AXONAL SPROUTING OF CA1 PYRAMIDAL CELLS IN HYPEREXCITABLE HIPPOCAMPALSLICES OF KAINATE-TREATED RATS

CA1 pyramidal cells become hyperexcitable following hippocampal kainat e lesions. To examine if axonal sprouting contributes to this epilepti form activity, the local axonal arborization of CA1 pyramidal cells wa s examined after intracellular labelling with biocytin in hippocampal slices from control rats and in hyperexcitable slices obtained from ra ts treated with kainate (bilateral intracerebroventricular injections) 2-4 weeks previously. Biocytin-labelled cells with an axon that could be followed from the soma to the alveus were drawn and reconstructed with a camera lucida (15 cells from control slices and 14 cells from h yperexcitable slices). Local axonal arborizations were more extensive in cells of hyperexcitable slices. This increase in axon collaterals w as generally seen in the alveus and in stratum oriens, but changes wer e more prominent in the latter. In stratum oriens, cells from hyperexc itable slices showed a significant increase in mean total axon length (1035 versus 373 mu m in control), in mean number of branching points (6.50 versus 0.67 in control) and in mean number of segment orders per axon (3.07 versus 1.47 in control). Their first-order axon segments w ere similar in length to those of control cells (236 versus 338 mu m i n control), but with significantly more branching points (2.86 versus 0.53 in control). Their second-order axon segments were significantly longer (381 versus 63 mu m in control) and also showed more branching points (2.71 versus 0.13 in control). Their third- and fourth-order ax on segments were also longer and with more branching points. Under hig h-power light microscopic examination, biocytin-labelled axonal varico sities in cells of hyperexcitable slices were often seen in close appo sition with their own dendrites, presumably making synaptic contact (f ive of nine cells examined). No such appositions were seen in any of t he control cells (seven cells examined). These results indicate that, following kainate lesions, there is sprouting of local axon collateral s of CA1 pyramidal cells in stratum oriens and in the alveus. This loc al increase in axon collaterals may contribute to the epileptiform act ivity in the CA1 area by providing recurrent excitation via newly form ed synaptic, and perhaps even autaptic, contacts with pyramidal cell d endrites.