Expression of somatostatin and somatostatin receptor subtypes in Apolipoprotein D (ApoD) knockout mouse brain: An immunohistochemical analysis

• Published in: Journal of chemical neuroanatomy 2009-09, Vol.38 (1), p.20-33
• Main Authors: Rajput, Padmesh S., Billova, Sabina, Patel, Shutish C., Kharmate, Geetanjali, Somvanshi, Rishi K., Kumar, Ujendra
• Format: Article
• Language: English
• Subjects: Amygdala - metabolism; Amygdala - ultrastructure; Animals; ApoD; Apolipoproteins D - genetics; Brain - cytology; Brain - metabolism; Brain Chemistry - physiology; Brain Mapping; Cell Membrane - metabolism; Cell Membrane - ultrastructure; Cerebral Cortex - metabolism; Cerebral Cortex - ultrastructure; Corpus Striatum - metabolism; Corpus Striatum - ultrastructure; Cytoplasm - metabolism; Cytoplasm - ultrastructure; Degeneration; Down-Regulation - physiology; Hippocampus - metabolism; Hippocampus - ultrastructure; Immunohistochemistry; Mice; Mice, Knockout; Neurons - metabolism; Neurons - ultrastructure; Neuropeptide; Receptors, Somatostatin - metabolism; Somatostatin; Somatostatin - metabolism; Somatostatin receptors; Substantia Nigra - metabolism; Substantia Nigra - ultrastructure
• ISSN: 0891-0618; 1873-6300
• DOI: 10.1016/j.jchemneu.2009.05.004

Apolipoprotein D (ApoD) is widely distributed in central and peripheral nervous system. ApoD expression has been shown to increase in several neurodegenerative and neuropsychiatric disorders, as well as during regeneration in the nervous system. Like ApoD, in the central nervous system somatostatin (SST) is widely present and functions as neurotransmitter and neuromodulator. The biological effects of SST are mediated via binding to five high-affinity G-protein coupled receptors termed SSTR1–5. Mice lacking ApoD exhibit reduced SST labeling in cortex and hippocampus and increased expression in striatum and amygdala without any noticeable changes in substantia nigra. Changes in SSTRs expressions have been described in several neurodegenerative disorders including Alzheimer's, Parkinson's and Huntington's diseases. In the present study, using SSTR1–5 receptor-specific antibodies, we mapped their distribution in wild type ( w t ) and ApoD knockout (ApoD −/−) mouse brain. SSTR1–5 expression was observed both as membrane and cytoplasmic protein and display regions and receptor specific differences between w t and ApoD −/− mice brains. In cortex and hippocampus, SSTR subtypes like immunoreactivity are decreased in ApoD −/− mice brain. Unlike cortex and hippocampus, in the striatum of ApoD −/− mice, projection neurons showed increased SSTR immunoreactivity, as compared to w t . Higher SSTR subtypes immunoreactivity is seen in substantia nigra pars compacta (SNpc) whereas lower in substantia nigra pars reticulata (SNpr) of ApoD −/− mice brains as compared to w t . Whereas, amygdala displayed SSTR subtypes changes in different nuclei of ApoD −/− mice in comparison to w t mice brain. Taken together, our results describe receptor and region specific changes in SST and SSTR subtypes expression in ApoD −/− mice brain, which may be linked to specific neurological disorders.