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Updated: Aug 11, 2026
Whole-Cell Recording of Calcium Release-Activated Calcium (CRAC) Currents in Human T Lymphocytes
Published on: December 21, 2010
Cytosolic free [Ca2+] in single T-lymphocytes from depressed patients and healthy controls
1Central Institute of Mental Health, Mannheim, Germany.
Insights
Depression impairs calcium signaling in T lymphocytes. Phytohaemagglutinin (PHA) stimulation caused a reduced intracellular calcium ([Ca2+]i) rise in T lymphocytes from depressed patients compared to controls.
Area of Science:
- Neuroimmunology
- Cellular Physiology
Background:
- Human lymphocytes serve as models for central neurons.
- Depression is associated with altered immune function, including impaired mitogen-induced proliferation.
- Dysregulated intracellular calcium ([Ca2+]i) may contribute to depression's pathophysiology.
Purpose of the Study:
- To investigate alterations in intracellular calcium ([Ca2+]i) regulation in T lymphocytes from patients with major depression.
- To analyze the phytohaemagglutinin (PHA)-induced calcium response in single T lymphocytes.
Main Methods:
- Measurement of PHA-induced intracellular calcium ([Ca2+]i) rise in single Fura-2 AM-loaded T11+ lymphocytes.
- Comparison between patients with major depression and healthy controls.
- Analysis of resting and stimulated [Ca2+]i levels.
Main Results:
- No significant difference in resting intracellular calcium ([Ca2+]i) was observed between depressed patients and controls.
- Phytohaemagglutinin (PHA) evoked a diminished [Ca2+]i rise in T lymphocytes from depressed patients (4/13 cells) compared to controls (7/14 cells).
- Elevated [Ca2+]i levels reached up to 200 nmol/l in depressed patients versus 400-500 nmol/l in controls.
Conclusions:
- Preliminary data suggest altered intracellular calcium ([Ca2+]i) regulation in lymphocytes of depressed patients.
- This finding supports the hypothesis that impaired calcium signaling may be implicated in the pathophysiology of depression.
Abstract:
Human lymphocytes are widely used as peripheral models for central neurones. Alterations in immune function have been reported in depressed patients, e.g. mitogen-induced proliferation is impaired during depression. One possible causative mechanism could be altered [Ca2+]i regulation. Phytohaemagglutinin (PHA)-induced rise of [Ca2+]i has been found to be diminished in lymphocyte suspensions from depressed patients (Ecker et al., this issue). We measured PHA-induced rise of [Ca2+]i in single Fura-2 AM-loaded T11+ lymphocytes of patients with major depression and controls to further analyse [Ca2+]i regulation in depression. The [Ca2+]i of resting lymphocytes was 57 +/- 2 nmol/l (mean +/- SEM). There was no difference in resting [Ca2+]i of resting lymphocytes of patients and controls. PHA evoked an increase of [Ca2+]i an 7 out of 14 cells from control subjects up to 400-500 nmol/l. In contrast, only 4 out of 13 cells from depressed patients showed an increase of [Ca2+]i up to 200 nmol/l. In a small fraction of cells from both groups the [Ca2+]i signal is oscillating. Our preliminary data confirm alteration of [Ca2+]i regulation in lymphocytes of depressed patients.
