HIPPOCAMPUS

SAHALA AFSUL SALEEM

2ND M Sc CLINICAL
PSYCHOLOGY
HIPPOCAMPUS

The hippocampus is an elongated structure located within the

inferior medial wall of the temporal lobe (posterior to the
amygdala); it surrounds, in part, the lateral ventricle. In
humans, the hippocampus consists of an anterior and posterior
region and is shaped somewhat like a telephone receiver.

There are three major neural pathways leading to and from the
hippocampus. These include the fornix-fimbrial fiber system, a
supracallosal pathway (i.e., the indusium griseum), which
passes through the cingulate, and through the entorhinal area,
sometimes referred to as the gateway to the hippocampus.
It is through the entorhinal area that the hippocampus
receives olfactory and amygdaloid projections (Carlsen
et aI., 1982; Gloor, 1955; Krettek & Price, 1976, Steward,
1977) and fibers from the orbital frontal and temporal
lobes (Van Hoesen et al., 1972). It is through the fornix
and fimbrial pathways that the hippocampus makes
major intercon nections with the thalamus, septal nuclei,
medial hypothalamus, and through which it exerts either
inhibitory or excitatory influences on these nuclei
(Feldman, Saphier, & Conforti, 1987; Guillary, 1957;
Poletti & Sujatanon, 1980).
Septal interactions: The hippocampus maintains a
particularly intimate relationship with the septal nuclei
(sometimes referred to as the septum-not to be confused
with the septum pelucidum). The septal nucleus partly
serves as in interactional relay center as it channels
hippocampal influences to other structures such as the
hypothalamus and reticular formation (and vice versa) and
as a major link through which the hippocampus and
amygdala sometimes interact (Hagino & Yamaoka, 1976).
Amygdala interactions: The hippocampus is greatly
influenced by the amygdala, which in turn monitors and
responds to hippocampal activity (Gloor, 1955; Green &
Adey, 1956; Steriade, 1964) .The amygdala also acts to relay
certain forms of information from the hippocampus to the
hypothalamus (Poletti & Sajatanon, 1980).Together the
hippocampus and amygdala complement and interact in
regard to attention, the generation of emotional and other
types of imagery, as well as learning and memory.
Aversion
the hippocampus appears to act in concert with the
medial hypothalamus and septal nuclei (with which it
maintains rich interconnections) so as to prevent
extremes in arousal and thus maintain a state of quiet
alertness (or quiescence). Moreover, as with the medial
hypothalamus, it has been reported that the subjective
components of aversive emotion in humans is correlated
with electrophysiological alternations in the
hippocampus and septal area (Heath, 1976).
Attention and Inhibition

The hippocampus participates in the elicitation of orienting

reactions and the mainte nance of an aroused state of attention
(Foreman & Stevens, 1987; Grastayan et al., 1959; Green &
Arduini, 1954; Routtenberg, 1968). When exposed to novel
stimuli or when engaged in active searching of the environment,
hippocampal theta appears (Adey et al., 1960). However, with
repeated presentations of a novel stimulus, the hippocampus
habit uates and theta disappears (Adey et al., 1960). Thus, as
information is attended to, recognized, and presumably learned
and/or stored in memory, hippocampal participation
diminishes. Theta also appears during the early stages
oflearning as well as when engaged in selective attention and
the making of discriminant responses (Grastyan et aI., 1959).
When the hippocampus is damaged or destroyed, animals have
great difficulty inhibiting behavioral responsiveness or shifting
attention. For example, Clark and Issac son (1965) found that
animals with hippocampal lesions could not learn to wait 20 sec
between bar presses, if first trained to respond to a continuous
schedule. There is an inability to switch from a continuous to a
discontinuous pattern, such that a marked degree of
perseveration and inability to change sets or inhibit a pattern of
behavior once initiated occurs (Douglas, 1967; Ellen, Wilson, &
Powell, 1964). Habituation is largely abolished, and the ability to
think or respond divergently is disrupted.
In part, this finding suggests that hippocampal damage
disrupts the ability to learn and thus remember-findings that
have been repeatedly demonstrated in humans. In animals,
disinhibition caused by hippocampal damage can even
prevent the learning of a passive-avoidance task, such as
simple ceasing to move (Kimura, 1958). When coupled with
the evidence presented above, it appears that the
hippocampus acts to enhance or diminish areas of neural
excitation selectively, which in tum allows for differential
selective attention and differential responding. When
damaged, the ability to shift from one set of perceptions to
another or to change behavioral patterns is disrupted, and
the organism becomes overwhelmed by a particular mode of
input.
Learning and Memory

