A model for the assessment, care, and treatment of suicidal risk within the military intelligence community.

This paper describes the development of a behavioral health and wellness model into the US Army Intelligence and Security Command (INSCOM) to address concerns about suicide within this community. In response to stresses existing within the intelligence community (IC), INSCOM partnered with the Army Public Health Center (APHC) to assess the health and wellbeing of Command personnel. A Community Health Assessment (CHA) survey was conducted (N = 2,704 Soldiers; N = 959 Civilians) that included focus groups across three installations and secondary source data. Six key areas were prioritized: suicide behavior, behavioral health access to care and health promotion, behavioral health stigma and maintaining clearances, workplace environment, sleep health, and overall fitness. Several actions were implemented to address the report's findings and recommendations. A Command Surgeon office was established within INSCOM. An INSCOM Health Assessment and Readiness Team (I-HART) was established. The Deputy Undersecretary of the Army provided support to address suicide within INSCOM by approving 4 highly qualified experts (HQE's) in behavioral health and clinical suicidology to provide research oversight and make recommendations. The Command General approved 8 behavioral health providers. There are planned research efforts within the command focusing on scalable and technology enabled care delivery to improve mental well-being and decrease suicides.

Bursting as a source of non-linear determinism in the firing patterns of nigral dopamine neurons.

Nigral dopamine (DA) neurons in vivo exhibit complex firing patterns consisting of tonic single-spikes and phasic bursts that encode information for certain types of reward-related learning and behavior. Non-linear dynamical analysis has previously demonstrated the presence of a non-linear deterministic structure in complex firing patterns of DA neurons, yet the origin of this non-linear determinism remains unknown. In this study, we hypothesized that bursting activity is the primary source of non-linear determinism in the firing patterns of DA neurons. To test this hypothesis, we investigated the dimension complexity of inter-spike interval data recorded in vivo from bursting and non-bursting DA neurons in the chloral hydrate-anesthetized rat substantia nigra. We found that bursting DA neurons exhibited non-linear determinism in their firing patterns, whereas non-bursting DA neurons showed truly stochastic firing patterns. Determinism was also detected in the isolated burst and inter-burst interval data extracted from firing patterns of bursting neurons. Moreover, less bursting DA neurons in halothane-anesthetized rats exhibited higher dimensional spiking dynamics than do more bursting DA neurons in chloral hydrate-anesthetized rats. These results strongly indicate that bursting activity is the main source of low-dimensional, non-linear determinism in the firing patterns of DA neurons. This finding furthermore suggests that bursts are the likely carriers of meaningful information in the firing activities of DA neurons.

Oscillatory firing of dopamine neurons: differences between cells in the substantia nigra and ventral tegmental area.

Neuronal oscillations have been suggested to play an important role in information processing in the brain. Using spectral analysis, we have recently shown that the repetitive burst-like firing in many dopamine (DA) neurons in the ventral tegmental area (VTA) can be described as a slow oscillation (SO) in firing rate. In this study, we examined whether DA neurons in the adjacent substantia nigra (SN) also display a SO. DA neurons were recorded extracellularly using the cells/track technique in chloral hydrate-anesthetized rats. Spectral analysis showed that firing patterns of SN DA neurons exhibited a SO similar to that observed in VTA DA neurons. The amplitude of the SO, however, was much reduced in the SN compared with that in the VTA and so was the number of DA neurons qualified as high-SO cells. In high-SO DA neurons, the amplitude of the SO was strongly correlated with the degree of bursting, and this correlation was observed in both the VTA and SN. In low-SO cells, however, the SO was more significantly correlated with the variability of firing than with firing rate and bursting. Since the generation of the SO depends on afferent inputs to DA neurons, a better understanding of its difference between the SN and VTA may provide important insights into the neural networks that control DA neurons in the two areas.

Functional coupling between the prefrontal cortex and dopamine neurons in the ventral tegmental area.

Stimulation of the prefrontal cortex (PFC) has been shown to have an excitatory influence on dopamine (DA) neurons. We report here that, under nonstimulated conditions, the activity of DA neurons in the ventral tegmental area (VTA) also covaries, on a subsecond timescale, with the activity of PFC cells. Thus, in 67% of VTA DA neurons recorded in chloral hydrate-anesthetized rats, the firing of the cell displayed a slow oscillation (SO) that was highly coherent with the activity of PFC neurons. The SO was suppressed by transections immediately caudal to the PFC or by intra-PFC infusion of tetrodotoxin, suggesting that it depends on inputs derived from the PFC. Unexpectedly, the SO in most VTA DA neurons was reversed in phase relative to PFC cell activity, suggesting that at least part of PFC information is transferred to DA neurons indirectly through inhibitory relay neurons. These results, together with those reported previously, suggest that the PFC can act through multiple pathways to exert both excitatory and inhibitory influences on DA neurons. The observed functional coupling between DA and PFC neurons further suggests that these pathways not only allow a bidirectional control of DA neurons by the PFC, but also enable action potential-dependent DA release to be coordinated, on a subsecond timescale, with glutamate release from PFC terminals. Further understanding of this coordinated activity may provide important new insights into brain functions and disorders thought to involve both VTA DA and PFC neurons.

Clozapine blocks D-amphetamine-induced excitation of dopamine neurons in the ventral tegmental area.

Current antipsychotic drugs are thought to inhibit central dopamine (DA) transmission by blocking DA receptors. Here, we provide evidence that the atypical antipsychotic drug clozapine may produce part of its effect by inhibiting a subset of excitatory inputs to DA neurons. Thus, in chloral hydrate-anesthetized rats, systemic administration of D-amphetamine produced two opposing effects on DA neurons in the ventral tegmental area. Under control conditions, D-amphetamine inhibited the firing of the cell through D2-like receptors. When D2-like receptors were blocked by raclopride, D-amphetamine excited DA neurons, instead of producing no effect. The excitation, expressed as an increase in firing rate and a slow oscillation in firing pattern, was suppressed by the adrenergic alpha1 receptor antagonist prazosin, suggesting an involvement of alpha1 receptors. In rats pretreated with the typical antipsychotic drug haloperidol, D-amphetamine also excited DA neurons. However, when given after clozapine, D-amphetamine produced no significant effects. The failure of D-amphetamine to produce an excitation is not due to an incomplete blockade of D2-like receptors by clozapine because co-treatment with clozapine and raclopride also failed to enable the excitatory effect of D-amphetamine. The suggestion that clozapine inhibits the excitatory effect of D-amphetamine is further supported by the finding that clozapine, given after D-amphetamine, reliably reversed D-amphetamine-induced excitation in raclopride-treated rats. Thus, different from raclopride and haloperidol, clozapine may inhibit DA transmission through two additive mechanisms: blockade of DA receptors and inhibition of an amphetamine-sensitive, excitatory pathway that innervates DA neurons.