schematically shows the major inputs to geniculate relay cells. In addition to the glutamatergic retinal input, there are local GABAergic inputs (from interneurons and cells of the thalamic reticular nucleus), feedback glutamatergic inputs from layer 6 of cortex, and inputs from various brainstem sites, these mostly being cholinergic inputs from the parabrachial region. For further details of these and other inputs, see [1
Figure 1 Schematic diagram of circuitry for the lateral geniculate nucleus. The inputs to relay cells are shown along with the relevant neurotransmitters and postsynaptic receptors (ionotropic and metabotropic) Abbreviations: ACh, acetylcholine; GABA, γ-aminobutyric (more ...)
These afferents all end on relay cell dendrites with conventional chemical synapses, meaning that their postsynaptic effects are dependent on postsynaptic receptors. These receptors come in two basic flavors: ionotropic and metabotropic. Ionotropic receptors include AMPA receptors for glutamate, GABAA
receptors, and nicotinic receptors for acetylcholine; the respective metabotropic receptors, are various metabotropic glutamate receptors, GABAB
receptors, and various muscarinic receptors. Ionotropic and metabotropic receptors differ along many parameters (for details, see [3
]), but one important to the present account is duration of effect: postsynaptic potentials from ionotropic receptors tend to be very brief, over within 10 or a few 10s of msec, whereas those from metabotropic receptors last 100s of msec to several sec.
shows that retinal input activates only ionotropic receptors, whereas all nonretinal inputs activate metabotropic receptors as well. This is good for information transfer of the retinal input, because the fast excitatory postsynaptic potentials can be matched one to one to retinal spikes, thereby maximizing information transfer for higher firing rates in the input. The advantage for nonretinal inputs may be the lengthy postsynaptic effects associated with metabotropic receptor activation. For example, this can have relatively long term effects on excitability of relay cells. Probably more germane is the fact that these relay cells, like cells throughout the central nervous system, have many voltage- and time-gated ion channels [5
], meaning that transmembrane ionic currents can flow when membrane potentials change sufficiently in amplitude and time. For instance, T-type Ca2+
channels determine the firing mode of relay cells—burst or tonic—and these have a time and voltage dependency well controlled by the combination of metabotropic receptors activated by nonretinal afferents to relay cells. That is, these T channels inactivate if held depolarized more positive than about −60 mV for ≥ 100 msec or so, but they de-inactivate if held more negative than about −70 mV for ≥100 msec or so, and once de-inactivated, they can be activated by a suitable depolarization, or EPSP. When these T channels become active, the relay cell responds in burst mode, and when they are inactive, the cell responds in tonic mode. These different response modes strongly affect the nature of information relayed [6
]. The point here is that the nonretinal inputs, by virtue of their activation of metabotropic receptors, can effectively control the activation of voltage- and time-gated ion channels.
Postsynaptic receptors are only one feature that distinguish retinal from nonretinal input. provides a more complete list of differences. From the pattern of differences, we have classified inputs to relay cells as driver or modulator. For the lateral geniculate nucleus, the driver input is the retinal input, and this represents the main information to be relayed. All the nonretinal inputs are modulators, and these serve to modulate retinogeniculate transmission. Other thalamic nuclei for which there is sufficient information have a similar classification of inputs to relay cells. For instance, the ventral posterior nucleus and the ventral portion of the medial geniculate nucleus have driver inputs from the medial lemniscus and inferior colliculus, respectively, and modulator inputs from most of the same sources as in .
Drivers and Modulators in LGN plus layer 5 Drivers
The important point to make here is that not all inputs to relay cells are equal, and they should not be treated as some sort of anatomical democracy. More to the point, if one can identify the driver input to a thalamic nucleus, one can at least gain insight into the source and type of information relayed by that nucleus. Identifying the driver inputs to certain thalamic nuclei, like most of the pulvinar, has also led to a division of thalamic relays into first order and higher order.