sinusoidal function Search Results


sinusoidal function  (GraphPad Software Inc)
90
GraphPad Software Inc sinusoidal function
A, perievent raster of SCN multi‐unit responses to electrical stimulation of the OC; synchronous with (left), or 250 ms after (right), optogenetic activation of GABAergic GHT projection neurons (for recording set‐up, see Fig. 5 F). B, normalized mean ± SEM OC‐driven responses of SCN subpopulations as a function of GHT pre‐stimulation latency: at most recording sites (n = 45/71 OC‐responsive sites from three slices; for classification details, see Methods), GHT pre‐stimulation evoked long‐lasting suppression of OC‐driven responses (two‐way RM ANOVA: GHT pre‐stimulation, Group and interaction, all P < 0.001; asterisks indicate significance differences between groups in Sidak's post hoc tests). C, GHT‐driven inhibition of OC‐evoked responses was significantly greater ipsilateral to the optogenetically stimulated LGN (n = 22 vs. n = 23 contralateral sites; t test, P < 0.05). D, perievent histograms of SCN responses (perievent rasters are depicted in A) showing enhanced OC‐driven responses during the late day/early projected evening. E, normalized mean ± SEM response of GHT‐responsive sites (n = 45) to OC‐stimulation: synchronous with (), or subsequent to (), optical activation of GABAergic GHT projection neurons. In both cases, an F test indicated a significantly better fit to a <t>sinusoidal</t> (24 h) vs. linear function (both P < 0.001 where a linear process generated the data). F, GHT‐driven inhibition of OC‐evoked responses (data from E, expressed as a percentage of the response observed under synchronous stimulation) varies significantly across the 24 h in vitro recording period (one‐way RM ANOVA of 6 h binned data; P < 0.001; asterisks indicate significance differences between timepoints in Tukey's post‐hoc tests). G, perievent raster of IGL/vLGN multi‐unit responses to OC and optical stimulation (as in Fig. ​Fig.55 C). H, normalized mean ± SEM IGL/vLGN population activity (n = 34 responding sites from three slices) under basal conditions (top), following direct ChR2 (middle) or OC stimulation (bottom). In none of the above cases did we observe evidence of pronounced day‐night variation (F test, all P = 0.999; which were more probably generated by a linear vs. sinusoidal model). Shaded areas in (A) and (E–H) represent projected night. In (B) and (F): * P < 0.05, ** P < 0.01 and *** P < 0.001, respectively.
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analytic sinusoidal function  (Respiratory Motion)
90
Respiratory Motion analytic sinusoidal function
A, perievent raster of SCN multi‐unit responses to electrical stimulation of the OC; synchronous with (left), or 250 ms after (right), optogenetic activation of GABAergic GHT projection neurons (for recording set‐up, see Fig. 5 F). B, normalized mean ± SEM OC‐driven responses of SCN subpopulations as a function of GHT pre‐stimulation latency: at most recording sites (n = 45/71 OC‐responsive sites from three slices; for classification details, see Methods), GHT pre‐stimulation evoked long‐lasting suppression of OC‐driven responses (two‐way RM ANOVA: GHT pre‐stimulation, Group and interaction, all P < 0.001; asterisks indicate significance differences between groups in Sidak's post hoc tests). C, GHT‐driven inhibition of OC‐evoked responses was significantly greater ipsilateral to the optogenetically stimulated LGN (n = 22 vs. n = 23 contralateral sites; t test, P < 0.05). D, perievent histograms of SCN responses (perievent rasters are depicted in A) showing enhanced OC‐driven responses during the late day/early projected evening. E, normalized mean ± SEM response of GHT‐responsive sites (n = 45) to OC‐stimulation: synchronous with (), or subsequent to (), optical activation of GABAergic GHT projection neurons. In both cases, an F test indicated a significantly better fit to a <t>sinusoidal</t> (24 h) vs. linear function (both P < 0.001 where a linear process generated the data). F, GHT‐driven inhibition of OC‐evoked responses (data from E, expressed as a percentage of the response observed under synchronous stimulation) varies significantly across the 24 h in vitro recording period (one‐way RM ANOVA of 6 h binned data; P < 0.001; asterisks indicate significance differences between timepoints in Tukey's post‐hoc tests). G, perievent raster of IGL/vLGN multi‐unit responses to OC and optical stimulation (as in Fig. ​Fig.55 C). H, normalized mean ± SEM IGL/vLGN population activity (n = 34 responding sites from three slices) under basal conditions (top), following direct ChR2 (middle) or OC stimulation (bottom). In none of the above cases did we observe evidence of pronounced day‐night variation (F test, all P = 0.999; which were more probably generated by a linear vs. sinusoidal model). Shaded areas in (A) and (E–H) represent projected night. In (B) and (F): * P < 0.05, ** P < 0.01 and *** P < 0.001, respectively.
