Hippocampus

The hippocampus is a seahorse-shaped structure within the brain’s temporal lobe that plays a vital role in forming memories, spatial navigation, and emotional processing.

Its name comes from the Greek word hippokampos, meaning “seahorse,” after its distinctive curved shape.

hippocampus location
There are two hippocampi in each hemisphere of the brain, located within the temporal lobe, just above each ear.

Key Takeaways

  • Memory: The hippocampus helps form new memories and recall past experiences.
  • Navigation: It builds spatial maps that let you find your way around familiar places.
  • Social Maps: This region also helps you process emotions and track how people are connected.
  • Damage: Losing hippocampal tissue causes memory loss and disorientation.
  • Protection: Exercise, stress management and mental stimulation support its health.

Where is the hippocampus located?

The hippocampus sits within the medial temporal lobes of your brain, just above each ear.

Everyone has two hippocampi, one in each hemisphere. The name comes from the Greek word for “sea horse,” which its curved shape resembles.

It’s part of the limbic system, a group of structures that help regulate emotions, memory, and learning.

The hippocampus also connects with other brain regions, including the amygdala and the prefrontal cortex, forming a network essential for processing experiences.

It is also unusual in another way. The hippocampus is one of the few brain regions where neurogenesis happens, meaning new neurons are still produced there in adulthood.

Hippocampus Functions

The hippocampus is best known for its role in memory. It does more than that, though. Here are its key functions:

The outline of a brain with the hippocampus location highlighted. 5 functions of the hippocampus in a list next to it: 1. forms new memories, 2. builds mental maps for navigation, 3. transfers information to long-term storage, 4. connects memory with emotions, and 5 creates social maps to help navigate interactions.

1. Memory formation

The hippocampus helps turn short-term experiences into long-term memories. It specializes in declarative memories. These are facts and events you can consciously recall.

For example, remembering what you had for breakfast or the name of a new colleague involves hippocampal processing.

Its close link to the amygdala also explains why emotional memories are often easier to remember.

When something feels important or intense, your brain tags it, and the hippocampus stores it more effectively.

A landmark case shows this. Scoville and Milner (1957) documented a patient known as HM.

Aim: To record how memory changes after both medial temporal lobes are surgically removed.

Method: In 1953, surgeon William Scoville removed about two-thirds of HM’s hippocampus on each side, along with the amygdala and entorhinal cortex, to stop severe seizures. Brenda Milner then tested him for years.

Results: HM developed anterograde amnesia: he could no longer form new long-term memories of facts and events. His IQ, digit span and pre-surgery memories were intact. He could still learn motor skills like mirror-drawing.

Conclusion: The hippocampus is needed to form new conscious memories. It is not needed to store old ones, or to run short-term memory and skill learning.

One caution matters. HM’s surgery cut beyond the hippocampus into neighbouring structures, so his deficits cannot be pinned on that structure alone.

2. Spatial Memory and Navigation

The rear (posterior) hippocampus builds a cognitive map. This is a mental representation of your surroundings that lets you navigate familiar places.

The idea began with place cells. O’Keefe and Dostrovsky (1971) recorded single neurons in freely moving rats. Some cells fired only when the animal sat in one particular spot.

O’Keefe and Nadel (1978) argued that these cells form a world-centred map of space. Grid cells supply its scale. In the neighbouring entorhinal cortex, they fire in a regular triangular lattice that works like neural graph paper (Hafting et al., 2005).

The strongest human evidence comes from London taxi drivers.

Aim: To test whether years of real-world navigation change the structure of the human hippocampus.

Method: Maguire et al. (2000) took structural MRI scans of 16 licensed London taxi drivers, who must memorise the whole street layout of the city. They compared them with 50 male controls.

Results: The drivers had more grey matter in the posterior hippocampi than controls, and less in the anterior. Posterior volume grew with the number of years spent driving.

Conclusion: The adult hippocampus reshapes itself in response to navigational demand, which is evidence of neuroplasticity.

The original study was correlational. Later work closed that gap. Bus drivers, matched for driving but not for flexible navigation, showed no such difference (Maguire et al., 2006).

Trainees who passed “The Knowledge” grew posterior grey matter, while those who failed did not (Woollett & Maguire, 2011). Navigation itself drove the change.

3. Memory Consolidation

The hippocampus does not store memories permanently. It binds the scattered fragments of an experience into one indexed trace, then prepares that trace for long-term storage in the cortex.

This slow hand-over is called systems consolidation (Squire, 1992).

Much of it happens during sleep. The hippocampus replays the trace again and again until the cortex can hold the memory on its own.

