Defensive conditioning inHelix lucorum and associated changes in command neuron activity

1983 ◽  
Vol 13 (3) ◽  
pp. 209-215 ◽  
Author(s):  
O. A. Maksimova
Keyword(s):  
Command Neuron ◽  
Neuron Activity ◽  
Defensive Conditioning

Control of Cricket Stridulation by a Command Neuron: Efficacy Depends on the Behavioral State

2000 ◽  
Vol 83 (2) ◽  
pp. 712-722 ◽  
Author(s):  
Berthold Hedwig
Keyword(s):  
Repetition Rate ◽  
Maximum Activity ◽  
Spike Frequency ◽  
Command Neuron ◽  
Calling Song ◽  
Neuron Activity ◽  
High Positive Correlation ◽  
Syllable Repetition ◽  
The Brain ◽  
Interneuron Activity

Crickets use different song patterns for acoustic communication. The stridulatory pattern-generating networks are housed within the thoracic ganglia but are controlled by the brain. This descending control of stridulation was identified by intracellular recordings and stainings of brain neurons. Its impact on the generation of calling song was analyzed both in resting and stridulating crickets and during cercal wind stimulation, which impaired the stridulatory movements and caused transient silencing reactions. A descending interneuron in the brain serves as a command neuron for calling-song stridulation. The neuron has a dorsal soma position, anterior dendritic processes, and an axon that descends in the contralateral connective. The neuron is present in each side of the CNS. It is not activated in resting crickets. Intracellular depolarization of the interneuron so that its spike frequency is increased to 60–80 spikes/s reliably elicits calling-song stridulation. The spike frequency is modulated slightly in the chirp cycle with the maximum activity in phase with each chirp. There is a high positive correlation between the chirp repetition rate and the interneuron's spike frequency. Only a very weak correlation, however, exists between the syllable repetition rate and the interneuron activity. The effectiveness of the command neuron depends on the activity state of the cricket. In resting crickets, experimentally evoked short bursts of action potentials elicit only incomplete calling-song chirps. In crickets that previously had stridulated during the experiment, short elicitation of interneuron activity can trigger sustained calling songs during which the interneuron exhibits a spike frequency of ∼30 spikes/s. During sustained calling songs, the command neuron activity is necessary to maintain the stridulatory behavior. Inhibition of the interneuron stops stridulation. A transient increase in the spike frequency of the interneuron speeds up the chirp rate and thereby resets the timing of the chirp pattern generator. The interneuron also is excited by cercal wind stimulation. Cercal wind stimulation can impair the pattern of chirp and syllable generation, but these changes are not reflected in the discharge pattern of the command neuron. During wind-evoked silencing reactions, the activity of the calling-song command neuron remains unchanged, but under these conditions, its activity is no longer sufficient to maintain stridulation. Therefore stridulation can be suppressed by cercal inputs from the terminal ganglia without directly inhibiting the descending command activity.

scholarly journals Orexin receptor antagonists reverse aberrant dopamine neuron activity and related behaviors in a rodent model of stress-induced psychosis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hannah B. Elam ◽  
Stephanie M. Perez ◽  
Jennifer J. Donegan ◽  
Daniel J. Lodge
Keyword(s):  
United States ◽  
Sensorimotor Gating ◽  
The United States ◽  
Dopamine Neuron ◽  
Neuron Activity ◽  
Sprague Dawley ◽  
Post Traumatic Stress ◽  
Neuron Population ◽  
Population Activity ◽  
Novel Approach