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sinusoidal function (with 24h periodicity) or a first order polynomial  (GraphPad Software Inc)
90
GraphPad Software Inc sinusoidal function (with 24h periodicity) or a first order polynomial
A, perievent raster of SCN multi‐unit responses to electrical stimulation of the OC; synchronous with (left), or 250 ms after (right), optogenetic activation of GABAergic GHT projection neurons (for recording set‐up, see Fig. 5 F). B, normalized mean ± SEM OC‐driven responses of SCN subpopulations as a function of GHT pre‐stimulation latency: at most recording sites (n = 45/71 OC‐responsive sites from three slices; for classification details, see Methods), GHT pre‐stimulation evoked long‐lasting suppression of OC‐driven responses (two‐way RM ANOVA: GHT pre‐stimulation, Group and interaction, all P < 0.001; asterisks indicate significance differences between groups in Sidak's post hoc tests). C, GHT‐driven inhibition of OC‐evoked responses was significantly greater ipsilateral to the optogenetically stimulated LGN (n = 22 vs. n = 23 contralateral sites; t test, P < 0.05). D, perievent histograms of SCN responses (perievent rasters are depicted in A) showing enhanced OC‐driven responses during the late day/early projected evening. E, normalized mean ± SEM response of GHT‐responsive sites (n = 45) to OC‐stimulation: synchronous with (), or subsequent to (), optical activation of GABAergic GHT projection neurons. In both cases, an F test indicated a significantly better fit to a <t>sinusoidal</t> (24 h) vs. linear function (both P < 0.001 where a linear process generated the data). F, GHT‐driven inhibition of OC‐evoked responses (data from E, expressed as a percentage of the response observed under synchronous stimulation) varies significantly across the 24 h in vitro recording period (one‐way RM ANOVA of 6 h binned data; P < 0.001; asterisks indicate significance differences between timepoints in Tukey's post‐hoc tests). G, perievent raster of IGL/vLGN multi‐unit responses to OC and optical stimulation (as in Fig. ​Fig.55 C). H, normalized mean ± SEM IGL/vLGN population activity (n = 34 responding sites from three slices) under basal conditions (top), following direct ChR2 (middle) or OC stimulation (bottom). In none of the above cases did we observe evidence of pronounced day‐night variation (F test, all P = 0.999; which were more probably generated by a linear vs. sinusoidal model). Shaded areas in (A) and (E–H) represent projected night. In (B) and (F): * P < 0.05, ** P < 0.01 and *** P < 0.001, respectively.