The synaptic mechanism is separate. Long-term potentiation strengthens the link between two neurons that fire together, and it was first demonstrated in the hippocampus (Bliss & Lømo, 1973).

4. Social Mapping

Recent research suggests the hippocampus also helps you track social relationships.

It creates social maps. These are mental representations of how people relate to one another, and they help you remember who is connected to whom (Montagrin et al., 2018).

The same relational machinery appears to organise non-spatial knowledge and imagined futures. Spatial navigation may simply be its original use.

Hippocampus Anatomy

hippocampus2

The hippocampus is comprised primarily of pyramidal cells, which are multipolar neurons that have excitatory and projective functions.

The hippocampus is not a uniform mass. It is divided into fields called CA1, CA2, CA3 and CA4, curled around a separate structure, the dentate gyrus.

Information travels through these fields along a mostly one-way, three-synapse loop known as the trisynaptic circuit. The entorhinal cortex feeds the dentate gyrus, the dentate gyrus feeds CA3, and CA3 feeds CA1.

Each stage does different work. The dentate gyrus performs pattern separation, keeping similar experiences apart so this morning’s breakfast is not confused with yesterday’s. CA3 performs pattern completion, rebuilding a whole memory from a fragment.

That is why one smell can revive a whole evening.

The hippocampus receives input and sends output to the rest of the brain via the entorhinal cortex.

This is an area strongly and reciprocally connected with many other parts of the cerebral cortex and serves as an interface between the hippocampus and other parts of the brain.

Its reach is wider still. The hippocampus receives input from the prefrontal cortex, the anterior cingulate gyrus and the premammillary region, and it can send signals back to each of them.

Long-Term Potentiation

How does a memory physically change the brain? The leading answer is long-term potentiation, or LTP: a lasting strengthening of the connection between two neurons after a brief burst of activity.

LTP was first demonstrated in the hippocampus. Bliss and Lømo (1973) stimulated the pathway into the dentate gyrus of anaesthetised rabbits and found that the synaptic response stayed enlarged for hours afterwards.

Two glutamate receptors explain the effect. AMPA receptors carry ordinary fast signals, while NMDA receptors act as coincidence detectors.

An NMDA receptor is normally plugged by a magnesium ion. It opens only when the sending neuron releases glutamate and the receiving neuron is already active, letting calcium flood in and strengthen the synapse.

So a synapse strengthens only when both cells fire together. This is the Hebbian principle, often summarised as “cells that fire together wire together.”

What Happens When the Hippocampus Is Damaged?

Damage to the hippocampus can seriously disrupt memory and spatial awareness.

Some common effects include:

  • Difficulty forming new memories (especially recent events)
  • Forgetting familiar places or losing your sense of direction
  • Struggling to remember words or learn new information

This kind of dysfunction is common in several conditions:

Alzheimer’s Disease

Alzheimer’s pathology starts in the entorhinal cortex, the hippocampus’s own gateway, and spreads into the hippocampus itself (Anand & Dhikav, 2012).

That anatomy explains the symptom order. Memory loss and confusion come first because the structure that forms new memories is damaged first.

Over time the region shrinks and its neurons deteriorate. Older memories are lost as well, and everyday orientation becomes difficult.

Depression and Chronic Stress

The hippocampus is packed with glucocorticoid receptors, the docking sites for stress hormones, so it is unusually sensitive to them. Sustained high cortisol can suppress and damage its neurons.

Videbech and Ravnkilde (2004) pooled MRI studies of patients with major depression. They found significantly smaller hippocampal volumes than in healthy controls, with reductions of up to 10%.

The traffic runs both ways. The hippocampus normally feeds back to dampen the body’s stress response, so damage here weakens the brake on stress itself.

Interestingly, electroconvulsive therapy (ECT) for depression has been shown to increase hippocampal volume (Nordanskog et al., 2010).

Psychiatric Disorders

People with schizophrenia or bipolar disorder often show reduced hippocampal volume and abnormal neural activity (Anand & Dhikav, 2012).

Reduced hippocampal volume is also reported in post-traumatic stress disorder. Whether trauma shrinks the hippocampus, or a smaller hippocampus raises the risk of PTSD, is still debated.

Volume differences of this kind are correlations. They cannot on their own tell you which came first.

Other Causes

Injury, stroke and oxygen deprivation can all harm the hippocampus, usually causing memory and orientation problems.

Epilepsy deserves a separate mention. The hippocampus is one of the most seizure-prone structures in the brain, and scarring of its tissue, called hippocampal sclerosis, is a common cause of temporal lobe epilepsy.

Memory can also fail when the hippocampus is intact. Damage further along its output pathway, to the mammillary bodies and thalamus, produces the amnesia of Korsakoff’s syndrome.

