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Adenosine A 1 and A 2A receptors differently control synaptic plasticity in the mouse dorsal and ventral hippocampus
Author(s) -
Reis Sara L.,
Silva Henrique B.,
Almeida Margarida,
Cunha Rodrigo A.,
Simões Ana P.,
Canas Paula M.
Publication year - 2019
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/jnc.14816
Subject(s) - neuroscience , excitatory postsynaptic potential , hippocampus , synaptic plasticity , adenosine , long term potentiation , long term depression , stimulation , neurotransmission , postsynaptic potential , hippocampal formation , biology , chemistry , endocrinology , inhibitory postsynaptic potential , nmda receptor , ampa receptor , receptor , biochemistry
The hippocampus is a brain region involved in processing both memory and emotions, through a preferential involvement of the dorsal hippocampus (DH) and ventral hippocampus (VH), respectively. Adenosine A 1 and A 2A receptors (A 1 R and A 2A R) control both mood and memory, but it is not known if there is a different adenosine modulation of synaptic plasticity along the hippocampal axis. Using adult, C57BL/6 male mice, we show that both A 1 R and A 2A R were more abundant in DH compared with VH. However, recordings of field excitatory postsynaptic potentials at Schaffer collaterals‐CA1 pyramidal synapses revealed that A 1 R were equi‐effective to inhibit basal excitatory synaptic transmission in DH and VH, but endogenous A 1 R activation was more effective to depress the probability of release in VH. In contrast, the selective A 2A R antagonist (SCH58261, 50 nM) controlled both long‐term potentiation (induced by a high frequency stimulation protocol) and long‐term depression (induced by a low frequency stimulation protocol) selectively in DH rather than VH, whereas the selective A 1 R antagonist (DPCPX, 100 nM) revealed a similar tonic inhibition of long‐term depression in DH and VH. These findings show a different control of synaptic plasticity by the adenosine modulation system in the dorsal and ventral poles of the hippocampus, which may underlie a different efficiency of the adenosine system to control mood and memory.