کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2012353 | 1067030 | 2009 | 8 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Cannabinoid CB1 receptors in rat medial prefrontal cortex are colocalized with calbindin but not parvalbumin- and calretinin-positive GABA-ergic neurons Cannabinoid CB1 receptors in rat medial prefrontal cortex are colocalized with calbindin but not parvalbumin- and calretinin-positive GABA-ergic neurons](/preview/png/2012353.png)
In the present study, we investigate putative localization of cannabinoid receptors 1 (CB1) protein on a population of cortical γ-aminobutyric acid (GABA) – positive interneurons characterized by expression of calciumbinding proteins in rat medial prefrontal cortex (MPC). Parvalbumin (PARV)/calretinin (CALR)- and calbindin (CALB)-positive neurons form two distinct populations of GABA-ergic interneurons that comprise the axo-somatic/axo-axonic and axo dendritic inhibitory systems of pyramidal cells. It has been found that CB1 receptor-positive cells are randomly distributed across the rat MPC. All spotted neurons that were positive for CB1 receptors were positive for GABA; however, the number of GABA-positive cells drastically exceeded the number of CB1 receptor-positive neurons. Subsequent experiments with double-labelling of CB1 receptors with PARV and CALR revealed no colocalization. CALB-positive neurons (e.g., double bouquet and bipolar cells) display colocalization: the degree of colocalization among CB1 receptor-positive cells reached 18%. The appearance of CB1 receptors in double bouquet and bipolar neurons indicates that CB1 receptors may control the activity of pyramidal neurons from presynaptic sites in axo dendritic synapses formed on apical and basilar dendrites of pyramidal neurons, as is characteristic for CALB-positive cortical interneurons. The phenotype of GABA-and CB1 receptor-positive but CALB-negative neurons may represent a population of inhibitory neurons that allow axosomatic control of information flow, governed by principal neurons of the MPC.
Journal: Pharmacological Reports - Volume 61, Issue 6, November–December 2009, Pages 1000–1007