Introduction: There has long been an interest in the effects of diet on mental health, and the interaction of the two with stress; however, the nature of these relationships is not well understood. Although associations between diet, obesity and the related metabolic syndrome (MetS), stress, and mental disorders exist, causal pathways have not been established. Methods: We reviewed the literature on the relationship between diet, stress, obesity and psychiatric disorders related to stress. Results: Diet and obesity can affect mood through direct effects, or stress-related mental disorders could lead to changes in diet habits that affect weight. Alternatively, common factors such as stress or predisposition could lead to both obesity and stress-related mental disorders, such as depression and posttraumatic stress disorder (PTSD). Specific aspects of diet can lead to acute changes in mood as well as stimulate inflammation, which has led to efforts to assess polyunsaturated fats (PUFA) as a treatment for depression. Bidirectional relationships between these different factors are also likely. Finally, there has been increased attention recently on the relationship between the gut and the brain, with the realization that the gut microbiome has an influence on brain function and probably also mood and behavior, introducing another way diet can influence mental health and disorders. Brain areas and neurotransmitters and neuropeptides that are involved in both mood and appetite likely play a role in mediating this relationship. Conclusions: Understanding the relationship between diet, stress and mood and behavior could have important implications for the treatment of both stress-related mental disorders and obesity.

https://www.mdpi.com/2072-6643/12/8/2428/pdf

Diet, Stress and Mental Health.

Cortical inhibitory neurons exhibit remarkable diversity in their morphology, connectivity, and synaptic properties. Here, we review the function of somatostatin-expressing (SOM) inhibitory interneurons, focusing largely on sensory cortex. SOM neurons also comprise a number of subpopulations that can be distinguished by their morphology, input and output connectivity, laminar location, firing properties, and expression of molecular markers. Several of these classes of SOM neurons show unique dynamics and characteristics, such as facilitating synapses, specific axonal projections, intralaminar input, and top-down modulation, which suggest possible computational roles. SOM cells can be differentially modulated by behavioral state depending on their class, sensory system, and behavioral paradigm. The functional effects of such modulation have been studied with optogenetic manipulation of SOM cells, which produces effects on learning and memory, task performance, and the integration of cortical activity. Different classes of SOM cells participate in distinct disinhibitory circuits with different inhibitory partners and in different cortical layers. Through these disinhibitory circuits, SOM cells help encode the behavioral relevance of sensory stimuli by regulating the activity of cortical neurons based on subcortical and intracortical modulatory input. Associative learning leads to long-term changes in the strength of connectivity of SOM cells with other neurons, often influencing the strength of inhibitory input they receive. Thus despite their heterogeneity and variability across cortical areas, current evidence shows that SOM neurons perform unique neural computations, forming not only distinct molecular but also functional subclasses of cortical inhibitory interneurons.

/pdf/somatostatin-expressing-inhibitory-interneurons-in-cortical-21dtblrqdk.pdf

Somatostatin-Expressing Inhibitory Interneurons in Cortical Circuits.

The basal forebrain cholinergic projection (BFC) system has been the focus of considerable attention as a result of evidence implicating it in a number of behavioral functions, including arousal, sensory processing, motivation, emotion, learning, and memory (Deutsch, 1983; Buzsaki et al., 1988; Richardson and DeLong, 1988; Durkin, 1989; Rolls 1989, Steriade and McCarley, 1990). Moreover, neuropathological changes in the BFC have been reported in a surprisingly large number of neurological diseases, including Alzheimer’s and Parkinson’s diseases (for ref. see Coyle et al., 1983; Mesulam and Geula, 1988; Arendt et al., 1989). BFC neurons in the rat are dispersed across a number of classically defined territories of the basal forebrain, as illustrated from a series of coronal sections in Fig. 1. However, using a computer graphic three-dimensional reconstruction technique (Schwaber et al., 1987) or manual reconstruction from camera lucida drawings (Fig. 2) it is evident that BFC neurons form a continuum, rather than being arranged as distinct nuclear groups.

