Sustained attention in combat-related posttraumatic stress disorder

There is substantial evidence that PTSD patients have information processing abnormalities for stimuli that are highly relevant to the traumas they have endured. The goal of the present study was to examine whether this extends to neutral stimuli as well. Twenty-four male Vietnam combat veterans with PTSD were compared to fifteen normal male comparison subjects on their performance on a sensitive measure of sustained attention, the Continuous Performance Test-Identical Pairs version (CPT-IP). PTSD subjects did not differ from controls in their ability to discriminate target stimuli from background noise on the CPT. Additionally they performed as well as controls, even in the presence of external distraction. Thus, this study did not find a generalized deficit in attention associated with PTSD on the CPT-IP. Nevertheless, further clarification of the nature of the information processing disturbance in PTSD is warranted.     

Muscarinic suppression in stratum radiatum of CA1 shows dependence on presynaptic M1 receptors and is not dependent on effects at GABA(B) receptors

Cholinergic modulation of synaptic transmission is vital to memory processes and may be responsible for setting network dynamics in the hippocampus appropriate for encoding of information. found evidence suggesting M1 receptors cause presynaptic inhibition of glutamatergic transmission, while research supports a role of the M2 receptor. We examined muscarinic inhibition of fEPSPs in stratum radiatum of mice lacking m1 subtype receptors (KO) compared to wild type (WT) controls. WT mice exhibit greater suppression of transmission by muscarine as compared to KO in a dose dependent fashion. Oxotremorine shows no significant difference in suppression between WT and KO, while MCN-A-343, an M1 agonist, exhibits a significant difference between KO and WT, with KO showing no suppression. One hundred micromolar SGS-742, a selective GABA(B) antagonist, fails to affect either normal transmission or muscarinic suppression in either WT or KO suggesting that differences in suppression between the groups is not attributable to differences in GABA(B) receptor activation due to muscarinic activation of GABAergic interneurons. These findings support a role for presynaptic m1 mAChRs in modulation of synaptic transmission in CA1, but indicate that other muscarinic receptor subtypes, such as M2, are also involved in suppression of synaptic potentials.     

Contextual modulation of memory consolidation

We investigate olfactory memory consolidation in honeybees. Three experiments are reported that include 1024 animals in 28 experimental groups. After one pairing of odorant and sucrose reward, retention is typically nonmonotonic with a minimum 3 min after conditioning. This corresponds to the “Kamin effect” in vertebrates; the postminimum rise in retention is usually interpreted as reflecting memory consolidation. First, we test for the generality of this effect across four different odorants. The postminimum rise in retention was reproducibly observed for 1-hexanol but not for 1-octanol, limonene, or geraniol. Second, we investigate whether previous learning about the training context modulates subsequent memory consolidation. On the day before training, a reward was applied either upon placement into the future training context for 1 min, halfway during exposure or just before removal from the context. In the latter group, the 3-min minimum in retention was eliminated; thus, in that group, forward pairings of context and reward (i.e., context exposure begins before reward is applied) lead to an associative context memory that can modulate subsequent olfactory memory consolidation. Third, we found no evidence for a modulation of olfactory memory consolidation by pre-exposure to the odorant.     

Learning to stand tall: Idiopathic scoliosis,behavioral electronics,and technologically-assisted patient participation in treatment,c. 1969–1992

Drawing on the archives of American learning psychologist Neal E. Miller, this article investigates the role of instrumentation in the expansion and diversification of the behavior therapy domain from the late 1960s to the early 1990s. Through the case of Miller's research on the use of biofeedback to treat idiopathic scoliosis, it argues that the post-World War II adoption of electronic technology by behavioral psychologists contributed to extending their subject matter to include physiological processes and somatic conditions. It also enabled a technologically-instrumented move outside the laboratory through the development of portable ambulatory treatment devices. Using the example of the Posture-Training Device that Miller and his collaborators invented for the behavioral treatment of idiopathic scoliosis, this paper considers how electromechanical psychological instrumentation illustrated a larger and ambiguous strategic shift in behavior therapy from an orientation toward external control to one of self-control.