Can you Strengthen your Hippocampus?

While you can’t change your brain’s structure overnight, certain habits can support hippocampal health and slow decline:

  • Exercise regularly: Physical activity promotes neurogenesis (new brain cell growth) in the hippocampus.
  • Manage stress: Practices like mindfulness and deep breathing can protect the hippocampus from stress-related shrinkage.
  • Stimulate your brain: Reading, writing, puzzles, and memory games help keep hippocampal pathways active.

Critical Evaluation

The hippocampus is often called the brain’s memory centre. That shorthand hides three real problems.

  • Not a Store: memories are consolidated into the cortex, so the hippocampus indexes them rather than holding them.
  • Memory or Space: whether its core job is memory or spatial mapping has never been settled.
  • Fragile Evidence: the human case rests on a few rare patients, and the mechanism on rodents.

Not a Memory Store

Squire (1992) drew this conclusion from the pattern of amnesia itself. Patients who lose the hippocampus keep memories laid down years earlier, which could not happen if those memories lived there.

The structure works as a temporary binding-and-indexing hub. It ties together the scattered cortical fragments of an event, then trains the cortex to hold the memory without help.

Old memories survive its loss because they no longer need it.

The practical consequence for a student is precise. Damage to the hippocampus should predict lost recent memories and no new ones, not a wiped-out past, and that is exactly what amnesic patients show.

Calling it the brain’s memory centre therefore mistakes an index for a library, and it is the most persistent misconception about the structure.

Memory or Spatial Map?

Two rival accounts have coexisted for decades. Squire (1992) treats the hippocampus as a declarative-memory system. O’Keefe and Nadel (1978) treat it as a spatial map.

Each camp has strong evidence.

Amnesic patients lose facts and events, not just their way around. Place cells, by contrast, fire for location, not for facts. Neither finding fully explains the other.

The modern synthesis says both are special cases of something more general: the hippocampus stores relational representations, records of how items connect to one another. Space is simply the most obvious kind of relation.

That reconciliation is useful. It is not a decisive win for either camp, and the dispute still shapes how new experiments are designed and interpreted.

Both camps still design studies meant to prove the other wrong.

Rare Cases and Rodent Brains

HM’s surgery removed the amygdala and entorhinal cortex as well as most of the hippocampus. His deficits therefore cannot be pinned on one structure.

He was also one man with an unusual operation, which makes generalising to healthy brains a real inferential leap.

The mechanistic backbone has the opposite problem. Place cells (O’Keefe & Dostrovsky, 1971) and long-term potentiation (Bliss & Lømo, 1973) were both found in rodents, and rodent circuits may not map cleanly onto human conscious memory.

LTP carries a further caveat.

It is induced artificially in the laboratory, so showing that the same synaptic change encodes a natural memory remains an open problem.

None of this sinks the account. It is the convergence of lesion cases, animal lesions, single-cell recording and synaptic physiology, rather than any one study, that licenses the general conclusion.

Contemporary Research

Recent work has moved from asking which structure supports memory to asking how its circuits do it, and where the evidence is weak.

The sharpest open question is adult neurogenesis, the birth of new neurons in the mature brain. Two 2018 papers reached opposite conclusions from human autopsy tissue.

Boldrini et al. (2018) counted markers of newly born neurons in whole hippocampi from 28 healthy people aged 14 to 79. Numbers of immature neurons were similar at every age.

Sorrells et al. (2018) ran a similar marker analysis and found young neurons dropping sharply through childhood and becoming undetectable in adults.

The disagreement turns on method: how tissue is preserved, how long after death it is sampled, and whether the markers are specific to new neurons.

Neither should be quoted as settled fact.

Plasticity in the healthy adult hippocampus is on firmer ground, because the taxi-driver work progressed from a cross-sectional difference to a longitudinal before-and-after design (Woollett & Maguire, 2011).

The third theme is generalisation. The relational map that codes space also appears to organise social relationships, abstract knowledge and imagined futures (Montagrin et al., 2018).

