Regulation of bat echolocation pulse acoustics by striatal dopamine.

The ability to control the bandwidth, amplitude and duration of echolocation pulses is a crucial aspect of echolocation performance but few details are known about the neural mechanisms underlying the control of these voice parameters in any mammal. The basal ganglia (BG) are a suite of forebrain nuclei centrally involved in sensory-motor control and are characterized by their dependence on dopamine. We hypothesized that pharmacological manipulation of brain dopamine levels could reveal how BG circuits might influence the acoustic structure of bat echolocation pulses. A single intraperitoneal injection of a low dose (5 mg kg(-1)) of the neurotoxin 1-methyl-4-phenylpyridine (MPTP), which selectively targets dopamine-producing cells of the substantia nigra, produced a rapid degradation in pulse acoustic structure and eliminated the bat's ability to make compensatory changes in pulse amplitude in response to background noise, i.e. the Lombard response. However, high-performance liquid chromatography (HPLC) measurements of striatal dopamine concentrations revealed that the main effect of MPTP was a fourfold increase rather than the predicted decrease in striatal dopamine levels. After first using autoradiographic methods to confirm the presence and location of D(1)- and D(2)-type dopamine receptors in the bat striatum, systemic injections of receptor subtype-specific agonists showed that MPTP's effects on pulse acoustics were mimicked by a D(2)-type dopamine receptor agonist (Quinpirole) but not by a D(1)-type dopamine receptor agonist (SKF82958). The results suggest that BG circuits have the capacity to influence echolocation pulse acoustics, particularly via D(2)-type dopamine receptor-mediated pathways, and may therefore represent an important mechanism for vocal control in bats.

Effect of vagus nerve stimulator magnet on programmable shunt settings.

OBJECTIVE: Vagus nerve stimulators and programmable shunt valves are used in the operative care of epilepsy and hydrocephalus, respectively. Both devices use magnetic fields to activate and program their various settings and functions. The authors conducted several ex vivo trials to better elucidate any interplay between the two systems. METHODS: A pulse generator controller (Cyberonics Corp., Houston, TX) was brought to within 4 cm of Strata programmable shunt valves (Medtronic Neurosurgery, Goleta, CA). Each of five valves was preset to either a low- or high-pressure setting and then challenged with the vagus nerve stimulator generator. Each valve was challenged 20 times, for a total of 100 trials. RESULTS: In 100 trials, 78 inadvertent pressure setting adjustments were recorded. In 46 attempts, the valve pressure was increased, and in 34 attempts, the pressure was decreased. CONCLUSION: This study provides some support to the anecdotal reports of inadvertent adjustments of programmable shunt valves by the external magnetic field created by vagus nerve stimulator pulse generator controllers. Further trials and a double-blind study are necessary to illustrate more clearly the possible relationship of these magnetically controlled neurosurgical devices.