AbstractPost-traumatic stress disorder (PTSD) is a prevalent condition affecting approximately 8% of the United States population and 20% of United States combat veterans. In addition to core symptoms of the disorder, up to 64% of individuals diagnosed with PTSD experience comorbid psychosis. Previous research has demonstrated a positive correlation between symptoms of psychosis and increases in dopamine transmission. We have recently demonstrated projections from the paraventricular nucleus of the thalamus (PVT) to the nucleus accumbens (NAc) can regulate dopamine neuron activity in the ventral tegmental area (VTA). Specifically, inactivation of the PVT leads to a reversal of aberrant dopamine system function and psychosis-like behavior. The PVT receives dense innervation from orexin containing neurons, therefore, targeting orexin receptors may be a novel approach to restore dopamine neuron activity and alleviate PTSD-associated psychosis. In this study, we induced stress-related pathophysiology in male Sprague Dawley rats using an inescapable foot-shock procedure. We observed a significant increase in VTA dopamine neuron population activity, deficits in sensorimotor gating, and hyperresponsivity to psychomotor stimulants. Administration of selective orexin 1 receptor (OX1R) and orexin 2 receptor (OX2R) antagonists (SB334867 and EMPA, respectively) or the FDA-approved, dual-orexin receptor antagonist, Suvorexant, were found to reverse stress-induced increases in dopamine neuron population activity. However, only Suvorexant and SB334867 were able to reverse deficits in behavioral corelates of psychosis. These results suggest that the orexin system may be a novel pharmacological target for the treatment of comorbid psychosis related to PTSD.

scholarly journals Evidence accumulation relates to perceptual consciousness and monitoring

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Michael Pereira ◽  
Pierre Megevand ◽  
Mi Xue Tan ◽  
Wenwen Chang ◽  
Shuo Wang ◽  
...  
Keyword(s):  
Posterior Parietal Cortex ◽  
Detection Threshold ◽  
Task Demands ◽  
Neuron Activity ◽  
Neural Responses ◽  
Neuronal Responses ◽  
Neural Basis ◽  
Perceptual Consciousness ◽  
Evidence Accumulation ◽  
Posterior Parietal

AbstractA fundamental scientific question concerns the neural basis of perceptual consciousness and perceptual monitoring resulting from the processing of sensory events. Although recent studies identified neurons reflecting stimulus visibility, their functional role remains unknown. Here, we show that perceptual consciousness and monitoring involve evidence accumulation. We recorded single-neuron activity in a participant with a microelectrode in the posterior parietal cortex, while they detected vibrotactile stimuli around detection threshold and provided confidence estimates. We find that detected stimuli elicited neuronal responses resembling evidence accumulation during decision-making, irrespective of motor confounds or task demands. We generalize these findings in healthy volunteers using electroencephalography. Behavioral and neural responses are reproduced with a computational model considering a stimulus as detected if accumulated evidence reaches a bound, and confidence as the distance between maximal evidence and that bound. We conclude that gradual changes in neuronal dynamics during evidence accumulation relates to perceptual consciousness and perceptual monitoring in humans.

scholarly journals Changes in Prefrontal Cortex–Thalamic Circuitry after Acoustic Trauma

Biomedicines ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 77
Author(s):  
Kristin M. Barry ◽  
Donald Robertson ◽  
Wilhelmina H. A. M. Mulders
Keyword(s):  
Electrical Stimulation ◽  
Prefrontal Cortex ◽  
Auditory System ◽  
Acoustic Trauma ◽  
Neuron Activity ◽  
Compensatory Mechanism ◽  
Efferent Connections ◽  
Medial Geniculate ◽  
Central Auditory Pathways ◽  
Stimulation Of

In the adult auditory system, loss of input resulting from peripheral deafferentation is well known to lead to plasticity in the central nervous system, manifested as reorganization of cortical maps and altered activity throughout the central auditory pathways. The auditory system also has strong afferent and efferent connections with cortico-limbic circuitry including the prefrontal cortex and the question arises whether this circuitry is also affected by loss of peripheral input. Recent studies in our laboratory showed that PFC activation can modulate activity of the auditory thalamus or medial geniculate nucleus (MGN) in normal hearing rats. In addition, we have shown in rats that cochlear trauma resulted in altered spontaneous burst firing in MGN. However, whether the PFC influence on MGN is changed after cochlear trauma is unknown. We investigated the effects of electrical stimulation of PFC on single neuron activity in the MGN in anaesthetized Wistar rats 2 weeks after acoustic trauma or sham surgery. Electrical stimulation of PFC showed a variety of effects in MGN neurons both in sham and acoustic trauma groups but inhibitory responses were significantly larger in the acoustic trauma animals. These results suggest an alteration in functional connectivity between PFC and MGN after cochlear trauma. This change may be a compensatory mechanism increasing sensory gating after the development of altered spontaneous activity in MGN, to prevent altered activity reaching the cortex and conscious perception.

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