Odor Detection Sensitivity Research Articles

Odor sensitivity is impaired in HIV-positive cognitively impaired patients

An estimated 7–28% of patients infected by the human immunodeficiency virus (HIV) develop dementia and at least 50% develop mild neurocognitive impairment. Past studies have shown odor identification impairments in HIV + neurocognitively impaired patients. It is difficult, however, based on an odor identification test to state with certainty that individuals with cognitive impairment have sensory olfactory deficits, because odor identification tests are known to draw upon cognitive skills. In the present study odor detection sensitivity was evaluated using an ascending, forced-choice, two-alternative, odor threshold test for butanol. Subjects were divided into three groups, HIV seropositive (HIV +) neurocognitively impaired, HIV + neurocognitively unimpaired, and HIV negative, based on neurological and psychological testing. An analysis of variance revealed significantly poorer odor sensitivity for the HIV + neurocognitively impaired group than for the two control groups. A significant negative correlation between degree of cognitive impairment and olfactory sensitivity was also found. We suspect that the olfactory deficits found in the HIV + neurocognitively impaired subjects are primarily due to damage to the central nervous system; however, nasal infection may be a contributing etiology.

Current recording from sensory cilia of olfactory receptor cells in situ. II. Role of mucosal Na+, K+, and Ca2+ ions.

Action potential-driven current transients were recorded from sensory cilia and used to monitor the spike frequency generated by olfactory receptor neurons, which were maintained in their natural position in the sensory epithelium. Both basal and messenger-induced activities, as elicited with forskolin or cyclic nucleotides, were dependent on the presence of mucosal Na+. The spike rate decreased to approximately 20% when mucosal Na+ was lowered from 120 to 60 mM (replaced by N-methyl-D-glucamine+), without clear changes in amplitude and duration of the recorded action potential-driven transients. Mucosal Ca2+ and Mg2+ blocked spike discharge completely when increased from 1 to 10 mM in Ringer solution. Lowering mucosal Ca2+ below 1 mM increased the spike rate. These results can be explained by the presence of a cyclic nucleotide-dependent, Ca(2+)-sensitive cation conductance, which allows a depolarizing Na+ inward current to flow through the apical membrane of in situ receptor cells. A conductance with these properties, thought to provide the receptor current, was first described for isolated olfactory cells by Nakamura and Gold (1987. Nature (Lond.). 325:442-444). The forskolin-stimulated spike rate decreased when l-cis-diltiazem, a known blocker of the cyclic nucleotide-dependent receptor current, was added to the mucosal solution. Spike rate also decreased when the mucosal K+ concentration was lowered. Mucosal Ba2+ and 4-aminopyridine, presumably by means of cell depolarization, rapidly increased the spike rate. This suggests the presence of apical K+ channels that render the receptor cells sensitive to the K+ concentration of the olfactory mucus. With a slower time course, mucosal Ba2+ and 4-aminopyridine decreased the amplitude and caused rectification of the fast current transients (prolongation of action potentials). Abolishment of the apical Na+ current (by removal of mucosal Na+), as indicated by a strong decrease in spike rate, could be counteracted by adding 10 mM Ba2+ or 1 mM 4-aminopyridine to the mucosal solution, which re-established spiking. Similarly, blockage of the apical cation conductance with 10 mM Ca could be counteracted by adding 10 mM Ba2+ or by raising the mucosal K+ concentration. Thus mucosal concentrations of Na+, K+, and Ca2+ will jointly affect the sensitivity of odor detection.