Sinusoidal Function (With 24h Periodicity) Or A First Order Polynomial, supplied by GraphPad Software Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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sinusoid function generator  (Tektronix inc)
90
Tektronix inc sinusoid function generator
A, perievent raster of SCN multi‐unit responses to electrical stimulation of the OC; synchronous with (left), or 250 ms after (right), optogenetic activation of GABAergic GHT projection neurons (for recording set‐up, see Fig. 5 F). B, normalized mean ± SEM OC‐driven responses of SCN subpopulations as a function of GHT pre‐stimulation latency: at most recording sites (n = 45/71 OC‐responsive sites from three slices; for classification details, see Methods), GHT pre‐stimulation evoked long‐lasting suppression of OC‐driven responses (two‐way RM ANOVA: GHT pre‐stimulation, Group and interaction, all P < 0.001; asterisks indicate significance differences between groups in Sidak's post hoc tests). C, GHT‐driven inhibition of OC‐evoked responses was significantly greater ipsilateral to the optogenetically stimulated LGN (n = 22 vs. n = 23 contralateral sites; t test, P < 0.05). D, perievent histograms of SCN responses (perievent rasters are depicted in A) showing enhanced OC‐driven responses during the late day/early projected evening. E, normalized mean ± SEM response of GHT‐responsive sites (n = 45) to OC‐stimulation: synchronous with (), or subsequent to (), optical activation of GABAergic GHT projection neurons. In both cases, an F test indicated a significantly better fit to a <t>sinusoidal</t> (24 h) vs. linear function (both P < 0.001 where a linear process generated the data). F, GHT‐driven inhibition of OC‐evoked responses (data from E, expressed as a percentage of the response observed under synchronous stimulation) varies significantly across the 24 h in vitro recording period (one‐way RM ANOVA of 6 h binned data; P < 0.001; asterisks indicate significance differences between timepoints in Tukey's post‐hoc tests). G, perievent raster of IGL/vLGN multi‐unit responses to OC and optical stimulation (as in Fig. ​Fig.55 C). H, normalized mean ± SEM IGL/vLGN population activity (n = 34 responding sites from three slices) under basal conditions (top), following direct ChR2 (middle) or OC stimulation (bottom). In none of the above cases did we observe evidence of pronounced day‐night variation (F test, all P = 0.999; which were more probably generated by a linear vs. sinusoidal model). Shaded areas in (A) and (E–H) represent projected night. In (B) and (F): * P < 0.05, ** P < 0.01 and *** P < 0.001, respectively.
Sinusoid Function Generator, supplied by Tektronix inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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forcing function of sinusoidal form  (Nonlinear Dynamics)
90
Nonlinear Dynamics forcing function of sinusoidal form
A, perievent raster of SCN multi‐unit responses to electrical stimulation of the OC; synchronous with (left), or 250 ms after (right), optogenetic activation of GABAergic GHT projection neurons (for recording set‐up, see Fig. 5 F). B, normalized mean ± SEM OC‐driven responses of SCN subpopulations as a function of GHT pre‐stimulation latency: at most recording sites (n = 45/71 OC‐responsive sites from three slices; for classification details, see Methods), GHT pre‐stimulation evoked long‐lasting suppression of OC‐driven responses (two‐way RM ANOVA: GHT pre‐stimulation, Group and interaction, all P < 0.001; asterisks indicate significance differences between groups in Sidak's post hoc tests). C, GHT‐driven inhibition of OC‐evoked responses was significantly greater ipsilateral to the optogenetically stimulated LGN (n = 22 vs. n = 23 contralateral sites; t test, P < 0.05). D, perievent histograms of SCN responses (perievent rasters are depicted in A) showing enhanced OC‐driven responses during the late day/early projected evening. E, normalized mean ± SEM response of GHT‐responsive sites (n = 45) to OC‐stimulation: synchronous with (), or subsequent to (), optical activation of GABAergic GHT projection neurons. In both cases, an F test indicated a significantly better fit to a <t>sinusoidal</t> (24 h) vs. linear function (both P < 0.001 where a linear process generated the data). F, GHT‐driven inhibition of OC‐evoked responses (data from E, expressed as a percentage of the response observed under synchronous stimulation) varies significantly across the 24 h in vitro recording period (one‐way RM ANOVA of 6 h binned data; P < 0.001; asterisks indicate significance differences between timepoints in Tukey's post‐hoc tests). G, perievent raster of IGL/vLGN multi‐unit responses to OC and optical stimulation (as in Fig. ​Fig.55 C). H, normalized mean ± SEM IGL/vLGN population activity (n = 34 responding sites from three slices) under basal conditions (top), following direct ChR2 (middle) or OC stimulation (bottom). In none of the above cases did we observe evidence of pronounced day‐night variation (F test, all P = 0.999; which were more probably generated by a linear vs. sinusoidal model). Shaded areas in (A) and (E–H) represent projected night. In (B) and (F): * P < 0.05, ** P < 0.01 and *** P < 0.001, respectively.
