Biology Reference
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memory storage (Runyan and Dash 2005), suggesting that short-term synaptic plasticity may
underlie these effects. This has been studied in rats in the radial maze, using the delayed non-
matching to place paradigm, a delayed spatial task. Connections between the hippocampus
and the PFC are known to be important for this task (Floresco et al. 1997; Seamans et al.
1998). Hippocampal inputs provide spatial information for executive function in this short-
term memory task over a 30 minute delay period, and are regulated by dopamine since
infusion of a D1 receptor antagonist into the prelimbic mPFC before the test phase impairs
performance in this task (Seamans et al. 1998). However infusion of lidocaine into the mPFC
in this task does not impair behavioural performance in a short-term spatial memory
paradigm, showing that the information for this task is not actively maintained in the mPFC
but instead stored in the hippocampus (Seamans et al. 1995; 1998).
In addition to playing a role in learning and utilising “rules”, in which the mPFC accesses
long-term memories stored in other brain regions for use with working memory to guide
actions, the mPFC is also important for conflict resolution in order to suppress habitual
responses. This is termed behavioural flexibility, and one example of this is extinction of fear
conditioning. Another is the delayed match to place task, which can be studied using an
adjusted Morris water maze test where the platform is moved following training and testing
(Runyan and Dash 2005). (The mPFC plays no role in spatial learning using a standard
Morris water maze (de Bruin et al. 1994; Compton et al. 1997).) In this delayed match to
place task, the mPFC has been shown to be important not just for working memory (lasting
up to 20 seconds) but for short-term memory that requires conflict resolution (lasting
minutes). This was shown to require activation of PKA because the short-term memory was
blocked by infusing a PKA inhibitor into the mPFC (Runyan and Dash 2005). In contrast
working memory is blocked by activation of PKA in the mPFC, showing distinct molecular
mechanisms underlying working memory and short-term memory in the mPFC (Taylor et al.
1999; Runyan and Dash 2005).
(iii) Consolidation of memories
In addition to the involvement of the mPFC in the consolidation of extinction of fear
memories (see above), the mPFC is also involved in the consolidation of other forms of
memory. Early evidence for the role of the mPFC in consolidation of memories was provided
by studies examining synaptic transmission at hippocampal-mPFC inputs, which showed a
delayed but sustained potentiation of this pathway following an associative learning task
(Doyere et al. 1993). Furthermore, expression of syntaxin-1B, a presynaptic protein that is a
marker for LTP, is also elevated in the mPFC following a spatial memory task (Davis et al.
1996).
The infralimbic and prelimbic mPFC are important in consolidation and reconsolidation
i.e. the stabilisation of long term memories once formed, of recognition memories (Akirav
and Maroun 2006). This function has been assessed using an object discrimination task,
which involves examining the spontaneous exploratory behaviour of a rat by measuring the
time spent exploring novel versus familiar objects. Rats usually spend more time exploring
novel objects, thus an impairment in memory formation is shown by rats exploring familiar
objects to the same extent as novel objects. Infusion of AP5 or a protein synthesis inhibitor
into the mPFC immediately following training impairs object recognition, as does infusion
