The state of mind is influenced by fluctuations in the brain's internal environment, which is composed of various ions, neurotransmitters, and metabolic products within and around brain cells. Blood vessels regulate this brain environment, while astrocytes serve as intermediaries between blood vessels and neurons. To observe astrocytic activity, fluorescent calcium sensor proteins were expressed in astrocytes, and changes in fluorescence were measured. Surprisingly, this approach revealed not only calcium dynamics within astrocytes but also provided insights into intracellular pH and local brain blood volume dynamics. Using this method, we investigated the epileptic brain and the transition to REM sleep, uncovering distinct changes in the brain's internal environment associated with each condition. Manipulating this brain environment holds potential as a novel therapeutic strategy.

Fear triggers several physiological responses, including freezing behavior, increased blood pressure, and changes in heart rate. However, our understanding of the detailed responses and roles of the hippocampal CA1 region, the hypothalamic paraventricular nucleus, and sympathetic nervous activity in fear responses remains unclear. We focused on the context that evokes fear memories and conducted fear conditioning learning by combining the context with a cue. We measured the hippocampal CA1 neuronal activity and the hypothalamic paraventricular nucleus neuronal activity, sympathetic nerve activity, arterial pressure, and heart rate in conscious rats. This review discusses the impact of context on renal and lumbar sympathetic nerve activity, arterial pressure, and heart rate in response to the cue, and the involvement of the hippocampal CA1 region and hypothalamic paraventricular nucleus in these processes.

The gut microbiota, comprising trillions of microorganisms, plays a central role in digestion, metabolism, immune regulation, and the bidirectional communication between the gut and brain, known as the gut–brain axis. Metabolites and neurotransmitters derived from intestinal microbes influence not only local immune system but also act through the vagal nerve and bloodstream to affect central nervous system activity, modulating stress responses, behavior, and systemic immunity. Alterations in the microbiota have been linked to neurological disorders including multiple sclerosis, Parkinson's disease, depression, anxiety, and stroke. Immune mediators such as cytokines interact with neural circuits, shaping neuroinflammation and disease progression. Microbial metabolites such as short-chain fatty acids and tryptophan derivatives regulate microglial maturation, barrier integrity, and neuroprotection. Conversely, microbial components such as lipopolysaccharides activate immune pathways that promote neuroinflammation. Stress-induced hypothalamic–pituitary–adrenal axis activity further links brain regulation to gut immunity. Clinical and experimental studies highlight that dysbiosis contributes to disease mechanisms: reduced butyrate-producing bacteria in multiple sclerosis and Parkinson's disease, vagal transmission of α-synuclein pathology from gut to brain in Parkinson’s models, and associations between mood disorders and inflammatory bowel disease. Stroke is aggravated by post-ischemic dysbiosis, which promotes peripheral T-cell migration into the brain. Therapeutically, fecal microbiota transplantation and vagal nerve stimulation have shown promise in restoring microbiota balance and modulating inflammation. Advances in chemogenetics, optogenetics, and neuromodulation enable precise dissection of gut–brain–immune networks. Targeting microbiota–neuroimmune crosstalk offers potential strategies for preventing and treating neurological and systemic diseases.

Parkinson’s disease exhibits various subtypes throughout the disease course, and the severity of autonomic dysfunction may be associated with more severe motor symptoms. On the other hand, similar to the dorsal nucleus of the vagus nerve, which is associated with autonomic dysfunction, the olfactory bulb is known to exhibit pathological changes from an early stage, and recently, techniques such as MRI-based olfactory bulb volume measurement have been employed. In the subtype classification, the olfactory bulb may serve as a potential biomarker.

The patient was a 68-year-old woman diagnosed with Parkinson’s disease. Five years after disease onset, at the age of 65, her lower limb motor akinesia worsened, prompting an increase in her selegiline hydrochloride dosage from 2.5 mg/day to 5 mg/day. Following this adjustment, she began to experience hypertensive episodes lasting approximately two hours during the day, accompanied by facial flushing, fatigue, and chest pain. As these episodes became more frequent, we performed 24-hour blood pressure monitoring and measured plasma noradrenaline (NA) levels during the episodes. Hypertensive crisis and high plasma NA levels were observed mainly during the daytime, especially post-lunch. When selegiline hydrochloride was discontinued and replaced by safinamide, the hypertensive episodes ceased. Although hypertension induced by low-dose selegiline hydrochloride is rare, it is important to remain vigilant in daily clinical practice.