BackgroundDopaminergic fibers originating from area A11 of the hypothalamus project to different levels of the spinal cord and represent the major source of dopamine. In addition, tyrosine hydroxylase, the rate-limiting enzyme for the synthesis of catecholamines, is expressed in 8-10% of dorsal root ganglia (DRG) neurons, suggesting that dopamine may be released in the dorsal root ganglia. Dopamine has been shown to modulate calcium current in DRG neurons, but the effects of dopamine on sodium current and on the firing properties of small DRG neurons are poorly understood.ResultsThe effects of dopamine and dopamine receptor agonists were tested on the tetrodotoxin-resistant (TTX-R) sodium current recorded from acutely dissociated small (diameter ≤ 25 μm) DRG neurons. Dopamine (20 μM) and SKF 81297 (10 μM) caused inhibition of TTX-R sodium current in small DRG neurons by 23% and 37%, respectively. In contrast, quinpirole (20 μM) had no effects on the TTX-R sodium current. Inhibition by SKF 81297 of the TTX-R sodium current was not affected when the protein kinase A (PKA) activity was blocked with the PKA inhibitory peptide (6–22), but was greatly reduced when the protein kinase C (PKC) activity was blocked with the PKC inhibitory peptide (19–36), suggesting that activation of D1/D5 dopamine receptors is linked to PKC activity. Expression of D1and D5 dopamine receptors in small DRG neurons, but not D2 dopamine receptors, was confirmed by Western blotting and immunofluorescence analysis. In current clamp experiments, the number of action potentials elicited in small DRG neurons by current injection was reduced by ~ 30% by SKF 81297.ConclusionsWe conclude that activation of D1/D5 dopamine receptors inhibits TTX-R sodium current in unmyelinated nociceptive neurons and dampens their intrinsic excitability by reducing the number of action potentials in response to stimulus. Increasing or decreasing levels of dopamine in the dorsal root ganglia may serve to adjust the sensitivity of nociceptors to noxious stimuli.

Positron emission tomography-computed tomography (PET-CT) scans with [18F]-fluorodeoxyglucose (FDG) and PET-magnetic resonance imaging (MRI) have become standard practice in staging and restaging of colorectal cancer patients by providing important information about the primary cancer as well as metastases. The PET portion of this imaging modality relies on the accumulation of radioactive glucose analog, FDG. In cancer cells, there is an overproduction of glucose transporters and, as a result, increased FDG uptake. However, not all PET-positive lesions are cancer, and in many instances, PET findings can be false positive.A few points need to be considered before understanding FDG. First, not all cancer cells use the same amount of glucose: some use more and some use less. Cancer cells with a faster metabolic rate such as colorectal adenocarcinoma are very FDG avid, whereas others such as mucinous cancers consume less glucose and therefore are less FDG avid. Inflammatory cells also have increased metabolic rates and, as a result, are FDG avid.Many of us have had patients or know of patients who were treated by the medical oncologist for stage IV cancer only to find out what was assumed to be a metastatic lesion was benign on pathology. Other patients have undergone multiple biopsies of supposed metastatic mesenteric lymph nodes that subsequently turned out to be fat necrosis or a granulomatous reaction. FDG-positive lesions often mean cancer, but not always. A variety of lesions have increased FDG radiotracer including infection, inflammation, autoimmune processes, sarcoidosis, and benign tumors. If such conditions are not identified accurately and in a timely manner, misdiagnosis can lead to inadequate therapies.Within the lower gastrointestinal tract, physiological FDG uptake can be highly variable and may range from mild to intense with a focal, diffuse, or segmental distribution. To add to the confusion, swallowed secretions, lymphoid tissue uptake, microbial uptake, infection, and benign tumors show increased FDG uptake. For example, incidental focal FDG uptake in the colon or rectum has only a 47 % probability of showing an underlying adenoma or malignant lesion on colonoscopy [1].It is well documented that surgical staples or suture lines following bowel resection can cause inflammatory or granulomatous changes with scar tissue formation with increased FDG uptake [2]. Often the only way to differentiate between benign and malignant pathology in this setting is by colonoscopy with biopsy. Chemotherapy and surgery itself can produce reactive lymphadenopathy. Radiation therapy can produce an intense inflammatory response that often develops months after treatment with reactive lymphadenopathy, peritoneal changes, and mass development. These changes can appear similar to cancer with increased FDG uptake that can last years after the cessation of therapy.Imaging with a complex technology as with PET-CT or PET-MRI can create a multitude of artifacts confounding diagnosis. PET-CT and PET-MRI use an attenuation-ba...

A 57-year-old-male presented for whole-body PET with CT for restaging of lung cancer. Besides revealing postradiation changes, we noticed an unusual pattern of FDG uptake in the myocardium, with prominent metabolic uptake involving 4 chambers of the heart. Later that day, the patient was referred to the emergency department for increased heart rate, but otherwise asymptomatic. CT angiography was performed, which showed scattered filling defects in bilateral pulmonary arteries consistent with pulmonary embolism. The finding of prominent FDG uptake involving all cardiac chambers in this patient is likely related to heart strain caused by acute pulmonary embolism.

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Two patients demonstrated an unusual pattern of intense bone and surrounding soft tissue hypermetabolic uptake in the posterior pelvis on fluorodeoxyglucose positron emission tomography with computed tomography PET-CT scans. After further investigation, we found that both patients underwent uncomplicated autologous bone marrow harvesting several weeks before imaging. These two cases illustrate a distinctive PET-CT appearance following bone marrow harvesting that the radiologist needs to recognize to not confuse the findings with metastatic disease.