Forcing Function Of Sinusoidal Form, supplied by Nonlinear Dynamics, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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sinusoidal functions  (National Research Council Canada)
90
National Research Council Canada sinusoidal functions
A, perievent raster of SCN multi‐unit responses to electrical stimulation of the OC; synchronous with (left), or 250 ms after (right), optogenetic activation of GABAergic GHT projection neurons (for recording set‐up, see Fig. 5 F). B, normalized mean ± SEM OC‐driven responses of SCN subpopulations as a function of GHT pre‐stimulation latency: at most recording sites (n = 45/71 OC‐responsive sites from three slices; for classification details, see Methods), GHT pre‐stimulation evoked long‐lasting suppression of OC‐driven responses (two‐way RM ANOVA: GHT pre‐stimulation, Group and interaction, all P < 0.001; asterisks indicate significance differences between groups in Sidak's post hoc tests). C, GHT‐driven inhibition of OC‐evoked responses was significantly greater ipsilateral to the optogenetically stimulated LGN (n = 22 vs. n = 23 contralateral sites; t test, P < 0.05). D, perievent histograms of SCN responses (perievent rasters are depicted in A) showing enhanced OC‐driven responses during the late day/early projected evening. E, normalized mean ± SEM response of GHT‐responsive sites (n = 45) to OC‐stimulation: synchronous with (), or subsequent to (), optical activation of GABAergic GHT projection neurons. In both cases, an F test indicated a significantly better fit to a <t>sinusoidal</t> (24 h) vs. linear function (both P < 0.001 where a linear process generated the data). F, GHT‐driven inhibition of OC‐evoked responses (data from E, expressed as a percentage of the response observed under synchronous stimulation) varies significantly across the 24 h in vitro recording period (one‐way RM ANOVA of 6 h binned data; P < 0.001; asterisks indicate significance differences between timepoints in Tukey's post‐hoc tests). G, perievent raster of IGL/vLGN multi‐unit responses to OC and optical stimulation (as in Fig. ​Fig.55 C). H, normalized mean ± SEM IGL/vLGN population activity (n = 34 responding sites from three slices) under basal conditions (top), following direct ChR2 (middle) or OC stimulation (bottom). In none of the above cases did we observe evidence of pronounced day‐night variation (F test, all P = 0.999; which were more probably generated by a linear vs. sinusoidal model). Shaded areas in (A) and (E–H) represent projected night. In (B) and (F): * P < 0.05, ** P < 0.01 and *** P < 0.001, respectively.
