Vocal-tract filtering by lingual articulation in a parrot

Human speech and bird vocalization are complex communicative behaviors with notable similarities in development and underlying mechanisms. However, there is an important difference between humans and birds in the way vocal complexity is generally produced. Human speech originates from independent modulatory actions of a sound source, e.g., the vibrating vocal folds, and an acoustic filter, formed by the resonances of the vocal tract (formants). Modulation in bird vocalization, in contrast, is thought to originate predominantly from the sound source, whereas the role of the resonance filter is only subsidiary in emphasizing the complex time-frequency patterns of the source (e.g., but see ). However, it has been suggested that, analogous to human speech production, tongue movements observed in parrot vocalizations modulate formant characteristics independently from the vocal source. As yet, direct evidence of such a causal relationship is lacking. In five Monk parakeets, Myiopsitta monachus, we replaced the vocal source, the syrinx, with a small speaker that generated a broad-band sound, and we measured the effects of tongue placement on the sound emitted from the beak. The results show that tongue movements cause significant frequency changes in two formants and cause amplitude changes in all four formants present between 0.5 and 10 kHz. We suggest that lingual articulation may thus in part explain the well-known ability of parrots to mimic human speech, and, even more intriguingly, may also underlie a speech-like formant system in natural parrot vocalizations.     

Intrathecal delivery of IFN-gamma protects C57BL/6 mice from chronic-progressive experimental autoimmune encephalomyelitis by increasing apoptosis of central nervous system-infiltrating lymphocytes

The exclusive detrimental role of proinflammatory cytokines in demyelinating diseases of the CNS, such as multiple sclerosis, is controversial. Here we show that the intrathecal delivery of an HSV-1-derived vector engineered with the mouse IFN-gamma gene leads to persistent (up to 4 wk) CNS production of IFN-gamma and inhibits the course of a chronic-progressive form of experimental autoimmune encephalomyelitis (EAE) induced in C57BL/6 mice by myelin oligodendrocyte glycoprotein (MOG)(35-55). Mice treated with the IFN-gamma-containing vector before EAE onset showed an earlier onset but a milder course of the disease compared with control mice treated with the empty vector. In addition, 83% of IFN-gamma-treated mice completely recovered within 25 days post immunization, whereas control mice did not recover up to 60 days post immunization. Mice treated with the IFN-gamma-containing vector within 1 wk after EAE onset partially recovered from the disease within 25 days after vector injection, whereas control mice worsened. Recovery from EAE in mice treated with IFN-gamma was associated with a significant increase of CNS-infiltrating lymphocytes undergoing apoptosis. During the recovery phase, the mRNA level of TNFR1 was also significantly increased in CNS-infiltrating cells from IFN-gamma-treated mice compared with controls. Our results further challenge the exclusive detrimental role of IFN-gamma in the CNS during EAE/multiple sclerosis, and indicate that CNS-confined inflammation may induce protective immunological countermechanisms leading to a faster clearance of encephalitogenic T cells by apoptosis, thus restoring the immune privilege of the CNS.     

Knockout of ERK1 MAP kinase enhances synaptic plasticity in the striatum and facilitates striatal-mediated learning and memory

Extracellular signal-regulated kinases (ERK1 and 2) are synaptic signaling components necessary for several forms of learning. In mice lacking ERK1, we observe a dramatic enhancement of striatum-dependent long-term memory, which correlates with a facilitation of long-term potentiation in the nucleus accumbens. At the cellular level, we find that ablation of ERK1 results in a stimulus-dependent increase of ERK2 signaling, likely due to its enhanced interaction with the upstream kinase MEK. Consistently, such activity change is responsible for the hypersensitivity of ERK1 mutant mice to the rewarding properties of morphine. Our results reveal an unexpected complexity of ERK-dependent signaling in the brain and a critical regulatory role for ERK1 in the long-term adaptive changes underlying striatum-dependent behavioral plasticity and drug addiction.     

Length–weight relationship of 37 fish species from the Taquari River (Paranapanema Basin,Brazil)

This work describes the length–weight relationship (LWR) of 37 fish species from the Taquari River, one of the tributaries of the Jurumirim Reservoir in the high Paranapanema Basin, São Paulo, Brazil. Information was not yet available in FishBase on LWRs of 22 of the fish species and maximum weights (Wt) of 24 of the fish species. New maximum standard lengths are presented for nine species as well as weights for two fish species.