Room Temperature Relaxometry of Single Nitrogen Vacancy Centers in Proximity to α-RuCl3 Nanoflakes.

Nitrogen vacancy (NV) center-based magnetometry has been proven to be a versatile sensor for various classes of magnetic materials in broad temperature and frequency ranges. Here, we use the longitudinal relaxation time T1 of single NV centers to investigate the spin dynamics of nanometer-thin flakes of α-RuCl3 at room temperature. We observe a significant reduction in the T1 in the presence of α-RuCl3 in the proximity of NVs, which we attribute to paramagnetic spin noise confined in the 2D hexagonal planes. Furthermore, the T1 time exhibits a monotonic increase with an applied magnetic field. We associate this trend with the alteration of the spin and charge noise in α-RuCl3 under an external magnetic field. These findings suggest that the influence of the spin dynamics of α-RuCl3 on the T1 of the NV center can be used to gain information about the material itself and the technique to be used on other 2D materials.

The development of microfabricated solenoids with magnetic cores for micromagnetic neural stimulation.

Electrical stimulation via invasive microelectrodes is commonly used to treat a wide range of neurological and psychiatric conditions. Despite its remarkable success, the stimulation performance is not sustainable since the electrodes become encapsulated by gliosis due to foreign body reactions. Magnetic stimulation overcomes these limitations by eliminating the need for a metal-electrode contact. Here, we demonstrate a novel microfabricated solenoid inductor (80 µm × 40 µm) with a magnetic core that can activate neuronal tissue. The characterization and proof-of-concept of the device raise the possibility that micromagnetic stimulation solenoids that are small enough to be implanted within the brain may prove to be an effective alternative to existing electrode-based stimulation devices for chronic neural interfacing applications.

Perinatal citalopram does not prevent the effect of prenatal stress on anxiety, depressive-like behaviour and serotonergic transmission in adult rat offspring.

It is still not clear whether the selective serotonin reuptake inhibitors frequently prescribed to depressed pregnant women improve the behavioural outcome in their children. The current study investigated whether administration of citalopram to pregnant rats could prevent anxiety and depressive-like behaviour induced by gestational stress in their offspring, and restore the expression of serotonin 1A autoreceptors in GABAergic interneurons in the medial prefrontal cortex and dorsal raphe nuclei in males, and of corticotropin-releasing factor type 2 receptors in GABAergic interneurons in the dorsal raphe nuclei in females. Activation of these receptors modulates serotonergic transmission to target areas and is reduced in a sex-dependent manner by prenatal stress. Citalopram (10 mg/kg/day), administered orally from day 7 of gestation until 21 days postpartum, prevented the increase in anxiety in stressed mothers but did not reduce anxiety and depressive-like behaviour in their offspring and even induced depressive-like behaviour in the offspring of control mothers. Citalopram failed to restore the reduction in the expression of serotonin 1A autoreceptors in the prefrontal cortex of males and in corticotropin-releasing factor type 2 receptors in the dorsal raphe nuclei of females induced by prenatal stress. Prenatal citalopram did not prevent the behavioural changes or reduction in serotonergic transmission to target areas induced by prenatal stress. It had adverse behavioural effects in the offspring of control rats, which, together with the lack of any change in prenatally-stressed rats, may be due to inhibition of the foetal serotonin transporter thereby preventing normal development of the serotonin system.

Sex dependent reduction by prenatal stress of the expression of 5HT1A receptors in the prefrontal cortex and CRF type 2 receptors in the raphe nucleus in rats: reversal by citalopram.

RATIONALE: Alterations in the serotonergic transmission and activity of corticotropin-releasing factor (CRF) family may underlie anxiety and depressive disorders. These could be corrected by treatment with SSRIs. OBJECTIVES: The objective of the current study is to determine whether the increased anxiety of prenatally stressed (PS) rats of both sexes is associated with changes in 5HT1A and CRF type 2 receptors (5HT1AR and CRFR2) in the prefrontal cortex (PFC)-dorsal raphe nuclei (DRN) axis, and how these are affected by chronic treatment with citalopram (10 mg/kg/day). We focussed on GABAergic cells that co-express parvalbumin and/or neuropeptide Y, and 5HT1AR in the medial prefrontal cortex (mPFC) and on cells that express 5HT, parvalbumin, 5HT1AR or CRFR2 in the DRN. RESULTS: Immunohistochemistry with fluorescent antibodies demonstrated sex differences in the expression of 5HT1AR and CRFR2 protein. Prenatal stress selectively reduced the expression of 5HT1AR on GABAergic cells in the mPFC in males and that of CRFR2 in the DRN of females. Citalopram treatment for 5 weeks abolished the increase in anxiety in both sexes, restored the intensity of expression of 5HT1AR in the mPFC in males and increased their expression in the mPFC and DRN in females. Citalopram reduced CRFR2 expression in control and PS males but increased it in PS females. CONCLUSIONS: Male and female rats show differences in the expression of 5HT1AR and CRFR2 protein that are selectively reduced by prenatal stress. Reversal by citalopram of the changes in the expression of these receptors induced by prenatal stress support their role in the aetiology of anxiety.