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Image Search Results


A, perievent raster of SCN multi‐unit responses to electrical stimulation of the OC; synchronous with (left), or 250 ms after (right), optogenetic activation of GABAergic GHT projection neurons (for recording set‐up, see Fig. 5 F). B, normalized mean ± SEM OC‐driven responses of SCN subpopulations as a function of GHT pre‐stimulation latency: at most recording sites (n = 45/71 OC‐responsive sites from three slices; for classification details, see Methods), GHT pre‐stimulation evoked long‐lasting suppression of OC‐driven responses (two‐way RM ANOVA: GHT pre‐stimulation, Group and interaction, all P < 0.001; asterisks indicate significance differences between groups in Sidak's post hoc tests). C, GHT‐driven inhibition of OC‐evoked responses was significantly greater ipsilateral to the optogenetically stimulated LGN (n = 22 vs. n = 23 contralateral sites; t test, P < 0.05). D, perievent histograms of SCN responses (perievent rasters are depicted in A) showing enhanced OC‐driven responses during the late day/early projected evening. E, normalized mean ± SEM response of GHT‐responsive sites (n = 45) to OC‐stimulation: synchronous with (), or subsequent to (), optical activation of GABAergic GHT projection neurons. In both cases, an F test indicated a significantly better fit to a sinusoidal (24 h) vs. linear function (both P < 0.001 where a linear process generated the data). F, GHT‐driven inhibition of OC‐evoked responses (data from E, expressed as a percentage of the response observed under synchronous stimulation) varies significantly across the 24 h in vitro recording period (one‐way RM ANOVA of 6 h binned data; P < 0.001; asterisks indicate significance differences between timepoints in Tukey's post‐hoc tests). G, perievent raster of IGL/vLGN multi‐unit responses to OC and optical stimulation (as in Fig. ​Fig.55 C). H, normalized mean ± SEM IGL/vLGN population activity (n = 34 responding sites from three slices) under basal conditions (top), following direct ChR2 (middle) or OC stimulation (bottom). In none of the above cases did we observe evidence of pronounced day‐night variation (F test, all P = 0.999; which were more probably generated by a linear vs. sinusoidal model). Shaded areas in (A) and (E–H) represent projected night. In (B) and (F): * P < 0.05, ** P < 0.01 and *** P < 0.001, respectively.

Journal: The Journal of Physiology

Article Title: Geniculohypothalamic GABAergic projections gate suprachiasmatic nucleus responses to retinal input

doi: 10.1113/JP273850

Figure Lengend Snippet: A, perievent raster of SCN multi‐unit responses to electrical stimulation of the OC; synchronous with (left), or 250 ms after (right), optogenetic activation of GABAergic GHT projection neurons (for recording set‐up, see Fig. 5 F). B, normalized mean ± SEM OC‐driven responses of SCN subpopulations as a function of GHT pre‐stimulation latency: at most recording sites (n = 45/71 OC‐responsive sites from three slices; for classification details, see Methods), GHT pre‐stimulation evoked long‐lasting suppression of OC‐driven responses (two‐way RM ANOVA: GHT pre‐stimulation, Group and interaction, all P < 0.001; asterisks indicate significance differences between groups in Sidak's post hoc tests). C, GHT‐driven inhibition of OC‐evoked responses was significantly greater ipsilateral to the optogenetically stimulated LGN (n = 22 vs. n = 23 contralateral sites; t test, P < 0.05). D, perievent histograms of SCN responses (perievent rasters are depicted in A) showing enhanced OC‐driven responses during the late day/early projected evening. E, normalized mean ± SEM response of GHT‐responsive sites (n = 45) to OC‐stimulation: synchronous with (), or subsequent to (), optical activation of GABAergic GHT projection neurons. In both cases, an F test indicated a significantly better fit to a sinusoidal (24 h) vs. linear function (both P < 0.001 where a linear process generated the data). F, GHT‐driven inhibition of OC‐evoked responses (data from E, expressed as a percentage of the response observed under synchronous stimulation) varies significantly across the 24 h in vitro recording period (one‐way RM ANOVA of 6 h binned data; P < 0.001; asterisks indicate significance differences between timepoints in Tukey's post‐hoc tests). G, perievent raster of IGL/vLGN multi‐unit responses to OC and optical stimulation (as in Fig. ​Fig.55 C). H, normalized mean ± SEM IGL/vLGN population activity (n = 34 responding sites from three slices) under basal conditions (top), following direct ChR2 (middle) or OC stimulation (bottom). In none of the above cases did we observe evidence of pronounced day‐night variation (F test, all P = 0.999; which were more probably generated by a linear vs. sinusoidal model). Shaded areas in (A) and (E–H) represent projected night. In (B) and (F): * P < 0.05, ** P < 0.01 and *** P < 0.001, respectively.

Article Snippet: We then tested whether the resulting normalized population datasets were better fit by a sinusoidal function (with 24 h periodicity) or a first‐order polynomial (via an F test; GraphPad).

Techniques: Activation Assay, Inhibition, Generated, In Vitro, Activity Assay