Behavioural brain research
-
Although we demonstrated willed movement (WM) therapy can facilitate the patients actively participating in the physical activities by cognitive and perceptual stimulation in our previous study, the molecular mechanisms of the willed movement on the patients remains unclear. We initially established the model of WM intervention for rats and identified possible effects of willed movement on motor recovery and on expression of Kainate/alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in ischemia core (IC) and ischemia penumbra (IP) regions of rats after cerebral ischemia reperfusion. ⋯ Early willed movement treatment can increase the expression level of AMPA receptor subunits and thus might increase synaptic transmission and enhance brain plasticity after focal brain ischemia at the subacute stage.
-
The roles of beta-NER (beta-noradrenergic receptor), GR (glucocorticoid) and mineral corticoid receptors (MR) in the consolidation of anxiogenic effects of predator stress were studied. One minute after predator stress, different groups of rats were injected (ip) with vehicle, propranolol (beta-NER blocker, 5 and 10 mg/kg), mifepristone (RU486, GR blocker, 20 mg/kg), spironolactone (MR blocker, 50 mg/kg), propranolol (5 mg/kg) plus RU486 (20 mg/kg) or the anxiolytic, chloradiazepoxide (CPZ, 10 mg/kg). One week later, rodent anxiety was assessed in elevated plus maze, hole board, light/dark box, social interaction and acoustic startle. ⋯ Consolidation of delay of habituation was blocked or attenuated by post stress MR block, GR plus beta-NER block and CPZ but not by post stress GR or beta-NER block alone. Taken together, present findings suggest consolidation of lasting anxiogenic effects of predator stress may share some of the same neurochemical mechanisms implicated in some forms of fear memory consolidation. Implications of these findings for the study of stress-induced changes in affect including posttraumatic stress disorder (PTSD) are discussed.
-
Nociceptive stimulation, at an intensity that elicits pain-related behavior, attenuates recovery of locomotor and bladder functions, and increases tissue loss after a contusion injury. These data imply that nociceptive input (e.g., from tissue damage) can enhance the loss of function after injury, and that potential clinical treatments, such as pretreatment with an analgesic, may protect the damaged system from further secondary injury. The current study examined this hypothesis and showed that a potential treatment (morphine) did not have a protective effect. ⋯ Rats treated with morphine alone also had significantly larger lesions than those treated with saline. These results suggest that nociceptive stimulation affects recovery despite a blockade of pain-elicited behavior. The results are clinically important because they suggest that opiate treatment may adversely affect the recovery of function after injury.
-
The object location task is a new procedure evaluating spatial memory abilities in the rat. The aim of the present study was to characterize this behavioural paradigm by pharmacologic means. For this purpose, the effects of the muscarinic receptor antagonist scopolamine and the inhibitor of the nitric oxide synthase L-NAME on object location were assessed in the rat. ⋯ These impairments seem to be centrally mediated since the peripheral muscarinic receptor antagonist methylscopolamine (0.2 mg/kg) did not affect object location under the same conditions. Finally, pre-training treatment with L-NAME (30 mg/kg but not 10 mg/kg) also induced delay-dependent performance deficits in the object location task. These results indicate that the object location test is sensitive to pharmacological treatment and could be used for assessing the therapeutic potential of promnesic compounds.
-
Bombesin (BB)-like peptides have been implicated in the mediation and/or modulation of the stress response. However, the impact of manipulating this peptidergic system has only been assessed in a limited number of anxiety and fear paradigms. Given that different behavioral paradigms reflect different aspects of anxiety, the objective of the present investigation was to assess the effects of two mammalian BB-related peptides, namely gastrin-releasing peptide (GRP) and neuromedin B (NMB), in paradigms thought to reflect fear and anxiety-related behaviors. ⋯ In the fear potentiated startle paradigm, pretreatment with either the BB(1) receptor antagonist or the BB(2) receptor agonist attenuated the fear potentiated startle response, without affecting basal startle amplitude. These data suggest that NMB and GRP do affect the stress response. However, whereas NMB manipulations affected both anxiety and fear responses, GRP alterations selectively affected fear-related responses.