The transient receptor potential vanilloid type 1 channel (TRPV1) (formerly called vanilloid receptor VR1) is known for its key role of functions in sensory nerves such as perception of inflammatory and thermal pain. Much less is known about the physiological significance of the TRPV1 expression in the brain. Here we demonstrate that TRPV1 knock-out mice (TRPV1-KO) show less anxiety-related behavior in the light-dark test and in the elevated plus maze than their wild-type littermates with no differences in locomotion. Furthermore, TRPV1-KO mice showed less freezing to a tone after auditory fear conditioning and stress sensitization. This reduction of conditioned and sensitized fear could not be explained by alterations in nociception. Also, tone perception per se was unaffected, as revealed by determination of auditory thresholds through auditory brainstem responses and distortion-product otoacoustic emissions. TRPV1-KO showed also less contextual fear if assessed 1 d or 1 month after strong conditioning protocols. These impairments in hippocampusdependent learning were mirrored by a decrease in long-term potentiation in the Schaffer collateral-commissural pathway to CA1 hippocampal neurons. Our data provide first evidence for fear-promoting effects of TRPV1 with respect to both innate and conditioned fear and for a decisive role of this receptor in synaptic plasticity.

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Adult mustached bats employ Doppler-sensitive sonar to hunt fluttering prey insects in acoustically cluttered habitats. The echolocation call consists of 4-5 harmonics, each composed of a long constant frequency (CF) component flanked by brief frequency modulations (FM). The 2nd harmonic CF component (CF2) at 61 kHz is the most intense, and analyzed by an exceptionally sharply tuned auditory system. The maturation of echolocation calls and the development of Doppler-shift compensation was studied in Cuba where large maternity colonies are found in hot caves. In the 1st postnatal week, infant bats did not echolocate spontaneously but could be induced to vocalize CF-FM signals by passive body motion. The CF2 frequency emitted by the smallest specimens was at 48 kHz (i.e., 0.4 octaves lower than the adult signal). CF-FM signals were spontaneously produced in the 2nd postnatal week at a CF2 frequency of 52 kHz. The CF2 frequencies of induced and spontaneous calls shifted upward to reach a value of 60.5 kHz in the 5th postnatal week. Standard deviations of CF2 frequency were large (up to +/-1.5 kHz) in the youngest bats and dropped to values of +/-250 Hz at the end of the 3rd postnatal week. Some individuals in the 4th and 5th postnatal weeks emitted with adultlike frequency precision of about +/-100 Hz. In the youngest bats, the 1st harmonic CF component (CF1) was up to 22 dB stronger than CF2. Adultlike relative levels of CF1 (-28 dB relative to CF2) were reached in the 5th postnatal week. In spontaneously emitted CF-FM calls, the duration of the CF2 component gradually increased with age from 5 ms to maximum values of 18 ms. Durations of the CF2 component in induced calls averaged 7 +/- 2.6 ms in the 1st postnatal week and 8.2 +/- 1.5 ms in the 5th postnatal week. There were no age-related changes in duration of the terminal FM sweep (3 +/- 0.4 ms) in both induced and spontaneous calls. The magnitude of the terminal FM sweep in spontaneous calls was not correlated with age (mean 13.5 +/- 2 kHz). Values for induced calls slightly increased with age from 11 +/- 2 to 13 +/- 2 kHz. The emission rate of induced CF-FM signals increased with age from values of 2.5 +/- 2 to 17 +/- 5 pulses/s. Values for spontaneously emitted calls were 4.4 +/- 3 and 9 +/- 4.5 pulses/s, respectively. Doppler-shift compensation, as tested in the pendulum task, emerged during the 4th postnatal week in young bats that were capable of very brief active flights, but before the time of active foraging outside the cave.

The role of inhibition in sensory cortical map plasticity is not well understood. Here we tested whether inhibition contributes to expression of receptive field plasticity in developing rat somatosensory (S1) cortex. In normal rats, microiontophoresis of gabazine (SR 95531), a competitive gamma-aminobutyric acid (GABA)-A receptor antagonist, preferentially disinhibited surround whisker responses relative to principal whisker responses, indicating that GABA(A) inhibition normally acts to sharpen whisker tuning. Plasticity was induced by transiently depriving adolescent rats of all but one whisker; this causes layer 2/3 (L2/3) receptive fields to shift away from the deprived principal whisker and toward the spared surround whisker. In units with shifted receptive fields, gabazine preferentially disinhibited responses to the deprived principal whisker, unlike in controls, suggesting that GABA(A) inhibition was acting to preferentially suppress these responses relative to spared whisker responses. This effect was not observed for L2/3 units that did not express receptive field plasticity or in layer 4, where receptive field plasticity did not occur. Thus GABA(A) inhibition promoted expression of sensory map plasticity by helping to sharpen receptive fields around the spared input.