Effects of midbrain central gray lesions on spontaneous and electrically induced aggression in the rat

Large electrolytic lesions were placed in the midbrain central gray of male rats. Their effects on hypothalamically induced aggression, switch-off behaviour, and locomotion were investigated. A number of these animals were also tested for territorial intermale aggression in order to compare electrically induced and spontaneous aggression. Large lesions resulted in an increase of the current threshold to induce aggression by hypo-thalamic stimulation. Smaller, but still quite large, lesions decreased the threshold current for hypothalamic aggression. After the operation a decrease in the threshold for switch-off was present, both in the experimental and the control group. Current thresholds for locomotion were decreased after the lesions only in the experimental group. Spontaneous aggression was temporarily decreased after the lesion. No indication was found that other behavioural elements of the animal were distorted by the lesion. The parallel between the effects on spontaneous and electrically induced aggression makes it attractive to ascribe a role to the neural circuit of hypothalamus and central gray in territorial aggression. However, even with large lesions the animals were still capable of fighting, hence the central gray is not indispensable. An attempt was made to explain the differential effects that differently sized central gray lesions have on hypothalamic aggression.     

Potassium gymnemate and the sweet and bitter taste provoked electrically

The sweetness or bitterness of taste solutions of saccharin and quinine may be blocked, while the sweetness or bitterness evoked by electrical stimulation of the tongue by cathodal polarization is unchanged. Electrical taste stimulation apparently bypasses the most peripheral process by which taste solutions elicit sweet and bitter and thus acts directly on the receptor and/or its afferent nerve terminals.     

Behavior of the rat after removal of the neocortex and hippocampal formation

After surgical removal of the neocortex and hippocampal formation, rats retained most of the movement patterns of locomotion, climbing, grooming, feeding, and fighting. However, forepaw immobility during swimming was abolished. Feeding behavior was suppressed temporarily but recovered partially. The distinctive postures of sleep and walking and a circadian rhythm of motor activity were retained. However, behaviors were often not performed at the appropriate time and place. The normal sequence of grooming behavior was disrupted; food hoarding and social behavior were essentially abolished. Removal of the neocortex alone had much the same effect as removal of neocortex and hippocampus together. Removal of hippocampus alone produced only a mild disruption of behavior. It is suggested that ascending nonspecific projections to the cerebral cortex play an important role in the moment-to-moment control of behavior but are not essential for the sleep-waking cycle.     

Gastrointestinal reactivity in rats lacking anterior insular neocortex

Behavioral and physiological studies have shown that the insular neocortex participates in a wide variety of special visceral processes, in particular, the higher-order integration of taste stimuli and the regulation of autonomic activity. The present experiment examined the involvement of the anterior insular (gustatory) neocortex (AIGN) in gastrointestinal reactivity and taste learning in rats by the use of a modified taste aversion training procedure. Normal rats and rats lacking AIGN demonstrated similar "illness thresholds" to the early onset symptoms of ingested LiCl. Conversely, animals lacking AIGN showed significant impairments in taste aversion learning ability. From a consideration of several research findings it is concluded that animals lacking AIGN can normally perceive tastes and illness, but these animals experience reliable impairments in taste aversion learning ability.     

Analysis of potentiation and overshadowing effects in the instrumental performance of pigeons

In each of two experiments, pigeons were trained on a multiple VI (variable interval) schedule with a 3-s delay of reinforcement. Different components were associated with different key colors. Experiment 1 (stage 2) confirmed a previous finding that the response rate is higher in a component having a signal (illumination of the houselight) filling the delay interval than in a component lacking the signal. This potentiation effect was replaced by an overshadowing effect (i.e., the rate was low in the signaled component) when in stage 1 of Experiment 1 the birds received concurrent experience of a component containing houselight presentations not correlated with reinforcement. In Experiment 2 it was found that this overshadowing effect was abolished when the signal used was the presentation of a pattern on the response key rather than illumination of the houselight. These results are interpreted in terms of an interaction between the rate-enhancing properties of the signal (perhaps a consequence of its conditioned reinforcing power) and the tendency of the signal in some conditions to evoke behavior that competes with the response being recorded.     

