The hippocampus is a structure in vertebrate brain that plays important roles in the formation of new memories, and, when damaged, in the cause of memory disorders and epileptic seizures.

Keywords: synaptic plasticity; learning; epilepsy; memory; long‐term potentiation

Figure 1.

Anatomy and synaptic connections of the hippocampus. (a) Position of the human hippocampus in relationship to the cerebral cortex and major subcortical structures. (b) Layers within the dentate gyrus (DG), CA3 and CA1, are indicated. (c) Differences in the density of the potassium channel Kv1.4 immunoreactivity demarcate the borders between strata in each region. (Redrawn from Cooper ED et al (1998) The Journal of Neuroscience18: 965–974 with permission.) Bar for (c) is 250 μm. alv, alveas; so, stratum oriens; sp, stratum pyramidale; sr, stratum radiatum; slm, stratum lacunosum‐moleculate; sc, schaffer collateral pathway; pp, perforant pathway; ml, molecular layer; gcl, granule cell layer; pml, polymorphic layer; sl, stratum lucidum; mf, mossy fibre pathway.

Figure 2.

Key features of hippocampal long‐term potentiation (LTP) in CA1. (a) Hippocampal transverse slice, illustrating principal fields and excitatory synaptic connections. (b) Preparation. Two independent sets of afferent fibres converge on a common population of CA1 pyramidal cells. Stimulating electrodes (S1 and S2) are placed in stratum radiatum on either side of the recording electrode, which is placed in stratum pyramidale. (c) Induction. (1) Potential changes evoked by stimulation with S1 before (left) and after (right) induction of LTP. The first, sharp deflection (*) is the stimulation artefact; the second, smaller one is the fibre action potential volley (′); the third, largest and slowest deflection (:) is the excitatory postsynaptic potential (EPSP) Initial slope of EPSP evoked by stimulation at S1 and S2 is plotted versus time in panels (2) and (3). Arrows indicate episodes of tetanic stimulation at S1 and S2. After weak tetanic stimulation at S1, S1‐evoked EPSPs are transiently increased (no LTP), and S2‐evoked EPSPs are unchanged. Strong tetanic stimulation at S2 induces LTP of S2‐evoked but not S1‐evoked responses (‘input specificity’). Next, tetanic stimuli at S1 and S2 are delivered simultaneously, resulting in additional LTP of S2‐evoked responses. In addition, such coincident activation results in LTP of S1‐evoked responses (‘associativity’). Data adapted from Bliss and Collingridge (1993). pp, perforant pathway; mf, mossy fibre pathway; fim, fimbria.

Figure 3.

Place‐specific activity of rat hippocampal neurons. (a) Illustration showing the experimental apparatus. Before the experiment a specialized four‐channel electrode, termed a ′tetrode′ is placed stereotactically into the CA1 region of the hippocampus of an anesthetized rat. When a neuron located near the recording tetrode fires an action potential, a brief signal or ′spike′ is detected by one or more of the channels. The spike size of these extracellulary‐recorded spikes differs based on how close an individual cell is to each of the four parts of the electrode, allowing the activity of several cells to be monitored simultaneously. After recovery from surgery, the rat is placed on a triangular track and is allowed to run in a clockwise direction seeking food rewards located in the centre of each side of the triangle. (b) Firing activity of eight CA1 pyramidal cells recorded during free movement around a triangular track. Each coloured dot represents the rat’s location at the moment a spike was fired; different colours indicate spikes of each of eight distinct neurons recorded. Each of the cells fire preferentially when the rat passes through a particular, small region of the track – the cell’s ‘place field’. Unpublished data kindly provided by William Skaggs and Bruce L. McNaughton.


Further Reading

Alvarez P, Zola‐Morgan S and Squire LR (1995) Damage limited to the hippocampal region produces long‐lasting memory impairment in monkeys. Journal of Neuroscience 15: 3796–3807.

Amaral DG and Witter MP (1995) Hippocampal formation. In: Paxinos G (ed.) The Rat Nervous System, pp. 433–495. San Diego: Academic Press.

Bliss TVP and Collingridge GL (1993) A synaptic model of memory: long‐term potentiation in the hippocampus. Nature 361: 31–39.

Cobb SR, Buhl EH, Halasy K, Paulsen O and Somogyi P (1995) Synchronization of neuronal activity in hippocampus by individual GABAergic interneurons. Nature 378: 75–78.

Engel J Jr (1996) Introduction to temporal lobe epilepsy. Epilepsy Research 26: 141–150.

Milner B, Squire LR and Kandel ER (1998) Cognitive neuroscience and the study of memory. Neuron 20: 445–468.

Morris R, Garrud P, Rawlins J and O’Keefe J (1982) Place navigation impaired in rats with hippocampal lesions. Nature 297: 681–683.

Nicoll RA and Malenka RC (1995) Contrasting properties of two forms of long‐term potentiation in the hippocampus. Nature 377: 115–118.

Parent JM and Lowenstein DH (1997) Mossy fiber reorganization in the epileptic hippocampus. Current Opinion in Neurology 10: 103–109.

Scoville W and Milner B (1957) Loss of recent memory after bilateral hippocampal lesions. Journal of Neurology, Neurosurgery and Psychiatry 20: 11–21.

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Cooper, Edward C, and Lowenstein, Daniel H(Jul 2003) Hippocampus. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1038/npg.els.0000144]