Behavioral and neural biology最新文献

We recently demonstrated that fetal brain implants produced a significant recovery in the ability of insular cortex (IC)-lesioned rats to learn a conditioned taste aversion (CTA). We now report effects on the recovery of CTA and of a second measure of learning, inhibitory avoidance (IA), of supplementing the implants with nerve growth factor (NGF). Four groups of male Sprague-Dawley animals showing disrupted taste aversion following IC lesions, plus two control groups, received different experimental treatments: Group 1, unlesioned control; Group 2, homotopic IC implants without NGF; Groups 3 and 4, IC implants + NGF; Group 5, heterotopic occipital cortical implants + NGF; and Group 6, without an implant as a lesioned control. All groups except Group 4 were trained pre- and postimplant in the CTA paradigm. Two days after CTA testing postimplant, all groups received IA training. Behavioral results showed that insular cortex implants with NGF promoted recovery to control levels of the ability to learn both tasks at 15 days postimplant. Those animals that received occipital implants with NGF or insular cortex with vehicle or remained without implants did not show any significant behavioral recovery at 15 days postimplant. These findings suggest that NGF associated with homotopic implants facilitates recovery of learning abilities in insular cortex-lesioned rats and suggest that similar treatments with NTFs may have analogous effects when lesions involve other brain areas.

Stimulation of regions of the cerebellar flocculus can elicit eyeblinks, but the relationship of this floccular eyeblink zone to eyeblink classical conditioning is unknown. In this experiment, New Zealand white rabbits received bilateral lesions of the flocculus and paraflocculus and were subsequently classically conditioned with tone and corneal airpuff on the left and then the right eye. All animals reached training criterion on both eyes, with the exception of one animal whose lesion included the superior cerebellar peduncle and who was unable to learn on the ipsilateral eye. The lesioned group was not significantly different from unlesioned controls in rate of acquisition or conditioned or unconditioned response amplitude. These results indicate that the flocculus and paraflocculus are not by themselves the essential site of plasticity for classical conditioning of the rabbit eyeblink response.

Mammalian neonates have been simultaneously described as having particularly poor memory, as evidenced by infantile amnesia, and as being particularly excellent learners with unusually plastic nervous systems that are easily influenced by experience. An understanding of the neurobiological constraints and mechanisms of early learning may contribute to a unified explanation of these two disparate views. Toward that end, we review here our work on the neurobiology of learning and memory in neonates. Specifically, we have examined the neurobiology of early learning using an olfactory classical conditioning paradigm. Olfactory classical conditioning in neonates at the behavioral level conforms well with the requirements and outcomes of classical conditioning described in adults. Furthermore, specific neural correlates of this behavioral conditioning have been described including anatomical and physiological changes, neural pathways, and modulatory systems. In this Review, we outline the behavioral paradigm, the identified neural Finally, we compare the neurobiology of early learning with that reported for mature animals, with specific reference to the role of US-CS convergence, memory modulation, consolidation, and distributed memory.

We recently demonstrated that insular cortex (IC) fetal implants supplemented by nerve growth factor (NGF) can accelerate the recovery of behavioral deficits induced by IC brain lesions. In the present report we describe results on in vivo assays of acetylcholine (ACh) turnover in the IC of rats subjected to the same brain lesion and implant treatments used in that research and for which detailed behavioral data are available. The neurochemical assays were carried out immediately after completion of the behavioral measurements. The assays showed that implants or NGF with heterotopic tissue continued to be associated with elevated levels of ACh and with deficits in learning and memory at a time postlesion when both behavior and ACh turnover in vivo, after treatment with homotopic implants and NGF combined, were at nonlesioned control levels. The results support the concept that, in vivo, the cholinergic neurotransmitter system is intimately involved in recovery from IC lesion-induced deficits in behavior and show that a combination of homotopic implant and NGF may be used as a means of manipulating that system to accelerate the repair of such deficits. Mechanisms by which this combination produces its effects are considered and the possibility is suggested that other neurotrophic factors (NTF) may also be useful when other types of brain lesions are involved.

There are reports by Diamond and her colleagues, based on measurements made shortly after parturition, that pregnancy increases the size of the cerebral cortex in rats. As a prelude to examining the cellular basis for this phenomenon, we measured the size of the cortex in three coronal planes in hooded rats on the last day of their pregnancy and in control, nonpregnant female littermates. No differences were found between the pregnant and control rats. We conclude that either the events on the day of parturition alter the size of the cortex or the effects of pregnancy on the cortex are not reliable.