Imaging high-resolution structure of GFP-expressing neurons in neocortex in vivo

To detect subtle changes in neuronal morphology in response to changes in experience, one must image neurons at high resolution in vivo over time scales of minutes to days. We accomplished this by infecting postmitotic neurons in rat and mouse barrel cortex with a Sindbis virus carrying the gene for enhanced green fluorescent protein. Visualized with 2-photon excitation laser scanning microscopy, infected neurons showed bright fluorescence that was distributed homogeneously throughout the cell, including axonal and dendritic arbors. Single dendritic spines could routinely be resolved and their morphological dynamics visualized. Viral infection and imaging were achieved throughout postnatal development up to early adulthood (P 8-30), although the viral efficiency of infection decreased with age. This relatively noninvasive method for fluorescent labeling and imaging of neurons allows the study of morphological dynamics of neocortical neurons and their circuits in vivo.     

Taste-mediated potentiation of noningestional stimuli in rats

Holtzman rats drank saccharin in a distinctive environmental chamber prior to lithium-induced toxicosis. This treatment was administered four times. These animals subsequently drank less water or familiar saline in the chamber than animals which received water in the environment during conditioning. In addition, these environmental stimuli blocked the formation of a lithium-mediated coffee aversion more if they were conditioned in the presence of saccharin than if they were conditioned in the presence of water. Such differential blocking provided further evidence that the presence of a taste during conditioning facilitated aversion learning to the environmental chamber.     

Co-induction of long-term potentiation and long-term depression at a central synapse in the leech

Most studies of long-term potentiation (LTP) have focused on potentiation induced by the activation of postsynaptic NMDA receptors (NMDARs). However, it is now apparent that NMDAR-dependent signaling processes are not the only form of LTP operating in the brain [Malenka, R. C., & Bear, M. F. (2004). LTP and LTD: An embarrassment of riches. Neuron, 44, 5–21]. Previously, we have observed that LTP in leech central synapses made by the touch mechanosensory neurons onto the S interneuron was NMDAR-independent [Burrell, B. D., & Sahley, C. L. (2004). Multiple forms of long-term potentiation and long-term depression converge on a single interneuron in the leech CNS. Journal of Neuroscience, 24, 4011–4019]. Here we examine the cellular mechanisms mediating T-to-S (T → S) LTP and find that its induction requires activation of metabotropic glutamate receptors (mGluRs), voltage-dependent Ca²⁺ channels (VDCCs) and protein kinase C (PKC). Surprisingly, whenever LTP was pharmacologically inhibited, long-term depression (LTD) was observed at the tetanized synapse, indicating that LTP and LTD were activated at the same time in the same synaptic pathway. This co-induction of LTP and LTD likely plays an important role in activity-dependent regulation of synaptic transmission.     

Behavioral stress impairs long-term potentiation in rodent hippocampus

A number of hormones secreted from the pituitary-adrenal system during stress affect learning and memory processes. The phenomenon of hippocampal long-term potentiation (LTP) is viewed by many as a putative mechanism of memory storage and has proved a most valuable model for study of neuronal plasticity at the cellular level. The present study was conducted to investigate the possibility that stressful events which occur prior (in vivo) to the preparation of brain slices may influence the electrophysiology of the in vitro hippocampal explant when tested for LTP. Adult male rats (Long-Evans male X Sprague-Dawley female) were pair-housed 1 week prior to testing. One animal in each pair was either placed in a restraining tube for 30 min and received no tail shocks (Restraint) or placed in a restraining tube and received tail shocks (1 microA, 1 s) every minute for 30 min (Restraint + Shock). The other animal in each pair was taken directly from the home cage and received no restraint or tail shock (Control). In vitro hippocampal slices were then prepared immediately from these animals according to standard methods. Our results demonstrate a marked impairment of LTP in hippocampal explants taken from rats exposed to stress. The significance of this result with respect to cellular mechanisms underlying the relationship between stress, cognition, and learning is discussed.     

