Inhibition of vasomotion in hippocampal cerebral arterioles during increases in neuronal activity.
The activity of small arterioles, internal diameter 9.9 +/- 0.8 microm (SEM), was investigated in the CA1 region of hippocampal slices maintained in vitro at 34 degrees C. Under resting conditions, the vessels were quiescent. However, in the presence of the thromboxane A2 agonist U46619 (75-100 nM),...
| Main Authors: | , , |
|---|---|
| Format: | Journal article |
| Language: | English |
| Published: |
2002
|
| _version_ | 1797079398655983616 |
|---|---|
| author | Brown, L Key, B Lovick, T |
| author_facet | Brown, L Key, B Lovick, T |
| author_sort | Brown, L |
| collection | OXFORD |
| description | The activity of small arterioles, internal diameter 9.9 +/- 0.8 microm (SEM), was investigated in the CA1 region of hippocampal slices maintained in vitro at 34 degrees C. Under resting conditions, the vessels were quiescent. However, in the presence of the thromboxane A2 agonist U46619 (75-100 nM), rhythmic contractile activity (vasomotion, 1.1-9.9 min(-1), mean 4.1 +/- 0.7 min(-1) SEM) developed in the smooth muscle cells of the vessel walls. Electrical stimulation of the Schaffer collateral fibre pathway was used to evoke increases in neuronal activity in CA1 in the vicinity of the vessels under investigation. A 3-min period of electrical stimulation of the Schaffer collateral fibre pathway produced a significant reduction in vasomotion in 8/8 vessels. During stimulation, vasomotion either ceased completely (n = 5) or the frequency decreased from 7.1, 3.3 and 3.2 min(-1) to 1.2, 0.4 and 0.6 min(-1), respectively (n = 3). In addition, the amplitude of the residual contractions was reduced by 66%, 12% and 52%. In the presence of 1 microM tetrodotoxin (TTX) (n = 4) to block the generation of action potentials, vasomotion was still present. However, the inhibition of vasomotion evoked by increased neuronal activity was blocked concomitant with the abolition of the field potentials recorded in CA1 in response to the stimulation of the Schaffer collaterals. These findings suggest that a reduction in vasomotion may contribute to the local hyperaemia, which accompanies increases in synaptic activity in the brain. |
| first_indexed | 2024-03-07T00:45:20Z |
| format | Journal article |
| id | oxford-uuid:847405ba-956e-43b3-884c-2cfa6782b0d1 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-07T00:45:20Z |
| publishDate | 2002 |
| record_format | dspace |
| spelling | oxford-uuid:847405ba-956e-43b3-884c-2cfa6782b0d12022-03-26T21:51:08ZInhibition of vasomotion in hippocampal cerebral arterioles during increases in neuronal activity.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:847405ba-956e-43b3-884c-2cfa6782b0d1EnglishSymplectic Elements at Oxford2002Brown, LKey, BLovick, TThe activity of small arterioles, internal diameter 9.9 +/- 0.8 microm (SEM), was investigated in the CA1 region of hippocampal slices maintained in vitro at 34 degrees C. Under resting conditions, the vessels were quiescent. However, in the presence of the thromboxane A2 agonist U46619 (75-100 nM), rhythmic contractile activity (vasomotion, 1.1-9.9 min(-1), mean 4.1 +/- 0.7 min(-1) SEM) developed in the smooth muscle cells of the vessel walls. Electrical stimulation of the Schaffer collateral fibre pathway was used to evoke increases in neuronal activity in CA1 in the vicinity of the vessels under investigation. A 3-min period of electrical stimulation of the Schaffer collateral fibre pathway produced a significant reduction in vasomotion in 8/8 vessels. During stimulation, vasomotion either ceased completely (n = 5) or the frequency decreased from 7.1, 3.3 and 3.2 min(-1) to 1.2, 0.4 and 0.6 min(-1), respectively (n = 3). In addition, the amplitude of the residual contractions was reduced by 66%, 12% and 52%. In the presence of 1 microM tetrodotoxin (TTX) (n = 4) to block the generation of action potentials, vasomotion was still present. However, the inhibition of vasomotion evoked by increased neuronal activity was blocked concomitant with the abolition of the field potentials recorded in CA1 in response to the stimulation of the Schaffer collaterals. These findings suggest that a reduction in vasomotion may contribute to the local hyperaemia, which accompanies increases in synaptic activity in the brain. |
| spellingShingle | Brown, L Key, B Lovick, T Inhibition of vasomotion in hippocampal cerebral arterioles during increases in neuronal activity. |
| title | Inhibition of vasomotion in hippocampal cerebral arterioles during increases in neuronal activity. |
| title_full | Inhibition of vasomotion in hippocampal cerebral arterioles during increases in neuronal activity. |
| title_fullStr | Inhibition of vasomotion in hippocampal cerebral arterioles during increases in neuronal activity. |
| title_full_unstemmed | Inhibition of vasomotion in hippocampal cerebral arterioles during increases in neuronal activity. |
| title_short | Inhibition of vasomotion in hippocampal cerebral arterioles during increases in neuronal activity. |
| title_sort | inhibition of vasomotion in hippocampal cerebral arterioles during increases in neuronal activity |
| work_keys_str_mv | AT brownl inhibitionofvasomotioninhippocampalcerebralarteriolesduringincreasesinneuronalactivity AT keyb inhibitionofvasomotioninhippocampalcerebralarteriolesduringincreasesinneuronalactivity AT lovickt inhibitionofvasomotioninhippocampalcerebralarteriolesduringincreasesinneuronalactivity |