For the proportion of postsynaptic GluR1 immunoreactivity to drop from 60% to 20%, a large portion of the pre-synaptic axons would have to be noncortical and nonthalamic. That the proportion of spines targeted by the thalamus or cortex may be small is not an unreasonable assumption. Another, thoroughly analyzed, brain region such as layer 4 of cortex receives as little as 6% (Ahmed et al., 1994) and no more than 20% (White, 1986) of its excitatory synaptic input from the thalamus. The current PEG result would be expected, if the proportion of spines receiving thalamic or cortical axons is about a third of all spines in the LA, and only those spines postsynaptic to the thalamic-plus-cortical axons express GluR1. What might be the source of nonthalamic/noncortical afferents to spines of the LA? One possibility is the spiny, projecting neurons of the LA, which presumably form axon collaterals to innervate other spiny neurons in the LA. The proportion of LA spines targeted by other LA neurons is a measurement that has not yet been examined, nor has it been determined whether
