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Inhibition of vasomotion in hippocampal cerebral arterioles during increases in neuronal activity
L A Brown1, B J Key, T A Lovick
1Department of Physiology, University of Birmingham, UK. l.a.brown@bham.ac.uk
Insights
Neuronal activity in the hippocampus reduces rhythmic contractions in small brain arteries. This suggests that decreased arterial vasomotion may contribute to increased blood flow during brain activity.
Area of Science:
- Neuroscience
- Vascular Biology
- Cerebral Blood Flow Regulation
Background:
- Small arterioles in the CA1 region of the hippocampus exhibit rhythmic contractile activity (vasomotion) when stimulated by the thromboxane A2 agonist U46619.
- Under resting conditions, these arterioles are quiescent.
Purpose of the Study:
- To investigate the effect of increased neuronal activity on the vasomotion of CA1 arterioles.
- To determine the role of neuronal signaling in regulating cerebral blood flow during synaptic activity.
Main Methods:
- In vitro electrophysiology and myography on rat hippocampal slices.
- Measurement of arteriolar vasomotion in response to U46619.
- Electrical stimulation of Schaffer collateral pathways to induce neuronal activity.
- Pharmacological blockade of action potentials using tetrodotoxin (TTX).
Main Results:
- Electrical stimulation of Schaffer collaterals significantly reduced or abolished arteriolar vasomotion.
- The reduction in vasomotion was observed in all tested vessels (8/8).
- In the presence of TTX, neuronal activity-induced inhibition of vasomotion was blocked, indicating a role for neuronal signaling.
Conclusions:
- Increased neuronal activity in the hippocampus leads to a reduction in the contractile activity of CA1 arterioles.
- This reduction in vasomotion may be a mechanism contributing to exercise-induced hyperemia (increased blood flow) in the brain.
- Neuronal signaling, independent of action potential generation in smooth muscle cells, mediates this effect.
Abstract:
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.
