Hormone-mediated neural remodeling orchestrates parenting onset during pregnancy.

During pregnancy, physiological adaptations prepare the female body for the challenges of motherhood. Becoming a parent also requires behavioral adaptations. Such adaptations can occur as early as during pregnancy, but how pregnancy hormones remodel parenting circuits to instruct preparatory behavioral changes remains unknown.

Catalytic Acceptorless Dehydrogenation (CAD) of Secondary Benzylic Alcohols into Value-Added Ketones Using Pd(II)-NHC Complexes.

For the creation of adaptable carbonyl compounds in organic synthesis, the oxidation of alcohols is a crucial step. As a sustainable alternative to the harmful traditional oxidation processes, transition-metal catalysts have recently attracted a lot of interest in acceptorless dehydrogenation reactions of alcohols. Here, using well-defined, air-stable palladium(II)-NHC catalysts (A-F), we demonstrate an effective method for the catalytic acceptorless dehydrogenation (CAD) reaction of secondary benzylic alcohols to produce the corresponding ketones and molecular hydrogen (H).

Pre- and post-synaptic modulation by GABA receptors of rat neuroendocrine dopamine neurones.

The secretion of prolactin from the pituitary is negatively controlled by tuberoinfundibular dopamine (TIDA) neurones. The electrical properties of TIDA cells have recently been identified as a modulatory target of neurotransmitters and hormones in the lactotrophic axis. The role of the GABA receptor in this control has received little attention, yet is of particular interest because it may act as a TIDA neurone autoreceptor.

Charting a Path toward Aggression.

Hypothalamic stimulation can elicit complex behaviors such as aggression, but how discrete motor components of such behaviors are organized at the circuit level remains largely unknown. In this issue of Neuron, Falkner et al. (2020) find that complex neural representations get transformed into a simplified action signal along a hypothalamic-midbrain pathway.

Network oscillation rules imposed by species-specific electrical coupling.

Electrical junctions are widespread within the mammalian CNS. Yet, their role in organizing neuronal ensemble activity remains incompletely understood. Here, in a functionally well-characterized system - neuroendocrine tuberoinfundibular dopamine (TIDA) neurons - we demonstrate a striking species difference in network behavior: rat TIDA cells discharge in highly stereotyped, robust, synchronized slow oscillations, whereas mouse oscillations are faster, flexible and show substantial cell-to-cell variability.

Hypocretin/Orexin Peptides Excite Rat Neuroendocrine Dopamine Neurons through Orexin 2 Receptor-Mediated Activation of a Mixed Cation Current.

Hypocretin/Orexin (H/O) neurons of the lateral hypothalamus are compelling modulator candidates for the chronobiology of neuroendocrine output and, as a consequence, hormone release from the anterior pituitary. Here we investigate the effects of H/O peptides upon tuberoinfundibular dopamine (TIDA) neurons - cells which control, via inhibition, the pituitary secretion of prolactin. In whole cell recordings performed in male rat hypothalamic slices, application of H/O-A, as well as H/O-B, excited oscillating TIDA neurons, inducing a reversible depolarising switch from phasic to tonic discharge.

Serotonin and Antidepressant SSRIs Inhibit Rat Neuroendocrine Dopamine Neurons: Parallel Actions in the Lactotrophic Axis.

Unlabelled: Selective serotonin reuptake inhibitors (SSRIs) are commonly prescribed for depression, but sexual side effects often compromise compliance. These reproductive dysfunctions are likely mediated by elevations of the hormone prolactin. Yet, how serotonin (5-HT) and SSRIs cause changes in prolactin secretion is not known.

Deficient Wnt signalling triggers striatal synaptic degeneration and impaired motor behaviour in adult mice.

Synapse degeneration is an early and invariant feature of neurodegenerative diseases. Indeed, synapse loss occurs prior to neuronal degeneration and correlates with the symptom severity of these diseases. However, the molecular mechanisms that trigger synaptic loss remain poorly understood.

The Subthalamic Nucleus becomes a Generator of Bursts in the Dopamine-Depleted State. Its High Frequency Stimulation Dramatically Weakens Transmission to the Globus Pallidus.

Excessive burst firing in the dopamine-depleted basal ganglia correlates with severe motor symptoms of Parkinson's disease that are attenuated by high frequency electrical stimulation of the subthalamic nucleus (STN). Here we test the hypothesis that pathological bursts in dopamine-deprived basal ganglia are generated within the STN and transmitted to globus pallidus neurons. To answer this question we recorded excitatory synaptic currents and potentials from subthalamic and pallidal neurons in the basal ganglia slice (BGS) from dopamine-depleted mice while continuously blocking GABA(A) receptors.

Subthalamic nucleus evokes similar long lasting glutamatergic excitations in pallidal, entopeduncular and nigral neurons in the basal ganglia slice.

The subthalamic nucleus (STN) modulates the activity of globus pallidus (GP), entopeduncular nucleus (EP) and substantia nigra pars reticulata (SNr) neurons via its direct glutamatergic projections. To investigate the mechanism by which STN affects activity in these structures and whether STN induced activity is comparable among STN target neurons, we performed patch clamp recordings in a tilted, parasagittal, basal ganglia slice (BGS) that preserves these functional connections. We report that single, brief stimulation of the STN generates a brief monosynaptic AMPA-mediated excitatory postsynaptic current (EPSC) in GP, EP and SNr neurons.

A mouse juvenile or adult slice with preserved functional nigro-striatal dopaminergic neurons.

The effect of endogenous dopamine on the activity of target neurons recorded with patch clamp or Ca2+ imaging techniques in slices has been studied to date with intra-striatal stimuli. Yet, this approach is severely handicapped by the nonphysiological and nonspecific stimulation of local neurons and fibers within the striatum. We now report a new juvenile and adult mouse slice preparation in which a component of the nigro-striatal dopaminergic pathway is preserved in its entirety, from cell bodies to axon terminals.

Latest view on the mechanism of action of deep brain stimulation.

How does deep brain stimulation (DBS) applied at high frequency (100 Hz and above, HFS) in diverse points of cortico-basal ganglia thalamo-cortical loops alleviate symptoms of neurological disorders such as Parkinson's disease, dystonia, and obsessive compulsive disorders? Do the effects of HFS stem solely or even largely from local effects on the stimulated brain structure or are they also mediated by actions of HFS on distal structures? Indeed, HFS as an extracellular stimulation is expected to activate subsets of both afferent and efferent axons, leading to antidromic spikes that collide with ongoing spontaneous ones and orthodromic spikes that evoke synaptic responses in target neurons. The present review suggests that HFS interfere with spontaneous pathological patterns by introducing a regular activity in several nodal points of the network. Therefore, the best site of implantation of the HFS electrode may be in a region where the HFS-driven activity spreads to most of the identified, dysrhythmic, neuronal populations without causing additional side effects.

Prostaglandin E1 inhibits calcium-dependent potentials in mammalian sympathetic neurons.

Prostaglandin E1 (PGE1, 10-500 nM) reversibly depressed 3 types of calcium-dependent potentials associated with the spike potential of rabbit superior cervical ganglion cells, namely, the spike after-hyperpolarization, the post-tetanic hyperpolarization, and the Ca2+ spike evoked in a Na+-free/high Ca2+ solution. The results suggest that PGE1 reduces Ca conductance and that this action may underlie its inhibitory action on transmitter release at adrenergic and cholinergic nerve terminals.