on learning and memory.

Such treatments thus confound the interpretation of the findings, making it difficult to assess the treatment-induced influence on mechanisms mediating memory formation and expression.

On the other hand, the use of posttraining injections of drugs that transiently affect neurobiological substrates of memory consolidation without producing permanent damage or long-term functional impairment enables the investigation of memory consolidation without affecting behavior during either the training or retention testing.

  1. McGaugh JL and Izquierdo I (2000) The contribution of pharmacology to research on the mechanisms of memory formation. Trends in Pharmacological Sciences 21: 208–210.
  2. Milner B, Squire LR, and Kandel ER (1998) Cogniive neuroscience and the study of memory. Neuron 20: 445–468.
  3. Müller GE and Pitzecker A (1900) Experimentelle betraege zur lehre vom gedaechtnis. Z Psychol Ergaenzungband 1: 1–300.
  4. Lechner HA, Squire LR, and Byrne JH (1999) 100 years of consolidation – remembering Müller and Pilzecker. Learning and Memory 6: 77–87.
  5. Pittenger C and Kandel ER (2003) In search of general mechanisms for long-lasting plasticity: Aplysia and the hippocampus. Philosophical Transactions of the Royal Society of London, Series B 358: 757–763.
  6. Ribot T (1890) Diseases of Memory. New York. Appleton and Company.
  7. Roozendaal B, Quirarte GL, and McGaugh JL (1997)) Stress-activated hormonal systems and the regulation of memory storage. Annals of the New York Academy of Sciences 821: 247–258.
  8. Routtenberg A and Rekart JL (2005) Post-translational protein modification as the substrate for long-lasting memory. Trends in Neuroscience 28: 12-19.
  9. Stough S, Shobe JL, and Carew TJ (2006) Intermediate-term processes in memory formation. Current Opinion in Neurobiology 16: 672–678.
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