Thirteen protein kinase inhibitors (PKIs) were investigated in chicks for their in vitro effects on PKC activity and for their in vivo effects on memory formation for a peck-avoidance task. Amnesia occurred by 15–30 min post-training when agents that inhibit primarily Ca²⁺/calmodulin were injected into brain. Amnesia occurred by 60 min post-training when agents that inhibit PKC-,PKA-, and/or PKG-dependent protein kinases, but not Ca²⁺/calmodulin, were injected. Enhancement of memory formation was accomplished by injecting bradykinin, but not forskolin. Both of these agents, however, attenuated the amnesia produced by H-7. These results are discussed as relevant neural processes involved in memory and synaptic plasticity.

Central components of the vomeronasal system appear to mediate extrahypothalamic control of gonadotropin release during male-induced acceleration of puberty onset in female rodents. In order to describe the bed nucleus of the stria terminalis (BNST) and to determine whether this component of the vomeronasal system is altered following early puberty onset, the anterior BNST of female Djungarian hamsters (Phodopus campbelli) was subdivided into three regions: medial, lateral, and ventral. The cross-sectional area, soma size, and neuronal density of each subdivision was compared among female hamsters in three groups: (1) young females showing accelerated reproductive development following a period of housing with an adult male, (2) young females matched by age with the accelerated females but housed alone during the same period, and (3) older females at the age of spontaneous puberty. Females housed with an adult male and undergoing accelerated puberty onset had significantly smaller lateral anterior BNST subdivisions than females housed alone for the same period (10 days following weaning) or housed alone until the age of spontaneous puberty onset (25 days following weaning). The size of the ventral and medial subdivisions was not different in the three groups. Furthermore, although soma size and neuronal density differed markedly among the anterior BNST subdivisions, these subdivision characteristics were similar in the accelerated, prepubertal, and older pubertal females. Our finding demonstrates that a central component of the vomeronasal system undergoes neuroanatomical alteration in response to environmental stimuli and recommends further examination of the BNST during this dynamic ontogenetic period.

Early-life undernutrition impairs the short-term memory capacity of adult rats (90 days of age) trained on a conditional—spatial discrimination task (Castro, Tracy, & Rudy, Behavioral Brain Research, 32, 255–264, 1989). While well-nourished control animals perform above 90% correct when the interval separating the forced run and choice run is 180 s, the performance of the undernourished animals falls to chance (50%) when the delay interval is increased to 90 s. We now report that this performance decrement can be attenuated by the administration of the anticholinesterase, physostigmine. However, the effects of physostigmine were dose dependent. While 0.02 mg/kg of physostigmine improved the performance of the undernourished animals so that they performed significantly above chance at the 180-s delay interval, neither 0.2 nor 0.002 mg/kg of physostigmine improved performance. We concluded that this effect was centrally mediated since scopolamine hydrobromide (1.0 mg/kg) which blocks both central and peripheral cholinergic receptors blocked physostigmine's performance-improving effect, while methyl-scopolamine (1.0 mg/kg) which blocks only peripheral receptors did not. These are the first results which suggest that the short-term memory impairments produced by early-life undernutrition can be attenuated by enhancing central cholinergic functioning.

A single oral treatment with 0.3 mg/kg of the competitive NMDA receptor blocker CGP 37 849 improved the retention performance of rats in a social memory paradigm. The effect disappeared with increasing doses: at 1 mg/kg a positive trend could still be observed; at 3 mg/kg no effect whatever was detectable.

Aplysia californica exhibit a dramatic defensive reaction, the release of a cloud of dark purple ink, in response to noxious stimuli. Although the neural control of this behavior has been studied rather extensively, the functional significance of the inking response is not well understood. We have found that ink released by animals that are subjected to noxious stimuli rapidly induces inhibition of the tail-elicited siphon withdrawal reflex in neighboring Aplysia. Further experiments indicated that the inhibitor is the ink itself, and not some other substance released by the donor animals. Finally, we examined whether ink-induced inhibition of siphon withdrawal might be a secondary consequence of an elevated competing response such as increased locomotion. We found that locomotion is not affected by the concentrations of ink we employed, indicating that the ink probably modulates the withdrawal reflex directly. Because the neural circuits responsible for both tail-elicited siphon withdrawal and the inking response have already been partly delineated, one can now bring the neurobiological advantages of Aplysia to bear on the ethologically important issue of signaling between conspecifics.