[Academisation of the Midwifery Profession (Part 2): Risks - and How they can Be Avoided as Best as Possible in the Degree Programs]. / Akademisierung des Hebammenberufs (Teil 2): Risiken ­ und wie sie in den Studiengängen bestmöglich vermieden werden können.

The full academisation of midwifery training, which thus far has been given in technical colleges, is now beginning in Germany and poses a great challenge for both the German federal states and the universities. Against this background, the aim of this article is to identify possible risks arising from the full academisation of training and the revision of the Midwifery Act and to show possible solution strategies to promote the implementation of study programmes.

Accumbal dopamine D2 receptors are important for sensorimotor gating in C3H mice.

One operational measure of sensorimotor gating that is deficient in many psychiatric disorders is prepulse inhibition (PPI) of the startle response. To investigate the role of dopamine D1 and D2 receptors within the nucleus accumbens (NAC) in sensorimotor gating in mice, we infused dopamine D1 and D2 receptor agonists (dihydrexidine and quinpirole respectively) directly into the NAC and measured the effects on PPI and on prepulse facilitation. Quinpirole infusions increased PPI and attenuated prepulse facilitation, whereas dihydrexidine had no effects. These results stand in contrast to data after systemic injections in mice and rats and intra-accumbal infusions in rats, suggesting that the role of dopamine D2 receptors within the NAC in mice differs from their role in rats.

Synaptic depression and short-term habituation are located in the sensory part of the mammalian startle pathway.

BACKGROUND: Short-term habituation of the startle response represents an elementary form of learning in mammals. The underlying mechanism is located within the primary startle pathway, presumably at sensory synapses on giant neurons in the caudal pontine reticular nucleus (PnC). Short trains of action potentials in sensory afferent fibers induce depression of synaptic responses in PnC giant neurons, a phenomenon that has been proposed to be the cellular correlate for short-term habituation. We address here the question whether both this synaptic depression and the short-term habituation of the startle response are localized at the presynaptic terminals of sensory afferents. If this is confirmed, it would imply that these processes take place prior to multimodal signal integration, rather than occurring at postsynaptic sites on PnC giant neurons that directly drive motor neurons. RESULTS: Patch-clamp recordings in vitro were combined with behavioral experiments; synaptic depression was specific for the input pathway stimulated and did not affect signals elicited by other sensory afferents. Concordant with this, short-term habituation of the acoustic startle response in behavioral experiments did not influence tactile startle response amplitudes and vice versa. Further electrophysiological analysis showed that the passive properties of the postsynaptic neuron were unchanged but revealed some alterations in short-term plasticity during depression. Moreover, depression was induced only by trains of presynaptic action potentials and not by single pulses. There was no evidence for transmitter receptor desensitization. In summary, the data indicates that the synaptic depression mechanism is located presynaptically. CONCLUSION: Our electrophysiological and behavioral data strongly indicate that synaptic depression in the PnC as well as short-term habituation are located in the sensory part of the startle pathway, namely at the axon terminals of sensory afferents in the PnC. Our results further corroborate the link between synaptic depression and short-term habituation of the startle response.

Experience increases the prepulse inhibition of the acoustic startle response in mice.

The authors have previously shown that inhibition of the acoustic startle response by a prepulse increases when it is repetitively elicited over days. The present experiments show in C3H and C57 mice that this change is caused by an increase in prepulse inhibition (PPI) and not by a decrease in prepulse facilitation. This PPI increase is only evoked if prepulses and startle stimuli are repeatedly given in a temporally paired ("contingent") order, proposing an associative learning process. (Only in C57 mice, PPI was additionally increased by adaptation in the same, but not in a different, context). As an underlying mechanism for this PPI increase by experience, the authors hypothesize Hebbian plasticity of an inhibitory synapse.

Neural cell adhesion molecule-null mice are not deficient in prepulse inhibition of the startle response.

Mice constitutively deficient in the neural cell adhesion molecule have morphological changes in the brain, which are hallmarks of schizophrenia. Schizophrenic patients are impaired in sensorimotor processing indicated by a deficit in prepulse inhibition of the acoustic startle response. Here we tested whether prepulse inhibition and prepulse facilitation are changed in neural cell adhesion molecule-deficient mice compared with their wild-type littermates. Neither prepulse inhibition nor prepulse facilitation (which occurred only at the lowest prepulse intensity used and was weak) was altered. This result is discussed in the light of the 'two-hit' hypothesis of schizophrenia, suggesting that in neural cell adhesion molecule-deficient mice, a prepulse inhibition deficit may become apparent only after treatment with a 'second hit' (such as increased stress).

Effects of sex and estrous cycle on modulation of the acoustic startle response in mice.

Potential sex differences in amplitude, habituation, prepulse inhibition (PPI) and prepulse facilitation (PPF) of the acoustic startle response (ASR) were investigated using male and female mice from the two different inbred mouse strains C57BL/6J (C57) and C3H. Furthermore, the effects of the estrous cycle were tested. The estrous cycle appeared to have no effect on ASR amplitude, habituation, PPF and PPI, the latter being in contrast to results in rats and humans. While sex had no effect on PPI or PPF, males exhibited higher startle amplitudes than females, irrespective of strain, which we discuss to be due to increased male anxiety. In addition, long-term habituation was stronger in C57 males and short-term habituation was weaker in C3H males with respect to females. These results provide evidence for influence of the reproductive hormones on startle reactivity and startle habituation; we therefore conclude that future studies involving genetic influences on behavior using inbred strains are only complete if both sexes are included.

Habituation of the acoustic and the tactile startle responses in mice: two independent sensory processes.

To test whether habituation is specific to the stimulus modality, the authors analyzed cross-habituation between the tactile startle response' (TSR) and the acoustic startle response (ASR). The acoustic artifacts of airpuffs used to elicit the TSR were reduced by using a silencer and were effectively masked by background noise of 90-100 dB sound-pressure level. ASR was elicited by 14-kHz tones. TSR and ASR habituated in DBA and BALB mice: both the TSR and ASR habituated to a greater extent in DBA mice than in BALB mice. In both strains, habituation of the TSR did not generalize to the ASR, and vice versa. From this, the authors concluded that habituation of startle is located in the sensory afferent branches of the pathway.

Factors governing prepulse inhibition and prepulse facilitation of the acoustic startle response in mice.

The influence of prepulses on the acoustic startle response (ASR) was measured in three inbred mouse strains, C57BL/6J, 129/SvHsd, and AKR/OlaHsd, and one hybrid strain produced by crossing wild mice and NMRI mice. Prepulse inhibition (PPI), i.e. reduction of ASR by prepulses, was maximal when the interval between prepulses and startle stimuli was in the range of 37.5-100 ms. Prepulse facilitation (PPF), i.e. increase of ASR by prepulses, was maximal when the prepulse preceded the startle stimulus by 12.5 ms. PPI increased with increasing prepulse SPL, PPF first increased then decreased when prepulse SPL was increased. Percent PPI was independent from startle stimulus SPL. All strains showed a long-term increase of PPI when tested for several days; one strain (129) also showed an increase of PPF over days. The present results clearly show that PPI and PPF are independent processes, which add to yield the final response change. PPF and the observed long-term changes of PPI and PPF are stronger expressed in mice than have been observed in rats under similar conditions. Since there were significant differences between the strains of mice with respect to PPI and PPF, genetically different strains of mice are a promising tool to study these two processes.