Long-Term Potentiation
Neurons are the basic processing units of the brain. They are instruments of communication—receiving, processing, and sending information to and from other neurons. Neurons are separated from each other by tiny gaps called synapses. Neurons communicate with each other by releasing hormones called neurotransmitters that travel across the synaptic gap. On the receiving neuron, these neurotransmitters are detected by receptors located on branching extensions of the nerve cell, called dendrites. These signals can either excite or inhibit the receiving neuron.
Long-term potentiation (LTP) is an increase in the strength of a synaptic connection that lasts from minutes to days. Synaptic strength is a measure of how easy it is for one neuron to be affected by inputs from another neuron. LTP means that after a given neuron (neuron A) is stimulated by another neuron (neuron B), it takes less signal strength for neuron A to stimulate neuron B in the future. A neural circuit is formed. This is because the stimulation causes formation of additional receptors in the receiving neuron. Any kind of learning consists of modifying synapses—making them more or less likely to receive and send signals in the presence of particular inputs.Long-Term Potentiation
Anatomy of Memory
The Hippocampus
Spatial memories and explicit memories depend on neural circuits formed in the hippocampus, a horseshoe-shaped structure located in the limbic system. It lies just below the cerebral cortex—the outer "rind" of the brain. The hippocampus does not permanently store memories. Instead, it moves them for storage in other parts of the brain. The hippocampus has many projections (nerve fibers) connecting it to other brain regions. These connections allow the formation of conscious memories that contain images, feelings, and words. Implicit procedural learning does not involve the hippocampus.
People are rarely able to recall memories of events that happened earlier than age three, a phenomenon referred to as childhood amnesia. Sigmund Freud, the Austrian neurologist considered the father of psychology, theorized that childhood amnesia was caused by repression of memories involving traumatic events or sexually threatening desires that occurred early in the child's psychosexual development. Neuroscientists, however, argue that the key to childhood amnesia lies in the development of the hippocampus.
The implicit memory system is functional at birth, but the hippocampal (explicit) memory system takes about three years to become functional. It takes another two years to develop full connections to the rest of the brain. During the initial phase of development, explicit memories can be acquired and maintained over the short term. However, these memories decay rapidly, resulting in amnesia for events during this developmental period. Adults who have sustained damage to the hippocampus or have had their hippocampus surgically removed experience profound anterograde amnesia.
The most famous case is that of American patient Henry Gustav Molaison (1926–2008), referred to in textbooks as H.M. At age seven, Molaison was knocked down by a bicycle and sustained a head injury. He began having epileptic seizures at age 16, which eventually became uncontrollable and life-threatening. When he was 27 years old, Molaison had brain surgery aimed at relieving the epileptic fits. The surgery involved removing about two-thirds of his hippocampus. After the surgery, he had normal working memory, normal retrograde memory (memories of his past), and normal implicit memory. However, he could no longer form new conscious (explicit) memories. Brenda Milner, a researcher who worked with him for more than 50 years, reported that Molaison never recognized her.
Researchers have also studied three young adults who suffered damage to the hippocampus during difficult births that interrupted their oxygen supplies. Like Molaison, the children could not form new episodic memories, such as remembering what activities they had engaged in during the day. But they learned to read, write, and spell, developed normal vocabularies, and performed well in school. This suggests that the hippocampus is crucial for forming and maintaining memories of personal experiences (episodic memory) but is less involved in the formation and maintenance of more general memories (semantic memory).
The Cortex, Cerebellum, and Basal Ganglia
Learning or executing a motor skill activates the motor cortex (which triggers voluntary movement), the cerebellum (involved in balance and muscle activity), and the basal ganglia (which help control voluntary movement). Damage to these areas results in impairment in learning, executing, and controlling motor movements. For example, Huntington's disease is a genetic disorder that causes neural degeneration in the basal ganglia. This damage leads to uncontrolled movements, difficulty learning new information, impaired thinking, irritability, and sadness.
An abundance of neuroscientific evidence shows that the semantic and episodic explicit memory systems are neurologically separable. Damage to left brain areas (such as the left front parietal and temporal regions) results in category-specific amnesia. In this condition, semantic memory for entire categories of information is wiped out, but episodic memory is spared. Conversely, other types of brain damage impair episodic memory but spare semantic memory. For example, in one case a patient with Alzheimer's dementia could remember how to play golf (implicit procedural memory), as well as golf rules and golf terminology (semantic memory), but could not remember any details of a round he had just played (episodic memory).Subcortical Memory
In 2005, neuroscientists Yoko Okada and Craig Stark repeated the experiment with a variety of video clips while people underwent functional magnetic resonance imaging (fMRI), a brain imaging technique that allowed them to view which areas of the brain were active during processing. They found that true memories involved a high level of activity in both the prefrontal cortex and hippocampus. False memories involved low activity in the prefrontal cortex. They concluded that activity in the prefrontal cortex encodes the source, or context, of a newly formed memory. If the prefrontal cortex is not actively engaged during exposure to misinformation, that misinformation is more easily embedded in the context of the first event, creating false memories. Researchers Scott Slotnick and Daniel Schacter reached similar conclusions using different methodology. They claimed that activity in the prefrontal cortex is a neural signature that distinguishes true from false memories. However, this kind of neural activity may not be accessible to conscious awareness. Activity in the prefrontal cortex is therefore crucial for "tagging" misinformation as inconsistent with original memory.