Afferents to basal forebrain cholinergic projection neurons: an update.

Cysteamine-induced depletion of central somatostatin-like immunoactivity: effects on behavior, learning, memory and brain neurochemistry.

1 Interactions among Neurotransmitters: Their Importance to the "Integrated Organism".- 2 The Cholinergic Basal Forebrain and its Telencephalic Targets: Interrelations and Implications for Cognitive Function.- 3 Synaptic Organization of Basal Forebrain Cholinergic Projection Neurons.- 4 Functional Pharmacology of Basal Forebrain Dopamine.- 5 Cholinergic/Noradrenergic Interactions and Memory.- 6 The Role of the Noradrenergic System in Higher Cerebral Functions-Experimental Studies About the Effects of Noradrenergic Modulation on Electrophysiology and Behavior.- 7 Septal Noradrenergic and Glutamatergic Influences on Hippocampal Cholinergic Activity in Relation to Spatial Learning and Memory in Mice.- 8 Neurotransmitter Interactions and Responsivity to Cholinomimetic Agents.- 9 The Importance of D1 and D2 Interactions with Nicotinic and Muscarinic Systems for Working Memory Function.- 10 Neurotransmitter Systems in Hippocampus and Prelimbic Cortex, Dopamine-Acetylcholine Interactions in Hippocampus, and Memory in the Rat.- 11 Nicotinic-Muscarinic Interactions in Cognitive Function.- 12 The Influence of Neurotensin upon Cholinergic Function.- 13 Serotonin Influences on Cholinergic Function: Possible Interactions in Learning and Memory.- 14 The Contribution of the Serotonergic Innervation of the Hippocampus to the Effects of Combined Cholinergic/Serotonergic Deficits.- 15 Overlapping Neural Substrates Underlying Defense Reactions, Aversive Memory, and Convulsive Behavior.- 16 Potentiation of the Effects of Antimuscarinic Drugs on Behavior by Serotonin Depletion: Specificity and Relation to Learning and Memory.- 17 Interactions of Neurotransmitters and Neuroanatomy: It's Not What You Do, It's the Place that You Do It.- 18 Intraseptal GABAergic Infusions Disrupt Memory in the Rat: Method and Mechanisms.- 19 Working Memory and Cholinergic Autoregulation in the Medial Septal Area.- 20 Modulation of Memory by Benzodiazepine-Acetylcholine Interactions.- 21 Cognition Enhancement Based on GABA-Cholinergic Interactions.- 22 Transmitter Interactions and Cognitive Function: Appreciation of the Concert.

Neurotransmitter interactions and cognitive function

In the present study the effects of somatostatin and cysteamine (a selective decreaser of the somatostatin level in the body) were compared in different behavioral tests on rats. Somatostatin inhibited the extinction of active avoidance behavior 8 hr and 24 hr after intracerebroventricular (ICV) treatment, while cysteamine facilitated it 4 hr and 8 hr after subcutaneous (SC) treatment. Somatostatin did not significantly influence the cysteamine-induced facilitation of the extinction. Somatostatin did not have a significant effect on T-maze spatial discrimination learning and reverse learning, whereas cysteamine markedly attenuated the performance 4 hr (1st day) after treatment. Somatostatin in a dose of 4 μg (ICV) increased the locomotor activity 10 min after treatment, while cysteamine markedly decreased all parameters of the open-field test. These effects of the drug had disappeared 24 hr after treatment. If different doses of somatostatin (4 μg or 10 μg ICV) were administered to cysteamine-pretreated rats, the peptide did not modify the drug-induced changes in the open-field test. The data suggest that the brain somatostatin might have a physiological role in the organization of certain types of behavior.

Comparative studies with somatostatin and cysteamine in different behavioral tests on rats.

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Comparative studies with somatostatin and cysteamine in different behavioral tests on rats.