These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Sex steroids modulate motor-correlated increases in cerebellar discharge.
    Author: Smith SS, Woodward DJ, Chapin JK.
    Journal: Brain Res; 1989 Jan 09; 476(2):307-16. PubMed ID: 2702471.
    Abstract:
    Adult female rats implanted with a microelectrode drive unit were trained to walk on a computer-controlled treadmill apparatus (10 s on every 20 s for 2 h) during recording of single Purkinje neurons in the paravermal area of the anterior cerebellum. Vigorous increases in the firing rate of individual units were found to be correlated with movement of specific limbs in particular stages of the step cycle during treadmill locomotion. Both spontaneous and motor-evoked discharge of individual Purkinje neurons were monitored before and after s.c. injection of either 17 beta estradiol (E2, 100 ng/kg) or progesterone (P, 50 micrograms). The percent increase in firing rate during locomotion versus rest was determined as a measure of the evoked:spontaneous discharge ratio. Drug-induced changes in this ratio indicate differential effects on the individual parameters, rather than simple excitatory or inhibitory effects. For all neurons tested, E2 augmented the movement-evoked discharge over pre-E2 control levels. The onset for this effect occurred at 15 min post-steroid, with a peak response noted at 30-35 min post-steroid. By 60-90 min, a partial recovery of the evoked:spontaneous ratio was noted, although absolute increases in both parameters were still observed, indicating long-term effects on neuronal activity. These effects were independent of the stage of the estrous cycle. In contrast, P decreased absolute firing rates of Purkinje cells during stationary and locomotor phases. However, the evoked:spontaneous ratio was decreased to an even greater degree. The latency for this effect was 9-12 min, with recovery to control levels of response seen at 30 min post-steroid. This response was typical of cells tested on estrus and diestrus 1. Cells tested on proestrus or diestrus 2, when E2 levels are increasing, were not modulated by P using the above paradigm.
    [Abstract] [Full Text] [Related] [New Search]