Abstract
The rodent primary visual cortex (V1) is densely innervated by serotonergic axons and previous in vitro work has shown that serotonin (5-HT) can modulate plasticity (e.g., long-term potentiation (LTP)) at V1 synapses. However, little work has examined the effects of 5-HT on LTP under in vivo conditions. We examined the role of 5-HT on LTP in V1 elicited by theta burst stimulation (TBS) of the lateral geniculate nucleus in urethane-anesthetized (adult and juvenile) rats. Thalamic TBS consistently induced potentiation of field postsynaptic potentials (fPSPs) recorded in V1. While 5-HT application (0.1–10 mM) itself did not alter LTP levels, the broad-acting 5-HT receptor antagonists methiothepin (1 mM) resulted in a clear facilitation of LTP in adult animals, an effect that was mimicked by the selective 5-HT1A receptor antagonist WAY 100635 (1 mM). Interestingly, in juvenile rats, WAY 100635 application inhibited LTP, indicative of an age-dependent switch in the role of 5-HT1A receptors in gating V1 plasticity. Analyses of spontaneous electrocorticographic (ECoG) activity in V1 indicated that the antagonist-induced LTP enhancement was not related to systematic changes in oscillatory activity in V1. Together, these data suggest a facilitating role of 5-HT1A receptor activation on LTP in the juvenile V1, which switches to a tonic, inhibitory influence in adulthood.
Highlights
Long-term potentiation (LTP), a form of brain plasticity characterized by a long-lasting increase in synaptic coupling of neurons, has been suggested as a candidate mechanism mediating processes of learning and memory in the nervous system [1, 2]
Characteristics of field postsynaptic potentials (fPSPs) in V1 Elicited by lateral geniculate nucleus (LGN) Stimulation
In agreement with previous work using this experimental preparation [14, 15, 18], fPSPs were composed mainly of a large amplitude, negative component, with a latency to peak of 16–18 ms following LGN stimulation (Figure 1)
Summary
Long-term potentiation (LTP), a form of brain plasticity characterized by a long-lasting increase in synaptic coupling of neurons, has been suggested as a candidate mechanism mediating processes of learning and memory in the nervous system [1, 2]. V1 of adult rodents [13,14,15], indicative of some fundamental differences in the induction of LTP in V1 between in vivo and in vitro conditions. A similar, facilitating effect on LTP is seen with histamine application directly in V1 of rats in vivo [18], highlighting the importance of a variety of neuromodulators as gating mechanism for the induction of plasticity at cortical synapses [19,20,21]. The central serotonergic (5-hydroxytryptamine, 5-HT) system has been implicated in the modulation of cortical synaptic
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