References

Anand, K. S., & Dhikav, V. (2012). Hippocampus in health and disease: An overview. Annals of Indian Academy of Neurology, 15(4), 239–246. https://doi.org/10.4103/0972-2327.104323

Bliss, T. V. P., & Lømo, T. (1973). Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path. The Journal of Physiology, 232(2), 331–356. https://doi.org/10.1113/jphysiol.1973.sp010273

Boldrini, M., Fulmore, C. A., Tartt, A. N., Simeon, L. R., Pavlova, I., Poposka, V., Rosoklija, G. B., Stankov, A., Arango, V., Dwork, A. J., Hen, R., & Mann, J. J. (2018). Human hippocampal neurogenesis persists throughout aging. Cell Stem Cell, 22(4), 589–599. https://doi.org/10.1016/j.stem.2018.03.015

Hafting, T., Fyhn, M., Molden, S., Moser, M. B., & Moser, E. I. (2005). Microstructure of a spatial map in the entorhinal cortex. Nature, 436(7052), 801–806. https://doi.org/10.1038/nature03721

Maguire, E. A., Gadian, D. G., Johnsrude, I. S., Good, C. D., Ashburner, J., Frackowiak, R. S., & Frith, C. D. (2000). Navigation-related structural change in the hippocampi of taxi drivers Proceedings of the National Academy of Sciences 97 (8), 4398-4403.

Maguire, E. A., Woollett, K., & Spiers, H. J. (2006). London taxi drivers and bus drivers: A structural MRI and neuropsychological analysis. Hippocampus, 16(12), 1091–1101. https://doi.org/10.1002/hipo.20233

Montagrin, A., Saiote, C., & Schiller, D. (2018). The social hippocampus. Hippocampus, 28 (9), 672-679.

Nordanskog, P., Dahlstrand, U., Larsson, M. R., Larsson, E. M., Knutsson, L., & Johanson, A. (2010). Increase in hippocampal volume after electroconvulsive therapy in patients with depression: a volumetric magnetic resonance imaging study. The journal of ECT, 26 (1), 62-67.

O’Keefe, J., & Dostrovsky, J. (1971). The hippocampus as a spatial map: Preliminary evidence from unit activity in the freely-moving rat. Brain Research, 34(1), 171–175. https://doi.org/10.1016/0006-8993(71)90358-1

O’Keefe, J., & Nadel, L. (1978). The hippocampus as a cognitive map. Oxford University Press.

Scoville, W. B., & Milner, B. (1957). Loss of recent memory after bilateral hippocampal lesions. Journal of Neurology, Neurosurgery, and Psychiatry, 20(1), 11–21. https://doi.org/10.1136/jnnp.20.1.11

Sheline, Y. I., Mittler, B. L., & Mintun, M. A. (2002). The hippocampus and depression. European Psychiatry, 17, 300-305.

Sorrells, S. F., Paredes, M. F., Cebrian-Silla, A., Sandoval, K., Qi, D., Kelley, K. W., James, D., Mayer, S., Chang, J., Auguste, K. I., Chang, E. F., Gutierrez, A. J., Kriegstein, A. R., Mathern, G. W., Oldham, M. C., Huang, E. J., Garcia-Verdugo, J. M., Yang, Z., & Alvarez-Buylla, A. (2018). Human hippocampal neurogenesis drops sharply in children to undetectable levels in adults. Nature, 555(7696), 377–381. https://doi.org/10.1038/nature25975

Squire, L. R. (1992). Memory and the hippocampus: A synthesis from findings with rats, monkeys, and humans. Psychological Review, 99(2), 195–231. https://doi.org/10.1037/0033-295X.99.2.195

Van Praag, H., Shubert, T., Zhao, C., & Gage, F. H. (2005). Exercise enhances learning and hippocampal neurogenesis in aged mice. Journal of Neuroscience, 25 (38), 8680-8685.

Videbech, P., & Ravnkilde, B. (2004). Hippocampal volume and depression: a meta-analysis of MRI studies. American Journal of Psychiatry, 161 (11), 1957-1966.

Weis, S., Llenos, I. C., Sabunciyan, S., Dulay, J. R., Isler, L., Yolken, R., & Perron, H. (2007). Reduced expression of human endogenous retrovirus (HERV)-W GAG protein in the cingulate gyrus and hippocampus in schizophrenia, bipolar disorder, and depression. Journal of neural transmission, 114 (5), 645-655.

Woollett, K., & Maguire, E. A. (2011). Acquiring “the Knowledge” of London’s layout drives structural brain changes. Current Biology, 21(24), 2109–2114. https://doi.org/10.1016/j.cub.2011.11.018

Saul McLeod, PhD

BSc (Hons) Psychology, MRes, PhD, University of Manchester

Chartered Psychologist (CPsychol)

Saul McLeod, PhD, is a qualified psychology teacher with over 18 years of experience in further and higher education. He has been published in peer-reviewed journals, including the Journal of Clinical Psychology.


Olivia Guy-Evans, MSc

Associate Editor for Simply Psychology

BSc (Hons) Psychology, MSc Psychology of Education

Olivia Guy-Evans is a writer and associate editor for Simply Psychology, where she contributes accessible content on psychological topics. She is also an autistic PhD student at the University of Birmingham, researching autistic camouflaging in higher education.