scholarly journals Circuit and synaptic organization of forebrain-to-midbrain pathways that promote and suppress vocalization

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Valerie Michael ◽  
Jack Goffinet ◽  
John Pearson ◽  
Fan Wang ◽  
Katherine Tschida ◽  
...  
Keyword(s):  
Preoptic Area ◽  
Brain Slices ◽  
Social Cues ◽  
Ultrasonic Vocalizations ◽  
Behavioral Effects ◽  
Inhibitory Neurons ◽  
Boundary Zone ◽  
Synaptic Organization ◽  
Two Populations ◽  
Synaptic Mechanisms

Animals vocalize only in certain behavioral contexts, but the circuits and synapses through which forebrain neurons trigger or suppress vocalization remain unknown. Here, we used transsynaptic tracing to identify two populations of inhibitory neurons that lie upstream of neurons in the periaqueductal gray (PAG) that gate the production of ultrasonic vocalizations (USVs) in mice (i.e. PAG-USV neurons). Activating PAG-projecting neurons in the preoptic area of the hypothalamus (POAPAG neurons) elicited USV production in the absence of social cues. In contrast, activating PAG-projecting neurons in the central-medial boundary zone of the amygdala (AmgC/M-PAG neurons) transiently suppressed USV production without disrupting non-vocal social behavior. Optogenetics-assisted circuit mapping in brain slices revealed that POAPAG neurons directly inhibit PAG interneurons, which in turn inhibit PAG-USV neurons, whereas AmgC/M-PAG neurons directly inhibit PAG-USV neurons. These experiments identify two major forebrain inputs to the PAG that trigger and suppress vocalization, respectively, while also establishing the synaptic mechanisms through which these neurons exert opposing behavioral effects.

scholarly journals Circuit and synaptic organization of forebrain-to-midbrain pathways that promote and suppress vocalization

2019 ◽  
Author(s):  
Valerie Michael ◽  
Jack Goffinet ◽  
John Pearson ◽  
Fan Wang ◽  
Katherine Tschida ◽  
...  
Keyword(s):  
Social Behavior ◽  
Brain Slices ◽  
Social Cues ◽  
Ultrasonic Vocalizations ◽  
Behavioral Effects ◽  
Inhibitory Neurons ◽  
Boundary Zone ◽  
Synaptic Organization ◽  
Two Populations ◽  
Synaptic Mechanisms

AbstractAnimals vocalize only in certain behavioral contexts, but the circuits and synapses through which forebrain neurons trigger or suppress vocalization remain unknown. Here we used transsynaptic tracing to identify two populations of inhibitory neurons that lie upstream of neurons in the periaqueductal gray that gate the production of ultrasonic vocalizations in mice (i.e., PAG-USV neurons). Activating PAG-projecting neurons in the preoptic hypothalamus (POAPAG neurons) elicited USV production in the absence of social cues. In contrast, activating PAG-projecting neurons in the central-medial boundary zone of the amygdala (AmgC/M-PAG neurons) transiently suppressed USV production without disrupting non-vocal social behavior. Optogenetics-assisted circuit mapping in brain slices revealed that POAPAG neurons directly inhibit PAG interneurons, which in turn inhibit PAG-USV neurons, whereas AmgC/M-PAG neurons directly inhibit PAG-USV neurons. These experiments identify two major forebrain inputs to the PAG that trigger and suppress vocalization, respectively, while also establishing the synaptic mechanisms through which these neurons exert opposing behavioral effects.

Behavioral effects of 3a-androstanediol II: Hypothalamic and preoptic area actions via a GABAergic mechanism

1996 ◽  
Vol 79 (1-2) ◽  
pp. 119-130 ◽  
Author(s):  
Cheryl A. Frye ◽  
Jennifer E. Duncan ◽  
Mark Basham ◽  
Mary S. Erskine
Keyword(s):  
Preoptic Area ◽  
Behavioral Effects

Synaptic Mechanisms of Thiopental-induced Alterations in Synchronized Cortical Activity

1996 ◽  
Vol 84 (6) ◽  
pp. 1425-1434 ◽  
Author(s):  
Heath S. Lukatch ◽  
Bruce M. MacIver
Keyword(s):  
Brain Slices ◽  
Afferent Input ◽  
Burst Suppression ◽  
Dependent Manner ◽  
Gamma Aminobutyric Acid ◽  
Patch Clamps ◽  
Concentration Dependent Manner ◽  
Direct Acting ◽  
Synaptic Mechanisms

