Neuroscience Terms Starting With L
Neuroscience Glossary: L
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Limbic System
/ LIM-bik SIS-tem / · Latin limbus (border, edge) + Greek systema
Limbic System is a set of interconnected brain structures surrounding the brain stem, including the hippocampus, amygdala, hypothalamus, thalamus, and cingulate cortex, that regulate emotion, memory, motivation, and basic survival behaviors.
Originally described by Paul Broca as the limbic lobe in 1878 and expanded by James Papez into a circuit concept in 1937, the limbic system integrates emotional experience with memory formation and behavioral response. The hippocampus links emotional context to memory, the amygdala evaluates emotional salience, and the hypothalamus generates visceral and hormonal responses. Modern neuroscientists have criticized the concept of the limbic system as anatomically imprecise, as many structures included are not solely involved in emotion and the emotional brain extends well beyond these regions.
The cingulate cortex, wrapping around the corpus callosum within the limbic system, integrates emotional and cognitive information. Neuroimaging studies have found that anterior cingulate activity during social rejection overlaps substantially with activity recorded during physical pain, suggesting that the same neural substrate processes both experiences.
The limbic system is not the only seat of emotion in the brain. The prefrontal cortex, brainstem, hypothalamus, and sensory networks also shape emotional experience and behavior, and no single structure or circuit has a monopoly on any emotion.
Kindling, the gradual development of full seizures from repeated low-intensity electrical stimulation of limbic structures, was first demonstrated in rats by Graham Goddard in 1967. Stimulating the amygdala or hippocampus at sub-seizure intensities as few as once per day eventually produces spontaneous generalized seizures, a model now widely used to study temporal lobe epilepsy.
Long-Term Depression
/ long term de-PRESH-un / · Old English lang, long; Latin terminus, end; Latin deprimere, to press down
Long-Term Depression is a persistent weakening of synaptic strength following prolonged low-frequency stimulation, representing the counterpart to long-term potentiation in the bidirectional regulation of synaptic efficacy.
LTD is triggered when a postsynaptic neuron experiences sustained low-level calcium influx, activating protein phosphatases that remove AMPA receptors from the synapse by endocytosis, reducing sensitivity to glutamate. In the cerebellum, LTD at parallel fiber-Purkinje cell synapses is critical for motor learning, refining movements by weakening inappropriate synaptic pathways. The balance between LTP and LTD allows neural circuits to both strengthen useful connections and prune unnecessary ones, providing the cellular basis for learning, memory consolidation, and adaptive forgetting.
Masao Ito and colleagues first characterized cerebellar LTD in rabbits during the 1980s by pairing parallel fiber stimulation with climbing fiber input, demonstrating that the coincidence of these two signals, rather than either alone, was sufficient to trigger lasting synaptic weakening at the Purkinje cell.
Long-term depression is not damage or pathology. It is a regulated form of synaptic plasticity that requires specific molecular signaling cascades, including activation of mGluR1 receptors and protein kinase C, and its disruption impairs motor learning and memory refinement.
How to become pathologist? →In the vestibulo-ocular reflex of rabbits, cerebellar LTD helps recalibrate eye movements when visual feedback indicates that the reflex is too strong. Training with magnifying or minifying lenses can change reflex gain by 20 to 40 percent over several days, and parallel fiber-Purkinje cell LTD provides one cellular mechanism for that adjustment.
Long-Term Potentiation
/ long term poh-ten-shee-AY-shun / · English long-term + Latin potentia (power) + -ation
Long-Term Potentiation is an activity-dependent strengthening of synaptic transmission that persists for hours to weeks, representing the leading cellular mechanism of learning and memory in the brain.
LTP is induced by high-frequency stimulation that activates NMDA receptors, which require both glutamate binding and postsynaptic depolarization to open, acting as molecular coincidence detectors for pre- and postsynaptic activity. Expression involves increased AMPA receptor insertion into the postsynaptic membrane, enlargement of dendritic spines, and in its late phase, new protein synthesis. Timothy Bliss and Terje Lømo discovered LTP in 1973 in the rabbit hippocampus, providing the first synaptic mechanism for Hebb’s theoretical rule that neurons that fire together wire together.
Blocking protein synthesis in the hours after a learning event selectively prevents late-phase LTP and erases long-term memory in rodents without affecting short-term memory, demonstrating that the two memory phases depend on distinct molecular processes.
Translation Biology →Long-term potentiation is not the only cellular mechanism of learning. Long-term depression also changes synaptic strength and helps refine neural circuits, and the two processes must be balanced for accurate memory storage and behavioral flexibility.
Transgenic mice lacking the NR1 subunit of NMDA receptors specifically in the hippocampus cannot form spatial memories in the Morris water maze, typically failing to locate a hidden platform within a 60-second trial even after days of training. Their escape latencies often remain above 40 seconds while control mice improve rapidly, linking NMDA-receptor-dependent LTP to spatial learning.