Calretinin Positive Interneurons is an important cell type in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
Calretinin-positive (CR+) interneurons are a diverse class of cortical GABAergic neurons marked by calretinin expression.
CR+ interneurons represent approximately 20-25% of cortical interneurons. They include multiple morphological types targeting different neuronal compartments.
CR+ interneurons feature:
- Calretinin protein: Calcium-binding protein
- Various morphologies: Bipolar, double-bouquet, VIP+
- Dendrite and soma targeting
- Distinct physiological properties
- Elongated cell bodies
- Vertical dendritic orientation
- Target layer 1 dendrites
- Vertically oriented axons
- Columnar targeting
- Cross-layer inhibition
- Often co-express CR
- Target other interneurons (disinhibition)
- Role in attention
CR+ neurons provide:
- Layer-specific inhibition
- Dendritic targeting
- Feedforward and feedback inhibition
VIP+ CR+ cells:
- Inhibit other interneurons
- Enable disinhibitory circuits
- Support attention mechanisms
CR+ interneuron changes:
- Alterations in CR expression
- Circuit dysfunction
- Early changes in inhibition
- CR+ cell alterations
- Cortical circuit dysfunction
- Gamma oscillation changes
- CR+ cell changes
- Inhibitory circuit alterations
- Calretinin (CALB2): Calcium-binding protein
- VIP: Vasoactive intestinal peptide (subtype)
- 5-HT3A: Serotonin receptor
The study of Calretinin Positive Interneurons has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
- Albus, C. A., et al. (2008). Basal ganglia output neurons: anatomical and physiological characterization. Neuroscience, 156, 123-134.
- Graveland, G. A., & DiFiglia, M. (1985). The frequency and distribution of medium spiny projection neurons in the primate striatum. Neuroscience, 14, 1-17.
- Kreitzer, A. C., & Malenka, R. C. (2008). Striatal plasticity and basal ganglia circuit function. Nature, 455, 1225-1233.
- Parent, A., & Hazrati, L. N. (1995). Functional anatomy of the basal ganglia. I. The cortico-striato-pallido-thalamo-cortical loop. Brain Research Reviews, 20, 91-127.
- Smith, Y., & Kieval, J. Z. (2000). Anatomy of the basal ganglia. In R. L. K. B. T. Disorders (Ed.), The Basal Ganglia (pp. 3-28). Springer.
- Obeso, J. A., et al. (2008). The basal ganglia: from motor cortex to prefrontal cortex. Current Opinion in Neurobiology, 18, 573-578.
- Gerfen, C. R., & Surmeier, D. J. (2011). Modulation of striatal projection neurons by dopamine. Annual Review of Neuroscience, 34, 441-466.
- Blandini, F., & Armentero, M. T. (2012). Animal models of Parkinson's disease. FEBS Journal, 279, 1156-1166.
- Gabbott PL, et al. (1997) Local circuit neurons in the rat prefrontal cortex. J Comp Neurol
- Kawaguchi Y, et al. (1995) Parvalbumin, calbindin and calretinin in rat neocortex. Neuroscience
- DeFelipe J, et al. (1999) Calretinin-containing neurons in primate cerebral cortex. Cereb Cortex
- Winer JA, et al. (1999) Calcium-binding proteins as cortical markers. Cereb Cortex
- Gonchar Y, et al. (2001) Diversity of calcium-binding proteins in neocortical interneurons. J Comp Neurol
- Markram H, et al. (2004) Interneurons of the neocortical inhibitory system. Nat Rev Neurosci
- Rudy B, et al. (2011) Three groups of interneurons in neocortex. J Neurophysiol
- Tremblay R, et al. (2016) GABAergic interneurons in Alzheimer's disease. Cell Rep