The Effects of the GABA Agonist Muscimol upon Blood Flow in Different Vascular Territories of the Rat Cortex

Kelly, Paul A.; Faulkner, Amanda J.; Burrow, A.

doi:10.1038/jcbfm.1989.108

Cited by 11 publications

(4 citation statements)

References 19 publications

(8 reference statements)

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“…The interpretation of these data is difficult because brain regions influence one another. The data of Roland and Friberg are consistent with animal studies showing that GABA agonists reduce CBF and glucose consumption to the same degree (Kelly et al, 1989) (Kelly and McCulloch, 1983). The effect of the GABA agonists was most pronounced in cortical layer IV, the layer of major termination of input from the specific thalamic relay nuclei, rather than in the superficial cortical layers that contained the highest density of GABA receptors.…”

Section: Neurotransmitters Do Not Contribute To Cerebral Blood Flow Increases In the Cerebellar Cortexsupporting

confidence: 83%

Relationship of Spikes, Synaptic Activity, and Local Changes of Cerebral Blood Flow

Lauritzen

2001

J Cereb Blood Flow Metab

238

133

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The coupling of electrical activity in the brain to changes in cerebral blood flow (CBF) is of interest because hemodynamic changes are used to track brain function. Recent studies, especially those investigating the cerebellar cortex, have shown that the spike rate in the principal target cell of a brain region (i.e. the efferent cell) does not affect vascular response amplitude. Subthreshold integrative synaptic processes trigger changes in the local microcirculation and local glucose consumption. The spatial specificity of the vascular response on the brain surface is limited because of the functional anatomy of the pial vessels. Within the cortex there is a characteristic laminar flow distribution, the largest changes of which are observed at the depth of maximal synaptic activity (i.e. layer IV) for an afferent input system. Under most conditions, increases in CBF are explained by activity in postsynaptic neurons, but presynaptic elements can contribute. Neurotransmitters do not mediate increases in CBF that are triggered by the concerted action of several second messenger molecules. It is important to distinguish between effective synaptic inhibition and deactivation that increase and decrease CBF and glucose consumption, respectively. In summary, hemodynamic changes evoked by neuronal activity depend on the afferent input function (i.e. all aspects of presynaptic and postsynaptic processing), but are totally independent of the efferent function (i.e., the spike rate of the same region). Thus, it is not possible to conclude whether the output level of activity of a region is increased based on brain maps that use blood-flow changes as markers.

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Section: Neurotransmitters Do Not Contribute To Cerebral Blood Flow Increases In the Cerebellar Cortexsupporting

confidence: 83%

Relationship of Spikes, Synaptic Activity, and Local Changes of Cerebral Blood Flow

Lauritzen

2001

J Cereb Blood Flow Metab

238

133

View full text Add to dashboard Cite

show abstract

“…These data are difficult to reconcile because one would expect increases in glucose consumption to be accompanied by increases in CBF and decreases in CBF to be accompanied by decreases in glucose consumption on the basis of the idea of a coupling between neural activity, glucose consumption, and blood flow. Nevertheless, the data of Roland and Friberg (1988) are consistent with animal studies, which demonstrated that intravenous injection of a GABA agonist reduced CBF and glucose consumption to the same degree (Kelly and McCulloch, 1983;Kelly et al, 1989). The effect of the GABA agonist was most pronounced in cortical layer IV rather than in the superficial cortical layers that contained the highest density of GABA receptors.…”

Section: Synaptic Inhibitionsupporting

confidence: 79%

Brain Function and Neurophysiological Correlates of Signals Used in Functional Neuroimaging

2003

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“…Ocular blood flow was measured using the [14C]-iodoantipyrine method derived by Sakurada et al 16 and described in detail previously17 with modifications for tissue sampling 18. Briefly, [14C]-iodoantipyrine (50 μCi/rat in 0.6 ml saline) was injected intravenously over 45 seconds via a femoral cannula, and timed femoral arterial blood samples were collected intermittently.…”

Section: Methodsmentioning

confidence: 99%

Possible role for nitric oxide releasing nerves in the regulation of ocular blood flow in the rat

Kelly

Buckley

Ritchie

et al. 1998

British Journal of Ophthalmology

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Aim-To investigate the role of nitrergic nerves in the regulation of ocular blood flow. Methods-Conscious, lightly restrained rats were treated with either the neuronal nitric oxide synthase inhibitor 7-nitroindazole (7-NI), or the nonselective inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), and ocular blood flow was measured ex vivo from tissue samples, using the fully quantitative [14C]-iodoantipyrine technique. Results-In the peripheral circulation, L-NAME produced an increase in arterial blood pressure (+22%) while 7-NI had no eVect. In contrast, both 7-NI and L-NAME produced significant decreases in ocular blood flow (−31% and −59% respectively). The ocular vascular resistance calculated from ocular blood flow and mean arterial blood pressure increased by 29% following 7-NI, but by 130% following L-NAME. Conclusions-Nitric oxide releasing neurons may play an important contributory role in regulating ocular blood flow. (Br J Ophthalmol 1998;82:1199-1202 There is evidence that ocular blood vessels are innervated by nitric oxide (NO) producing neurons 1-3 and studies of ocular blood vessels in vitro suggest a functional role for these nerves in determining vascular calibre in the eye. [4][5][6] Cerebral vessels are similarly endowed 7 8 and it has become apparent that NO released from neurons innervating small cerebral resistance vessels may regulate blood flow by providing a tonic dilator influence. 9There is some in vivo evidence that NO releasing nerves can similarly influence blood flow in the avian eye, 10 but these authors have also reported that anaesthesia can fundamentally alter the cardiovascular response to pharmacological inhibition of neuronal nitric oxide synthase (nNOS), 11 and others have identified species diVerences in eYcacy and time course of eVects.12 13 The purpose of the present study was to investigate the eVects upon ocular blood flow of a single intraperitoneal injection of the nNOS inhibitor 7-nitroindazole (7-NI), which in vivo is relatively selective for the neuronal isoform of the enzyme, 14 and to compare these with the eVects of the arginine analogue, NG-nitro-L-arginine methyl ester (L-NAME), a nonselective NOS inhibitor. Materials and methods ANIMAL PREPARATIONA total of 19 male Sprague-Dawley rats (250-300 g) were used in this study. All experiments adhered to the ARVO Statement on the Use of Animals in Ophthalmic and Vision Research, and complied with British Home OYce regulations. Protocols did not involve any direct manipulation of the eye. On the day of the experiment the rats were anaesthetised and prepared surgically as described in detail previously.9 Following surgery, the rats were allowed to recover from the eVects of the anaesthesia for at least 2 hours before any further experimental manipulation, and all subsequent measurements were performed on fully conscious animals. Mean arterial blood pressure (MABP) was monitored continuously, and blood gases were measured immediately before the initiation of the measurement procedures for ocular blood flow. D...

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The Effects of the GABA Agonist Muscimol upon Blood Flow in Different Vascular Territories of the Rat Cortex

Cited by 11 publications

References 19 publications

Relationship of Spikes, Synaptic Activity, and Local Changes of Cerebral Blood Flow

Relationship of Spikes, Synaptic Activity, and Local Changes of Cerebral Blood Flow

Brain Function and Neurophysiological Correlates of Signals Used in Functional Neuroimaging

Possible role for nitric oxide releasing nerves in the regulation of ocular blood flow in the rat

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