A CEREBELLAR LONG-TERM DEPRESSION UPDATE - RESPONSE

Two major themes have emerged in the commentaries elicited by the targ et articles that concern cerebellar long-term depression (LTD) (CREPEL , VINCENT, and LINDEN). First, is a lively debate concerning the poten tial role of a nitric oxide/cGMP cascade in cerebellar LTD induction. Second is a much broader issue relating to the interchange of informat ion between cerebellar physiologists concerned with mechanisms at a ce llular and synaptic level and those working at the level of systems ph ysiology, behavior, or modeling. What contributions can cellular physi ologists make to the study of motor learning? Cellular physiologists c an provide testable hypotheses to help determine if these synaptic phe nomena do underlie particular behaviors (e.g., if cerebellar LTD under lies vestibulo-ocular reflex [VOR] adaptation or eyeblink conditioning , then blockade of cerebellar LTD via, say, mGluR1 inhibition, should interfere with these forms of motor learning). In addition, we can pro vide descriptive parametric information about basal synaptic function and use-dependent synaptic modifications that can constrain the range of models proposed to underlie a given behavior (e.g., are the timing constraints on LTD induction consistent with VOR adaptation or eyeblin k conditioning?)