Background Anesthetic depth after barbiturate administration has been correlated with distinct electroencephalogram (EEG) patterns. The current study used a rat neocortical brain slice micro-EEG preparation to investigate synaptic mechanisms underlying thiopental-induced transitions in synchronized neuronal activity. Methods Concentration-dependent cellular actions of thiopental were investigated in brain slices using specific pharmacologic probes, whole cell patch clamps, and extracellular field recordings. Theta-Like micro-EEG oscillations were elicited in neocortical slices by mimicking subcortical cholinergic and gamma-aminobutyric acid (GABA) afferent input with carbachol (100 microM), a cholinergic agonist, and bicuculline (10 microM) a GABAA antagonist. Results In the presence of 20 microM thiopental, micro-EEG slowing from theta (7.3 +/- 0.9 Hz, mean +/- SD, n = 19) to delta frequencies (2.5 +/- 0.5 Hz, n = 11) was associated with a threefold prolongation of inhibitory currents. Burst suppression activity occurred at 50 microM thiopental, and appeared to result from direct activation of GABAA-gated chloride currents, observed with voltage clamp recordings, and mimicked with a direct acting GABAA agonist, muscimol (1 microM). Isoelectric activity occurred at 100 microM thiopental, and likely resulted from reduced glutamatergic transmission, evidenced by depressed excitatory postsynaptic potentials. Glutamatergic excitation was required for burst suppression activity, because glutamate receptor antagonists blocked thiopental-induced bursts; forcing a transition to isoelectric activity. Conclusions Thiopental produced a continuum of EEG-like states in brain slices similar to those observed in vivo. The progression of thiopental-induced effects appear to have resulted from specific cellular actions that were recruited in a concentration-dependent manner. Progressive enhancement of synaptic inhibition followed by depression of excitatory transmission led to micro-EEG frequency slowing, burst suppression, and isoelectric activity.

scholarly journals SOCIAL INFORMATION AND BIOLOGICAL INVASIONS: CHORUS SONGS ARE MORE ATTRACTIVE TO EUROPEAN STARLINGS IN MORE RECENTLY ESTABLISHED POPULATIONS.

2021 ◽  
Author(s):  
Alexandra Rodriguez ◽  
Martine Hausberger ◽  
Laurence Henri ◽  
Philippe Clergeau
Keyword(s):  
Biological Invasions ◽  
Social Information ◽  
Acoustic Stimulus ◽  
Social Cues ◽  
Habitat Characteristics ◽  
European Starlings ◽  
Breeding Sites ◽  
Social Species ◽  
Long Time ◽  
Two Populations

When biological invasions by animals occur, the individuals arriving in novel environments can be confronted with unpredictable or unfamiliar resources and may need social interaction to improve survival in the newly colonized areas. Gathering with conspecifics and using social information about their activities may reveal the location of suitable feeding and breeding sites. This could compensate for the absence of individual information about new habitats and constitute an advantage for new settlers. If a tendency to gather in response to social stimuli is transmitted from one generation to the next, and if the benefit of gathering is lower in long time established populations, there should be behavioural differences in receptivity to social cues in populations with different colonizing histories. We hypothesized that individuals of a social species like the European starling from relatively recently-established populations would be more responsive to social cues than individuals belonging to long-established populations. We conducted playback experiments using a starling chorus to test its acoustic attractiveness to populations of starlings with different colonizing histories. We compared the reaction of individuals from two populations in rural Brittany, western France, established for a long time, with three more recently settled ones: two populations from a propagation front in southern Italy and one urban population from Rennes city in Brittany. Our data supported our hypothesis: individuals from more recent populations were more responsive to the acoustic stimulus, and gave more calls in flight than individuals from populations with an older settlement history. We discuss the different behavioural responses we observed in the different populations and the potential effects of habitat characteristics and starling densities.

scholarly journals MeCP2 Is Required for Normal Development of GABAergic Circuits in the Thalamus

2010 ◽  
Vol 103 (5) ◽  
pp. 2470-2481 ◽  
Author(s):  
Zhong-Wei Zhang ◽  
Joseph D. Zak ◽  
Hong Liu
Keyword(s):  
Neurodevelopmental Disorder ◽  
Brain Slices ◽  
Inhibitory Neurons ◽  
Gene Encoding ◽  
Vertebrate Brain ◽  
Gabaergic Synapses ◽  
And Function ◽  
Kinetics Of ◽  
Whole Cell Recordings

Methyl-CpG binding protein 2 (MeCP2) is highly expressed in neurons in the vertebrate brain, and mutations of the gene encoding MeCP2 cause the neurodevelopmental disorder Rett syndrome. This study examines the role of MeCP2 in the development and function of thalamic GABAergic circuits. Whole cell recordings were carried out in excitatory neurons of the ventrobasal complex (VB) of the thalamus and in inhibitory neurons of the reticular thalamic nucleus (RTN) in acute brain slices from mice aged P6 through P23. At P14–P16, the number of quantal GABAergic events was decreased in VB neurons but increased in RTN neurons of Mecp2-null mice, without any change in the amplitude or kinetics of quantal events. There was no difference between mutant and wild-type mice in paired-pulse ratios of evoked GABAergic responses in the VB or the RTN. On the other hand, unitary responses evoked by minimal stimulation were decreased in the VB but increased in the RTN of mutants. Similar changes in the frequency of quantal events were observed at P21–P23 in both the VB and RTN. At P6, however, quantal GABAergic transmission was altered only in the VB not the RTN. Immunostaining of vesicular GABA transporter showed opposite changes in the number of GABAergic synaptic terminals in the VB and RTN of Mecp2-null mice at P18–P20. The loss of MeCP2 had no significant effect on intrinsic properties of RTN neurons recorded at P15–P17. Our findings suggest that MeCP2 differentially regulates the development of GABAergic synapses in excitatory and inhibitory neurons in the thalamus.

