European Journal of Neuroscience. Jun2018, Vol. 47 Issue 12, p1482-1503. 22p. 1 Diagram, 1 Chart, 13 Graphs.
RETICULAR formation, NEURONS, SLEEP-wake cycle, WAKEFULNESS, SLOW wave sleep, and RAPID eye movement sleep
Abstract: The medullary reticular formation (RF) is involved in the maintenance of several vital physiological functions and level of vigilance. In this study, in nonanesthetised, head‐fixed mice, I examined the role of medullary RF neurons in the control of sleep‐wake states, that is, wakefulness (W), slow‐wave sleep (SWS) and paradoxical (or rapid eye movement) sleep (PS). I showed, for the first time, that the mouse medullary RF contains presumed SWS‐promoting, SWS‐on neurons that remain silent during W, display a sharp increase in discharge rate at sleep onset, and discharge tonically and selectively during SWS. In addition, I showed the presence in the medullary RF of both PS‐on and PS‐off neurons, which, respectively, commence discharging or cease firing selectively just prior to, and during, PS. PS‐off neurons were located in the raphe nuclei and ventral medulla, while PS‐on neurons were found in both the lateral part of the ventral gigantocellular reticular nucleus and the raphe nuclei, as were SWS‐on neurons. PS‐off and SWS‐on neurons appear to play an important role in both the W‐SWS and SWS‐PS switches, while PS‐on and PS‐off neurons play an important role in the PS‐W switch. The present findings on the trends in spike activity at the transitions from SWS to PS and from PS to W are in line with the reciprocal interaction hypothesis according to which PS occurs as a result of the cessation of discharge of PS‐off neurons, while PS ends as a result of the start of discharge of PS‐off neurons. [ABSTRACT FROM AUTHOR]
European Journal of Neuroscience. May2018, Vol. 47 Issue 9, p1110-1126. 17p. 1 Black and White Photograph, 1 Chart, 12 Graphs.
SLEEP-wake cycle, NEURONS, CIRCADIAN rhythms, WAKEFULNESS, and SLEEP interruptions
Abstract: A total of 668 single units were recorded in the mouse periaqueductal gray (PAG) and adjacent deep mesencephalic nucleus (DpMe) to determine their role in the switching of sleep–wake states, that is, wakefulness (W), slow‐wave sleep (SWS) and paradoxical (or rapid eye movement) sleep (PS) in general, and, in particular, to determine whether PS‐on and PS‐off neurons involved in PS state switching are present in these structures and to identify neuronal substrates for the SWS‐PS switching mediated by DpMe neurons. Both structures were found to contain similar percentages of W/PS‐active neurons, which discharge at a higher rate during W and PS than during SWS, while W‐active neurons, which discharge maximally during W, were found mainly in the PAG. Both also contained similar percentages of SWS/PS‐active neurons, which discharge at higher rates during SWS and PS than during W, and PS‐active neurons, which discharge maximally during PS, while SWS‐active neurons, which discharge maximally during SWS, were found almost exclusively in the PAG. Both structures contained virtually no PS‐on or PS‐off neurons, which, respectively, discharge or cease firing selectively and tonically just prior to, and during, PS. Unlike the PAG, the DpMe contained many SWS/PS‐on neurons, which discharge selectively at high rates during SWS and PS, but show a decrease in discharge rate at the transition from SWS to PS. Analysis of discharge profiles and trends in spike activity at the state transitions strongly suggests that PAG and DpMe neurons play an important role in the W‐SWS, SWS‐PS and/or PS‐W switches. [ABSTRACT FROM AUTHOR]
Kosmidis, Efstratios K., Contoyiannis, Yiannis F., Papatheodoropoulos, Costas, and Diakonos, Fotios K.
European Journal of Neuroscience. Sep2018, Vol. 48 Issue 6, p2343-2353. 11p. 6 Graphs.
MEMBRANE potential, PYRAMIDAL neurons, HIPPOCAMPUS (Brain), NEURAL circuitry, HUMAN information processing, EXCITATION (Physiology), and NEURAL networks (Neurobiology)
Abstract: Evidence that neural circuits are operating near criticality has been provided at various levels of brain organisation with a presumed role in maximising information processing and multiscale activity association. Criticality has been linked to excitation at both the single‐cell and network levels, as action potential generation marks an obvious phase transition from a resting to an excitable state. Using in vitro intracellular recordings, we examine irregular, small amplitude membrane potential fluctuations from CA1 pyramidal neurons of Wistar male rats. We show that these fluctuations, confounded with noise, carry information relevant to the neuronal state. The underlying dynamics exhibit intermittent characteristics shown to describe the temporal fluctuations of the order parameter of a macroscopic system at its critical point even in the absence of firing. An externally applied stimulus serves as the control parameter, driving the system in and out of its critical state. Based on our experimental observations we calculate the equivalent of the isothermal critical exponent δh finding a value which depends on the applied stimulus. For each neuron there is a stimulus amplitude for which the critical behaviour becomes most pronounced. The corresponding mean value of δh in the considered ensemble of neurons is δh ≈ 1.89, close to theoretical predictions for critical networks. Finally, we show that the firing rate of a neuron decreases exponentially with δh. [ABSTRACT FROM AUTHOR]
Wyrofsky, Ryan R., Reyes, Beverly A. S., Yu, Daohai, Kirby, Lynn G., and Van Bockstaele, Elisabeth J.
European Journal of Neuroscience. Sep2018, Vol. 48 Issue 5, p2118-2138. 21p. 1 Color Photograph, 1 Black and White Photograph, 2 Illustrations, 1 Diagram, 1 Chart, 3 Graphs.
