ABSTRACT
Elucidating the neural basis of fear allows for more effective treatments for maladaptive fear often observed in psychiatric disorders. Although the basal forebrain (BF) has an essential role in fear learning, its function in fear expression and the underlying neuronal and circuit substrates are much less understood. Here we report that BF glutamatergic neurons are robustly activated by social stimulus following social fear conditioning in male mice. And cell-type-specific inhibition of those excitatory neurons largely reduces social fear expression. At the circuit level, BF glutamatergic neurons make functional contacts with the lateral habenula (LHb) neurons and these connections are potentiated in conditioned mice. Moreover, optogenetic inhibition of BF-LHb glutamatergic pathway significantly reduces social fear responses. These data unravel an important function of the BF in fear expression via its glutamatergic projection onto the LHb, and suggest that selective targeting BF-LHb excitatory circuitry could alleviate maladaptive fear in relevant disorders.
Subject(s)
Basal Forebrain , Fear , Habenula , Neurons , Animals , Habenula/physiology , Male , Fear/physiology , Basal Forebrain/physiology , Basal Forebrain/metabolism , Mice , Neurons/physiology , Neurons/metabolism , Optogenetics , Mice, Inbred C57BL , Social Behavior , Behavior, Animal/physiology , Neural Pathways/physiology , Glutamic Acid/metabolism , Conditioning, Classical/physiologyABSTRACT
Sociability is fundamental for our daily life and is compromised in major neuropsychiatric disorders. However, the neuronal circuit mechanisms underlying prosocial behavior are still elusive. Here we identify a causal role of the basal forebrain (BF) in the control of prosocial behavior via inhibitory projections that disinhibit the midbrain ventral tegmental area (VTA) dopamine (DA) neurons. Specifically, BF somatostatin-positive (SST) inhibitory neurons were robustly activated during social interaction. Optogenetic inhibition of these neurons in BF or their axon terminals in the VTA largely abolished social preference. Electrophysiological examinations further revealed that SST neurons predominantly targeted VTA GABA neurons rather than DA neurons. Consistently, optical inhibition of SST neuron axon terminals in the VTA decreased DA release in the nucleus accumbens during social interaction, confirming a disinhibitory action. These data reveal a previously unappreciated function of the BF in prosocial behavior through a disinhibitory circuitry connected to the brain's reward system.
Subject(s)
Dopaminergic Neurons/physiology , Prosencephalon/physiology , Social Behavior , Ventral Tegmental Area/physiology , Animals , Dopaminergic Neurons/metabolism , GABAergic Neurons/metabolism , GABAergic Neurons/physiology , Male , Mice , Neural Inhibition , Prosencephalon/cytology , Reward , Somatostatin/genetics , Somatostatin/metabolism , Ventral Tegmental Area/cytologyABSTRACT
Cancer is a critical health problem in Taiwan. The range of physical, psychological, social, and existential stressors associated with cancer diagnosis and treatment can cause significant distress in cancer patients and survivors. The focus of cancer research has broadened in the past decade from the disease itself to factors that can have a positive influence on the health and life quality of cancer patients. However, few studies have explored how patients adapt and become resilient to the life challenges of their disease. This article introduces the concept of resilience and its influence factors. We analyze study findings and introduce four nursing interventions that have been used to nurture resilience in cancer patients. The authors hope findings help strengthen nurse competencies in order to enhance cancer patient quality of care.