Astrocytic iNOS-Dependent Enhancement of Synaptic Release in Mouse Neocortex

2010 ◽  
Vol 103 (3) ◽  
pp. 1322-1328 ◽  
Author(s):  
Yossi Buskila ◽  
Yael Amitai
Keyword(s):  
Pyramidal Neurons ◽  
Brain Slices ◽  
Selective Inhibition ◽  
Inhibitory Neurons ◽  
Small Subset ◽  
Excitatory Synapses ◽  
Brain Areas ◽  
Synaptic Release ◽  
Cellular Source ◽  
Inos Inhibition

Nitric oxide (NO) has been recognized as an atypical neuronal messenger affecting synaptic transmission, but its cellular source has remained unresolved as the neuronal NO synthase isoform (nNOS) in brain areas such as the neocortex is expressed only by a small subset of inhibitory neurons. The involvement of the glial NOS isoform (iNOS) in modulating neuronal activity has been largely ignored because it has been accepted that this enzyme is regulated by gene induction following detrimental stimuli. Using acute brain slices from mouse neocortex and electrophysiology, we found that selective inhibition of iNOS reduced both spontaneous and evoked synaptic release. Moreover, iNOS inhibition partially prevented and reversed the potentiation of excitatory synapses in layer 2/3 pyramidal neurons. NOS enzymatic assay confirmed a small but reliable Ca2+-independent activity fraction, consistent with the existence of functioning iNOS in the tissue. Together these data point to astrocytes as a source for the nitrosative regulation of synaptic release in the neocortex.

066 Noradrenaline and acetylcholine inhibit sleep-promoting neurons of ventrolateral preoptic area through a local GABAergic circuit

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A27-A28
Author(s):  
Roberto De Luca ◽  
Stefano Nardone ◽  
Lin Zhu ◽  
Elda Arrigoni
Keyword(s):  
Muscarinic Receptors ◽  
Inhibitory Action ◽  
Preoptic Area ◽  
Brain Slices ◽  
Inhibitory Effect ◽  
Gabaergic Neurons ◽  
Optogenetic Stimulation ◽  
Direct Inhibitory Effect ◽  
Afferent Inputs ◽  
Stimulation Of

Abstract Introduction The ventrolateral preoptic (VLPO) nucleus is a key area involved in the initiation and maintenance of sleep. During wakefulness, sleep-promoting galanin neurons in the VLPO are directly inhibited by arousal signals including noradrenaline and acetylcholine. We have found that while these neurotransmitters directly inhibit VLPO galanin neurons, they also activate GABAergic neurons in the VLPO that do not express galanin. We propose that when activated by monoaminergic and cholinergic inputs, these local VLPO GABAergic neurons provide an additional inhibition of the VLPO galanin sleep-promoting neurons. We tested this model in brain slices in mice. Methods We studied VLPO galanin neurons in mouse brain slices using patch-clamp recordings. We recorded from fluorescently labeled VLPO galanin neurons following the injection of a cre-dependent AAV encoding for mCherry, into the VLPO of Gal-cre mice. For the optogenetic studies we expressed channelrhodopsin-2 (ChR-2) in VLPO VGAT neurons and mCherry in galanin neurons by injecting a flp-dependent and a cre-dependent AAV encoding respectively for ChR2 and mCherry into the VLPO of VGAT-flp::Gal-cre mice. We photo-stimulated local GABAergic neurons and recorded from labeled VLPO galanin neurons. Noradrenaline, carbachol and receptor antagonists were bath-applied. Results Noradrenaline and carbachol inhibited VLPO galanin neurons by alpha-2 and muscarinic receptors and these effects were maintained in the presence of tetrodotoxin (TTX) indicating, as previously proposed, a direct inhibitory effect of noradrenaline and carbachol on VLPO galanin neurons. In addition, both noradrenaline and carbachol increased the frequency of spontaneous inhibitory post-synaptic currents (sIPSCs) of VLPO galanin neurons, suggesting an additional inhibitory action on VLPO galanin neurons. Finally, optogenetic stimulation of local VLPO GABAergic neurons produced short latency, TTX-resistant, opto-evoked IPSCs in VLPO galanin neurons. Both noradrenaline and carbachol increased the amplitude of these opto-evoked IPSCs by the activation of alpha-1 and muscarinic receptors. Conclusion Our results demonstrate that noradrenaline and acetylcholine inhibit VLPO galanin neurons directly and indirectly. Both noradrenaline and acetylcholine increase GABAergic afferent inputs to VLPO galanin neurons by activating local GABAergic neurons. We propose that during wakefulness this feedforward inhibition provides additional inhibition of VLPO galanin sleep-promoting neurons. Support (if any) NS091126 and HL149630

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