Excitatory inputs to four types of spinocerebellar tract neurons in the cat and the rat thoraco-lumbar spinal cord.

The cerebellum receives information from the hindlimbs through several populations of spinocerebellar tract neurons. Although the role of these neurons has been established in electrophysiological experiments, the relative contribution of afferent fibres and central neurons to their excitatory input has only been estimated approximately so far. Taking advantage of differences in the immunohistochemistry of glutamatergic terminals of peripheral afferents and of central neurons (with vesicular glutamate transporters VGLUT1 or VGLUT2, respectively), we compared sources of excitatory input to four populations of spinocerebellar neurons in the thoraco-lumbar spinal cord: dorsal spinocerebellar tract neurons located in Clarke's column (ccDSCT) and in the dorsal horn (dhDSCT) and ventral spinocerebellar tract (VSCT) neurons including spinal border (SB) neurons. This was done on 22 electrophysiologically identified intracellularly labelled neurons in cats and on 80 neurons labelled by retrograde transport of cholera toxin b subunit injected into the cerebellum of rats. In both species distribution of antibodies against VGLUT1 and VGLUT2 on SB neurons (which have dominating inhibitory input from limb muscles), revealed very few VGLUT1 contacts and remarkably high numbers of VGLUT2 contacts. In VSCT neurons with excitatory afferent input, the number of VGLUT1 contacts was relatively high although VGLUT2 contacts likewise dominated, while the proportions of VGLUT1 and VGLUT2 immunoreactive terminals were the reverse on the two populations of DSCT neurons. These findings provide morphological evidence that SB neurons principally receive excitatory inputs from central neurons and provide the cerebellum with information regarding central neuronal activity.

Self-medication in Primary Dysmenorrhea among Undergraduate Students in a Medical College: A Descriptive Cross-sectional Study.

Introduction: Primary dysmenorrhea is painful menstruation in women with normal pelvic anatomy, usually beginning during adolescence, primarily associated with a normal ovulatory cycle. There is an increased likelihood of self-medication among medical students. The aim of this study is to find out the prevalence of self-medication in primary dysmenorrhea among undergraduate students in a medical college. Methods: A descriptive cross-sectional study was conducted in a medical college among undergraduate female students with primary dysmenorrhea from 1 February 2022 to 31 May 2022. Ethical approval was obtained from the Institutional Review Committee of the same institute (Reference number: 254/2021). Convenience sampling was done. Data were collected through a self-administered questionnaire. Point estimate and 95% Confidence Interval were calculated. Results: Among 213 students with primary dysmenorrhea, self-medication was found to be in 78 (36.62%) (30.15-43.09, 95% Confidence Interval)). Among all the self-medications used, mefenamic acid was most common, used by 45 (57.69%) students, followed by paracetamol 11 (14.10%). Conclusions: The prevalence of self-medication practice in primary dysmenorrhea among undergraduate students was lower when compared to similar studies done in similar settings. Keywords: dysmenorrhea; menstruation; prevalence; self medication.

Two-pore potassium ion channels are inhibited by both G(q/11)- and G(i)-coupled P2Y receptors.

Two-pore potassium (K(2P)) ion channels and P2Y receptors modulate the activity of neurones and are targets for the treatment of neuronal disorders. Here we have characterised their interaction. In cells coexpressing the Galpha(i)-coupled hP2Y(12) receptor, ADP and ATP significantly inhibited hK(2P)2.1 currents. This was abolished by pertussis toxin (PTX), the hP2Y(12) antagonist AR-C69931MX, the hP2Y(1) antagonist MRS2179 and by mutating potential PKA/PKC phosphorylation sites in the channel C terminal. In cells coexpressing the Galpha(q/11)-coupled hP2Y(1) receptor, ADP and ATP also inhibited hK(2P)2.1 currents, which were abolished by MRS2179, but unaffected by AR-C69931MX and PTX. When both receptors were coexpressed with K(2P)2.1 channels, ADP-induced inhibition was antagonised by AR-C69913MX and MRS2179, but not PTX. Thus, both Galpha(q/11)- and Galpha(i)-coupled P2Y receptors inhibit K(2P) channels and the action of hP2Y(12) receptors appears to involve co-activation of endogenous hP2Y(1) receptors. This represents a novel mechanism by which P2Y receptors may modulate neuronal activity.