The authors particularly wish to express their thanks to Professor IX (). Hcbb, who provided germinal ideas for the research and who backed it with enthusiastic encouragement as well as laboratory facilities and funds. The authors are also grateful to Miss Joann Fcindcl, who performed the histological reconstructions reported here.

Behavioral reinforcement by stimulation of diencephalic structures is by now well established. Delgado, Roberts, and Miller ('54), after the work of Hess ('54), Gastaut et al. ( ' 5 2 ) , Kaada, ('51), and Masserman ('41, ' 4 2 ) , established negative reinforcement to diencephalic stimulation in the region of the ventral posterior thalamic nuclei. Work of our own (Olds and Milner, '54; Olds, '56, '60) has established positive reinforcement on stimulation in a system based in medial forebrain bundle regions of the lateral hypothalamus and also in the other brain regions tied together by the widely distributed medial forebrain bundle.Roberts ('58a, b), Brown and Cohen ('59), and Bower and Miller ('58) have indicated some regions where both approach and avoidance are evoked by stimulation of the same point. Brodie et al. ('60) have shown, to the contrary, that some points yielding positive reinforcement in medial forebrain bundle regions of the macaque could not be made to yield any escape or avoidance reactions at all. Lilly ('58) has reported a focal point near the anterior commissure of the macaque where approach was produced by very low stimulation levels, and a point much lower (near the optic chiasma) where escape was produced by very low stimulation levels. In the rat, we ('60) have found points in medial forebrain bundle regions where stimulation produced positive reinforcement only, points in dorsomedial tegmentum where stimulation produced negative reinforcement only, and points in between these two types, where stimulation produced both positive and negative reinforcement.Questions remain unanswered concerning the pervasiveness of the areas of pure positive reinforcement, of pure negative reinforcement, and of overlap. More specifically, the questions are concerned with which areas are involved in each phenomenon. The present study takes up these questions with respect to diencephalic centers and some bordering regions of midbrain and telencephalon in the rat. MATERIALS AND METHODS Subjects.One electrode pair was implanted in each of 123 male albino rats.(As explained later in the paper, only 96 of the pairs could be tested for both approach and avoidance behavior.) The electrodes were bipolar, twisted silver wires, 0.01 inch in diameter and insulated except for the cross section of the tips. The two tips were separated only by their insulation; since the distance between electrodes was only about 0.003 inches, the pair could be thought of as stimulating at a single point. Each pair was held in a plastic block screwed to the skull, permitting firm attachment of the light lead wires from the stimulator. The placement of the stimulating tips of the pairs was varied 1 mm from rat to rat in order to form a loose grid of diencephalon and related structures.A straight line passing from the primary skull marking, bregma, and through the anterior commissure and optic chiasma was used for reference. Points were denoted by ( 1 ) their anterior or posterior distance from this line, ( 2 ) their lateral distance...

Activation of protein kinase C (PKC) can mimic the biophysical effects of associative learning on neurons. Furthermore, classical conditioning of the rabbit nictitating membrane (a form of associative learning) produces translocation of PKC activity from the cytosolic to the membrane compartments of the CA1 region of the hippocampus. Evidence is provided here for a significant change in the amount and distribution of PKC within the CA1 cell field of the rabbit hippocampus that is specific to learning. This change is seen at 1 day after learning as focal increments of [3H]phorbol-12,13-dibutyrate binding to PKC in computer-generated images produced from coronal autoradiographs of rabbit brain. In addition, 3 days after learning, the autoradiographs suggest a redistribution of PKC within CA1 from the cell soma to the dendrites.

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