The hippocampus is most usually associated with learning

and memory encoding (e.g., long-term storage and retrieval
of newly learned information), particularly the anterior
regions (Fedio & Van Buren, 1974; Milner, 1966; 1970;
Penfield & Milner, 1958; Rawlins, 1985; Scoville & Milner,
1957). Many other brain areas, such as the mamillary
bodies and dorsal-medial nucleus of the thalamus, are also
important in memory functioning.
Bilateral destruction of the anterior hippocampus results in
striking and profound disturbances involving memory and new
learning (i.e., anterograde amnesia). For example, one such patient
who underwent bilateral destruction of this nuclei (H.M.), was
subsequently found to have almost completely lost the ability to
recall anything experienced after surgery. Dr. Brenda Milner has
worked with H.M. for almost 20 years, and yet she is an utter
stranger to him. H.M. is in fact so amnesic for everything that has
occurred since his surgery (al though memory for events prior to
his surgery is comparatively exceedingly well pre served), that
every time he rediscovers that his favorite uncle died (years after
his surgery) he suffers the same grief as if he had just been
informed for the first time. Despite his lack of memory for new
(nonmotor) information, Henry (or H.M.), has adequate
intelligence, is painfully aware of his deficit, and constantly
apologizes for his problem.
The hippocampus acts to protect memory and the
encoding of new information during the storage and
consolidation phase via the gating of afferent streams of
information and the filtering/exclusion (or dampening)
of irrelevant and interfering stimuli. When the
hippocampus is damaged, input overload results, the
neuroaxis is overwhelmed by neural noise, and the
consolidation phase of memory is disrupted such that
relevant information is not properly stored or even
attended to. Consequently, the ability to form
associations (e.g., between stimulus and response) or to
alter preexisting schemas (such as occurs during
learning) is attenuated (Douglas, 1967).
Hippocampal and Amygdaloid Interactions:
Memory
It has been argued that significant impairments involving
memory (in man) cannot be produced by lesions
restricted to the hippocampus (cf. Horel, 1978). Thus, in
some instances with restricted lesions, good recall of new
information is possible for at least several minutes
(Horel, 1978; Penfield & Milner, 1958). Rather, there is
evidence that strongly suggests that the hippocampus
plays an interdependent role with the amygdala in regard
to memory (Kesner & Andrus, 1982; Mishkin, 1978;
Sarter & Markowitsch, 1985).
Interestingly, nuclei such as the dorsal-medial region ofthe
thalamus, which have also been shown to be important in
memory (Squire & Moore, 1979), maintain rich
interconnections with the amygdala (Krettek & Price,
1977b; Nauta, 1971).
Nevertheless, although psychic blindness is produced by
damage to the amygdala, striking anterograde deficits in
recall do not seem to occur (Horel, 1978; Scoville & Milner,
1957). Rather, the role of the amygdala in memory and
learning seems to involve activities related to reward,
orientation, and attention, as well as emotional arousal
(Sarter & Markowitsch, 1985). If some event is associated
with positive or negative emotional states, it is more likely
to be learned and remembered .
The amygdala seems to reinforce and maintain
hippocampal activity through the identification of
motivationally significant information and the
generation of pleasurable rewards (through action on
the lateral hypothalamus). That is, reward increases
the probability of attention being paid to a particular
stimulus or consequence as a function of its
association with reinforcement (Douglas, 1967;
Kesner & Andrus, 1982).
However, the amygdala and hippocampus may act
differentially in regard to the effects of positive
versus negative reinforcement on learning and
memory. For example, whereas the hippocampus
produces theta in response to noxious stimuli, the
amygdala increases its activity following the
reception of a reward (Norton, 1970). Thus, if
errors are made during acquisition (negative
emotional state), possibly the hippocampus
modulates the appropriate reaction, whereas when
presented with a reward, the amygdala reinforces
the organism's response.
Thus, the hippocampus acts to reduce or enhance
extremes in arousal associated with information
reception and storage in memory, whereas the
amygdala acts to identify the social-emotional-
motivational characteristics of the stimuli as well as
to generate (in conjunction with the hippocampus)
appropriate emotional rewards to reinforce learning
and memory. We find that when both the amygdala
and hippocampus are damaged, striking and
profound disturbances in memory functioning result
(Kesner & Andrus, 1982; Mishkin, 1978).
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