METABOTROPIC GLUTAMATE RECEPTORS SWITCH VISUAL RESPONSE-MODE OF LATERAL GENICULATE-NUCLEUS CELLS FROM BURST TO TONIC

1. Metabotropic glutamate receptors (mGluRs) on relay cells of the lat eral geniculate nucleus appear to be activated exclusively by cortical inputs. We thus sought to manipulate these receptors in an effort to gain insight into the possible role of the corticogeniculate pathway. We used in vivo recording and pharmacological techniques in cats to ac tivate or inactivate these receptors on geniculate neurons while analy zing their response properties. 2. Iontophoretic application of the mG luR agonist 1-amino-cyclopentane-1,3-dicarboxylic acid (ACPD) to X and Y cells in the geniculate A laminae diminished or abolished burst act ivity characteristic of low-threshold Ca2+ spikes. This was accompanie d by pronounced changes in the visual response, including a decrease i n signal detectability as measured with receiver operating characteris tic curves. 3. ACPD effects appear specific to mGluRs, because a speci fic antagonist of ionotropic glutamate receptors (iGluRs) failed to af fect the ACPD-evoked responses, and antagonists of ACPD failed to affe ct iGluR-mediated responses. We found that 3,5-dihydroxyphenylglycine, an agonist reported to be specific for phosphatidylinositol (PI)-link ed mGluRs, had effects similar to those of ACPD, implying that these e ffects are mediated by PI-coupled mGluRs. Furthermore, antagonists rep orted to be effective against PI-linked mGluRs were effective in antag onizing the ACPD-mediated effects, and substances reported to be agoni sts to mGluRs coupled to the adenosine 3',5'-cyclic monophosphate casc ade did not affect neuronal responses on their own. These data, when a dded to our preliminary anatomic data, indicate that the receptor resp onsible for the observed effects may be mGluR1, or a functionally equi valent mGluR. 4. Activation of mGluRs produces changes in geniculate r elay cell activity consistent with depolarization of these cells seen during in vitro studies. Such membrane depolarization has been shown t o control the activation state of a voltage-dependent Ca2+ conductance . and this, in turn, determines whether the relay cell fires in tonic or burst mode. Our data show that application of ACPD produces a shift in response mode from burst to tonic. Because response mode is an imp ortant characteristic of the geniculate relay and because the activati on state of certain mGluRs, which helps determine response mode, may b e controlled by corticogeniculate input, we conclude that an important function of this input is to provide a visuotopically discrete transi tion from burst to tonic response mode.