PubMed · 592884
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T J Sejnowski. 1977-11-21. Statistical constraints on synaptic plasticity.. https://doi.org/10.1016/0022-5193(77)90146-1
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RATIONALE: The depressive phase of bipolar disorder (bipolar depression) is a difficult-to-treat form of depression. The olanzapine/fluoxetine combination (Symbyax) is the only medication approved to treat this disorder. The precise neural mechanisms responsible for its efficacy are not clearly understood. OBJECTIVES: In order to further elucidate the neurobiological mechanisms responsible for the beneficial clinical effects of the olanzapine/fluoxetine combination, the current experiment was designed to investigate the effects of chronic coadministration of olanzapine and fluoxetine on electrophysiological activity in the locus coeruleus (LC). METHODS: Rats received olanzapine for 3 weeks via subcutaneous osmotic pumps while simultaneously receiving daily intraperitoneal injections of fluoxetine. These chronically treated rats were anesthetized, and single-unit recordings of LC neurons were made. RESULTS: Chronic administration of olanzapine alone significantly increased firing of LC neurons, while, as reported previously, chronic administration of fluoxetine alone significantly reduced firing of LC neurons. However, in the combination condition, olanzapine was able to block the fluoxetine-induced suppression of the LC, and a significant increase in LC activity was observed. CONCLUSIONS: The observed increase in firing of LC neurons could lead to enhanced levels of norepinephrine release in projection areas and amelioration of the clinical symptoms of bipolar depression.
An evaluation of electron micrographs of stimulated nerve fibers used to investigate the effect of action potential generation on the structure-function relationship between axons and its associated glial cells revealed that what was at first thought to be stimulation-induced damage to the glia was, in fact, limited to volume expansion and disaggregation of the glial tubular lattice. All other structures appeared well preserved and otherwise normal. Using a 4-point subjective scale for evaluation by two investigators, 50-Hz stimulation for 2 min was observed to cause a volume expansion and disaggregation of the tubular lattice. Quantitatively, the internal diameter of the stimulated tubular lattice increased 65% above the unstimulated control (50.96 +/- 2.09 nm and 30.81 +/- 0.87 nm, respectively, P < or = 0.001). Stimulation had its greatest effect on tubular lattice volume and organization in the adaxonal glial layer and a decreasing effect as distance from the giant axon increased. These effects are reversible since the tubular lattice diameter and degree of disaggregation preserved 10 min after the cessation of stimulation were not found to be different from their unstimulated paired controls. Axons injected with TEA, a voltage-gated potassium channel blocker, prevented stimulation-induced volume expansion and disaggregation of tubular lattice structure. These results are consistent with an active uptake of K+ with obligated water or, alternatively, hyperosmotic K+ uptake and a fixation-induced increase in water permeation. Either mechanism of K+ uptake would result in tubular lattice volume expansion and disaggregation and suggests that the tubular lattice serves a larger role than a simple trans-glial diffusion pathway.
Extracellular neuronal responses were recorded from the posterior insular cortex. In three of 20 neurons, fluctuations in their spontaneous discharge were observed during recording without stimulation. In these recordings, fluctuations were also observed in arterial blood pressure (BP) and heart rate (HR) recorded simultaneously. For 3 neurons, the relationships among the fluctuations in the spontaneous discharge of the insular cortex neuron (INSneu), mean arterial pressure (MAP), and HR were analyzed using Pearson's correlation coefficient (r). In unit A, there was a negative correlation between INSneu and MAP (r = -0.30). The r between INSneu and HR was -0.02. In unit B, the data were divided into two groups according to HR (HR < 400 and HR > or = 400). The differential results in the correlations for INSneu-MAP were obtained in the two groups (r = -0.2, HR < 400; r = 0.51, HR > or = 400). For unit C, the INSneu was positively correlated with BP (r = 0.31) and HR (r = 0.36). From the correlation analysis concerning the time, changes in INSneu seem to precede (or delay) changes in BP. These results showed that fluctuations in neuronal activity in the posterior insular cortex are positively or negatively correlated with BP (or HR). The data suggest that some of the neurons in the posterior insular cortex may play a role in the homeostatic (and/or regulatory) control of the autonomic system.