Experience-dependent changes in dendritic arbor and spine density in neocortex vary qualitatively with age and sex

Male and female Long-Evans hooded rats were placed in the complex environments for 3 months either at weaning (22 days), in young adulthood (120 days), or in senescence (24 months). The dendritic morphology of both the apical and basilar fields of layer III pyramidal cells was analyzed in both parietal and visual cortex. There were two novel results. First, although spine density was increased significantly with complex-housing in adulthood, it was decreased significantly by the same housing during development. Second, dendritic length was increased in both parietal and occipital cortex at all ages in males and was increased in adult females as well, but juvenile females showed no change in dendritic length in the occipital cortex and only a small effect on the apical field in parietal cortex. Thus, there are qualitative differences in the changes in spine density at different ages and the dendritic changes in response to complex versus isolated housing vary with sex, and in females, the changes vary with age as well. These results may explain some of the apparent inconsistencies in reports of spine and dendrite changes in the literature.     

SGK protein kinase facilitates the expression of long-term potentiation in hippocampal neurons

Previous studies showed that the serum- and glucocorticoid-inducible kinase (sgk) gene plays an important role in long-term memory formation. The present study further examined the role of SGK in long-term potentiation (LTP). The dominant-negative mutant of sgk, SGKS422A, was used to inactivate SGK. Results revealed a time-dependent increase in SGK phosphorylation after tetanization with a significant effect observed 3 h and 5 h later. Transfection of SGKS422A impaired the expression, but not the induction, of LTP. Furthermore, the constitutively active sgk, SGKS422D, up-regulated postsynaptic density-95 expression in the hippocampus. These results together support the role of SGK in neuronal plasticity.     

Impairment of spatial learning and hippocampal synaptic potentiation in c-kit mutant rats

The c-kit receptor tyrosine kinase encoded by the white-spotting (W) gene is highly expressed in rat hippocampal CA1–CA4 regions. We found an impaired spatial learning and memory in homozygous c-kit (Ws/Ws) mutant rats that have a 12-base deletion in the tyrosine kinase domain of the c-kit gene and a very low kinase activity. Electrophysiological studies in hippocampal slices revealed that the long-term potentiation (LTP) induced by the tetanic stimulation (100 Hz, 1 sec) in the mossy fiber (MF)–CA3 pathway, but not in the Schaffer collaterals/commissural–CA1 pathway, was significantly reduced in c-kit mutants compared with wild-type (+/+) rats. The paired-pulse facilitation (PPF) was measured before the tetanus and after the establishment of the LTP in each slice. The initial PPF in the MF–CA3 pathway positively correlated with the amplitude of the LTP in the wild-type rats but not in the c-kit mutant rats. Furthermore, they failed to show the normal characteristics observed in the MF–CA3 pathway of +/+ rats; that is, the negative correlation between the initial PPF and the changes in PPF measured after the LTP. These findings suggest an involvement of SCF/c-kit signaling in hippocampal synaptic potentiation and spatial learning and memory.     

Corticosterone time-dependently modulates beta-adrenergic effects on long-term potentiation in the hippocampal dentate gyrus

Previous experiments in the hippocampal CA1 area have shown that corticosterone can facilitate long-term potentiation (LTP) in a rapid non-genomic fashion, while the same hormone suppresses LTP that is induced several hours after hormone application. Here, we elaborated on this finding by examining whether corticosterone exerts opposite effects on LTP depending on the timing of hormone application in the dentate gyrus as well. Moreover, we tested rapid and delayed actions by corticosterone on β-adrenergic-dependent changes in LTP. Unlike the CA1 region, our in vitro field potential recordings show that rapid effects of corticosterone do not influence LTP induced by mild tetanization in the hippocampal dentate gyrus, unless GABA_A receptors are blocked. In contrast, the β-adrenergic agonist isoproterenol does initiate a slow-onset, limited amount of potentiation. When corticosterone was applied concurrently with isoproterenol, a further enhancement of synaptic strength was identified, especially during the early stage of potentiation. Yet, treatment with corticosterone several hours in advance of isoproterenol fully prevented any effect of isoproterenol on LTP. This emphasizes that corticosterone can regulate β-adrenergic modulation of synaptic plasticity in opposite directions, depending on the timing of hormone application.