Chronic reduction of cerebral blood flow in the adult rat: late-emerging CA1 cell loss and memory dysfunction

1996 ◽  
Vol 708 (1-2) ◽  
pp. 50-58 ◽  
Author(s):  
B.A. Pappas ◽  
J.C. de la Torre ◽  
C.M. Davidson ◽  
M.T. Keyes ◽  
T. Fortin
2010 ◽  
Vol 103 (1) ◽  
pp. 172-182 ◽  
Author(s):  
Wojciech Margas ◽  
Saifeldin Mahmoud ◽  
Victor Ruiz-Velasco

The sphenopalatine ganglion (SPG) neurons represent the parasympathetic branch of the autonomic nervous system involved in controlling cerebral blood flow. In the present study, we examined the coupling mechanism between mu (μ) opioid receptors (MOR) and muscarinic acetylcholine receptors (mAChR) with Ca2+ channels in acutely dissociated adult rat SPG neurons. Successful MOR activation was recorded in ∼40–45% of SPG neurons employing the whole cell variant of the patch-clamp technique. In addition, immunofluorescence assays indicated that MOR are not expressed in all SPG neurons while M2 mAChR staining was evident in all neurons. The concentration-response relationships generated with morphine and [d-Ala2-N-Me-Phe4-Glycol5]-enkephalin (DAMGO) showed IC50 values of 15.2 and 56.1 nM and maximal Ca2+ current inhibition of 26.0 and 38.7%, respectively. Activation of MOR or M2 mAChR with morphine or oxotremorine-methiodide (Oxo-M), respectively, resulted in voltage-dependent inhibition of Ca2+ currents via coupling with Gαi/o protein subunits. The acute prolonged exposure (10 min) of neurons to morphine or Oxo-M led to the homologous desensitization of MOR and M2 mAChR, respectively. The prolonged stimulation of M2 mAChR with Oxo-M resulted in heterologous desensitization of morphine-mediated Ca2+ current inhibition, and was sensitive to the M2 mAChR blocker methoctramine. On the other hand, when the neurons were exposed to morphine or DAMGO for 10 min, heterologous desensitization of M2 mAChR was not observed. These results suggest that in rat SPG neurons activation of M2 mAChR likely modulates opioid transmission in the brain vasculature to adequately maintain cerebral blood flow.


1989 ◽  
Vol 9 (5) ◽  
pp. 579-588 ◽  
Author(s):  
Astrid Nehlig ◽  
Anne Pereira de Vasconcelos ◽  
Sylvette Boyet

The postnatal changes in local cerebral blood flow in freely moving rats were measured by means of the quantitative autoradiographic [14C]iodoantipyrine method. The animals were studied at 10, 14, 17, 21, and 35 days and at the adult stage. At 10 days after birth, rates of blood flow were very low and quite homogeneous in most cerebral structures except in a few posterior areas. From these relatively uniform levels, values of local cerebral blood flow rose notably to reach a peak at 17 days in all brain regions studied. Rates of blood flow decreased between 17 and 21 days after birth and then increased from weaning time to reach the known characteristic distribution of the adult rat. The postnatal evolution of local cerebral blood flow in the rat is in good agreement with previous studies in other species such as dog and humans that also show higher rates of cerebral blood flow and glucose utilization at immature stages. However, in the rat, local cerebral blood flow and local cerebral glucose utilization are not coupled over the whole postnatal period studied, since blood flow rates reach peak values at 17 days whereas glucose utilization remains still quite low at that stage. The high rate of cerebral blood flow in the 17-day-old rat may reflect the energetic and biosynthetic needs of the actively developing brain that are completed by the summation of glucose and ketone body utilization.


1992 ◽  
Vol 12 (3) ◽  
pp. 533-533 ◽  

Exercise and the Brain: Angiogenesis in the Adult Rat Cerebellum After Vigorous Physical Activity and Motor Skill Learning Krystyna R. Isaacs, Brenda J. Anderson, Adriana A. Alcantara, James E. Black, and William T. Greenough [Originally published in Journal of Cerebral Blood Flow and Metabolism 1992;12:110-9.] In the first row of Table 1 on page 116 of the above (Isaacs et al., 1992), the IC value was erroneously listed as 0.2 ± 0.3 μm. The correct value is 4.2 ± 0.3 μm. The table appears below with this correction. The author regrets this error. [Table: see text]


2001 ◽  
Vol 120 (5) ◽  
pp. A637-A637
Author(s):  
Y RINGEL ◽  
D DROSSMAN ◽  
T TURKINGTON ◽  
B BRADSHAW ◽  
R COLEMAN ◽  
...  

2008 ◽  
Vol 22 (2) ◽  
pp. 81-90 ◽  
Author(s):  
Natalie Werner ◽  
Neval Kapan ◽  
Gustavo A. Reyes del Paso

The present study explored modulations in cerebral blood flow and systemic hemodynamics during the execution of a mental calculation task in 41 healthy subjects. Time course and lateralization of blood flow velocities in the medial cerebral arteries of both hemispheres were assessed using functional transcranial Doppler sonography. Indices of systemic hemodynamics were obtained using continuous blood pressure recordings. Doppler sonography revealed a biphasic left dominant rise in cerebral blood flow velocities during task execution. Systemic blood pressure increased, whereas heart period, heart period variability, and baroreflex sensitivity declined. Blood pressure and heart period proved predictive of the magnitude of the cerebral blood flow response, particularly of its initial component. Various physiological mechanisms may be assumed to be involved in cardiovascular adjustment to cognitive demands. While specific contributions of the sympathetic and parasympathetic systems may account for the observed pattern of systemic hemodynamics, flow metabolism coupling, fast neurogenic vasodilation, and cerebral autoregulation may be involved in mediating cerebral blood flow modulations. Furthermore, during conditions of high cardiovascular reactivity, systemic hemodynamic changes exert a marked influence on cerebral blood perfusion.


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