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“Chronic treatment with the selective serotonin reuptake inhibitor, citalopram, normalizes several behavioral and neurochemical abnormalities in the olfactory bulbectomized (OBX) rat model of depression.
To assess the changes in regional cerebral glucose utilization (rCGU) following chronic treatment with citalopram in OBX and sham-operated rats.
Male Sprague Dawley rats (160-190 g) were used. Two weeks following the surgeries, the rats were implanted with osmotic minipumps which delivered 10 mg/kg/day of citalopram (the sham-CTP and OBX-CTP groups) or saline (to the sham-SAL and OBX-SAL groups) for 2 weeks. Following the treatment, the rates of rCGU were determined in 43 brain regions Lonafarnib datasheet using 2-[(14)C]deoxyglucose (2-[(14)C]DG) autoradiography.
The general linear model statistical analysis
revealed learn more significantly lower rCGU in the OBX-SAL group compared to the sham-SAL group in the medial prefrontal cortex and the median forebrain bundle. The sham-CTP group had significantly lower rCGU relative to the sham-SAL group in the medial prefrontal cortex. The OBX-CTP group had significantly lower rCGU than the OBX-SAL group in the anterior olfactory nucleus, orbitofrontal cortex, frontal cortex, anterior cingulate cortex, visual cortex, and substantia nigra-pars reticulata. The rCGU in the OBX-CTP group was significantly lower than that in the sham-CTP group in the anterior olfactory nucleus, orbitofrontal cortex, visual cortex, and substantia nigra-pars reticulata.
The results imply that chronic citalopram treatment, shown previously to result in behavioral normalization in OBX rats, establishes a new pattern of rCGU, rather than
normalizing it to the pattern of the sham-CTP rats.”
“Background: This prospective cohort study investigated the serum levels of brain-derived neurotrophic factor (BDNF), which mediates synaptic plasticity crucial for fear memory extinction, in patients severely injured in Gemcitabine solubility dmso motor vehicle accidents (MVAs). Method: A nested, case-controlled study was conducted with 103 MVA survivors: 8 medication-naive patients who met the criteria for full diagnosis of posttraumatic stress disorder (PTSD) at 6 months after MVA, 10 medication-naive patients with partial PTSD and 85 patients with no PTSD. PTSD was evaluated by the Clinician-Administered PTSD Scale (CAPS). Serum BDNF levels were measured shortly after the MVA (baseline) and at 6-month follow-up. Results: Posttrauma serum BDNF levels differed between the 3 groups after controlling for age and sex (F = 3.41, p = 0.04), with unexpectedly higher serum BDNF levels seen in the full-PTSD group compared with the no-PTSD group. Additional analysis of patients with serum samples taken at baseline and at 6 months revealed the full-PTSD group had significantly higher serum BDNF levels over the 6 months than the no-PTSD group after controlling for age and sex (F = 6.44, p < 0.01).