CANNABINOIDS, NORADRENERGIC neurons, NORADRENALINE, PREFRONTAL cortex, and MENTAL illness
Abstract: Cannabinoids are capable of modulating mood, arousal, cognition and behavior, in part via their effects on the noradrenergic nucleus locus coeruleus (LC). Dysregulation of LC signaling and norepinephrine (NE) efflux in the medial prefrontal cortex (mPFC) can lead to the development of psychiatric disorders, and CB1r deletion results in alterations of α2‐ and β1‐adrenoceptors in the mPFC, suggestive of increased LC activity. To determine how CB1r deletion alters LC signaling, whole‐cell patch‐clamp electrophysiology was conducted in LC‐NE neurons of male and female wild type (WT) and CB1r‐knock out (KO) mice. CB1r deletion caused a significant increase in LC‐NE excitability and input resistance in male but not female mice when compared to WT. CB1r deletion also caused adaptations in several indices of noradrenergic function. CB1r/CB2r‐KO male mice had a significant increase in cortical NE levels and tyrosine hydroxylase and CRF levels in the LC compared to WT males. CB1r/CB2r‐KO female mice showed a significant increase in LC α2‐AR levels compared to WT females. To further probe actions of the endocannabinoid system as an anti‐stress neuromediator, the effect of CB1r deletion on CRF‐induced responses in the LC was investigated. The increase in LC‐NE excitability observed in male and female WT mice following CRF (300 nM) bath application was not observed in CB1r‐KO mice. These results indicate that cellular adaptations following CB1r deletion cause a disruption in LC‐NE signaling in males but not females, suggesting underlying sex differences in compensatory mechanisms in KO mice as well as basal endocannabinoid regulation of LC‐NE activity. [ABSTRACT FROM AUTHOR]
Cunha, Alexandra Olimpio Siqueira, Ceballos, Cesar Celis, de Deus, Junia Lara, and Leão, Ricardo Maurício
European Journal of Neuroscience. Jun2018, Vol. 47 Issue 11, p1401-1413. 13p. 1 Chart, 6 Graphs.
PYRAMIDAL neurons, NEURONS, NEURAL transmission, ACOUSTIC stimulation, and NEUROSCIENCES
Abstract: Afferent neurotransmission to hippocampal pyramidal cells can lead to long‐term changes to their intrinsic membrane properties and affect many ion currents. One of the most plastic neuronal currents is the hyperpolarization‐activated cationic current (Ih), which changes in CA1 pyramidal cells in response to many types of physiological and pathological processes, including auditory stimulation. Recently, we demonstrated that long‐term potentiation (LTP) in rat hippocampal Schaffer‐CA1 synapses is depressed by high‐intensity sound stimulation. Here, we investigated whether a long‐term high‐intensity sound stimulation could affect intrinsic membrane properties of rat CA1 pyramidal neurons. Our results showed that Ih is depressed by long‐term high‐intensity sound exposure (1 min of 110 dB sound, applied two times per day for 10 days). This resulted in a decreased resting membrane potential, increased membrane input resistance and time constant, and decreased action potential threshold. In addition, CA1 pyramidal neurons from sound‐exposed animals fired more action potentials than neurons from control animals; however, this effect was not caused by a decreased Ih. On the other hand, a single episode (1 min) of 110 dB sound stimulation which also inhibits hippocampal LTP did not affect Ih and firing in pyramidal neurons, suggesting that effects on Ih are long‐term responses to high‐intensity sound exposure. Our results show that prolonged exposure to high‐intensity sound affects intrinsic membrane properties of hippocampal pyramidal neurons, mainly by decreasing the amplitude of Ih. [ABSTRACT FROM AUTHOR]
Polter, Abigail M., Barcomb, Kelsey, Tsuda, Ayumi C., and Kauer, Julie A.
European Journal of Neuroscience. May2018, Vol. 47 Issue 10, p1208-1218. 11p. 2 Diagrams, 4 Graphs.
DOPAMINERGIC neurons, MATERIAL plasticity, GABAERGIC neurons, INTERNEURONS, and OPTOGENETICS
Abstract: Ventral tegmental area (VTA) dopaminergic neurons are key components of the reward pathway, and their activity is powerfully controlled by a diverse array of inhibitory GABAergic inputs. Two major sources of GABAergic nerve terminals within the VTA are local VTA interneurons and neurons in the rostromedial tegmental nucleus (RMTg). Here, using optogenetics, we compared synaptic properties of GABAergic synapses on VTA dopamine neurons using selective activation of afferents that originate from these two cell populations. We found little evidence of co‐release of glutamate from either input, but RMTg‐originating synaptic currents were reduced by strychnine, suggesting co‐release of glycine and GABA. VTA‐originating synapses displayed a lower initial release probability, and at higher frequency stimulation, short‐term depression was more marked in VTA‐ but not RMTg‐originating synapses. We previously reported that nitric oxide (NO)‐induced potentiation of GABAergic synapses on VTA dopaminergic cells is lost after exposure to drugs of abuse or acute stress; in these experiments, multiple GABAergic afferents were simultaneously activated by electrical stimulation. Here we found that optogenetically‐activated VTA‐originating synapses on presumptive dopamine neurons also exhibited NO‐induced potentiation, whereas RMTg‐originating synapses did not. Despite providing a robust inhibitory input to the VTA, RMTg GABAergic synapses are most likely not those previously shown by our work to be persistently altered by addictive drugs and stress. Our work emphasises the idea that dopamine neuron excitability is controlled by diverse inhibitory inputs expected to exert varying degrees of inhibition and to participate differently in a range of behaviours. [ABSTRACT FROM AUTHOR]