Preferential Potentiation of Weaker Inputs to Primary Visual Cortex by Activation of the Basal Forebrain in Urethane Anesthetized Rats

Abstract

The ability of the brain to store information and adapt to changes in the sensory environment stems from the capability of neurons to change their communication with other neurons (“synaptic plasticity”). However, the ability of synapses to change (e.g., strengthen) is profoundly influenced by various chemical signals released in the nervous system (neuromodulators). Such modulatory effects may be preferential for different types of synapses. For example, cortical acetylcholine (ACh) has been shown to result in a relative enhancement of thalamocortical over intracortical synapses. Here, I tested the hypothesis that field postsynaptic potentials (fPSPs) in the rat primary visual cortex (V1) evoked by single pulse stimulation of the lateral geniculate nucleus (LGN) can be potentiated when LGN stimulation is paired with short bursts of stimuli applied to the basal forebrain (BF), the major source of ACh released in the cortex. Stimulation of the ipsi- and contralateral LGN elicited fPSPs in V1, with fPSPs triggered from the contralateral LGN exhibiting longer latencies and smaller amplitudes relative to fPSPs in ipsilateral projections. Stimulation bursts applied to the BF, paired with single, delayed LGN pulses, resulted in an enhancement of fPSP amplitude (~25%) for contralateral inputs at short (130 ms), but not longer (200-1000 ms) pairing intervals, while ipsilateral fPSPs failed to show significant potentiation over these intervals. The enhancement of the contralateral LGN-V1 fiber system induced by BF pairings was abolished by systemic or V1 application of the muscarinic receptor antagonist scopolamine, while systemic nicotinic receptor blockade was ineffective. These data suggest that there is a differential capacity for plasticity induction between strong, ipsilateral and weaker, contralateral fiber inputs to V1, with weaker inputs exhibiting greater synaptic enhancement following pairing with BF stimulation to elicit cortical ACh release. This preferential readiness for synaptic potentiation in normally weaker, non-dominant fiber inputs to V1 may facilitate the detection and integration of separate sensory signals originating in thalamic sensory nuclei.