Infection of neonatal Lewis rats with lymphocytic choriomeningitis virus (LCMV) produces distinct retinal, cerebellar, and hippocampal neuropathology. To understand the neurophysiological consequences of LCMV-induced hippocampal pathology, we studied evoked monosynaptic potentials and electro-encephalographic (EEG) activity in the dentate gyrus and CA1 and CA3 subfields of the hippocampus in vivo. Lewis rats were inoculated intracerebrally with LCMV at postnatal day 4. In rats studied 84-107 d postinfection, virus was cleared from the dentate gyrus and the number of dentate granule cells was decreased by 70%. No viral antigen or cell loss was apparent in CA1 or CA3. The hippocampal EEG of LCMV-infected rats 84-102 d postinfection was dominated by continuous theta. Although evoked potentials elicited in CA1 and CA3 by monosynaptic afferent stimulation revealed no differences between sham- and LCMV-infected rats, there was a site-specific dissociation of synaptic [population excitatory postsynaptic potential (pEPSP)] and cellular (population spike) responses and a suppression of GABA-mediated recurrent inhibition in the dentate gyrus of LCMV-infected rats. These findings indicate that GABA-mediated inhibition was markedly decreased in LCMV-infected rats. In support of this, parvalbumin-immunoreactive cell bodies and neuronal processes were decreased in LCMV-infected rats, suggesting that a subpopulation of GABA interneurons was affected. These findings indicate that abnormalities in synaptic function persist after clearance of infectious virus from the central nervous system and suggest that decreased inhibition subsequent to pathological sequence in a subpopulation of GABA interneurons may be implicated in the hyperexcitability of dentate granule cells.
Single-unit recordings of nucleus accumbens septi (NAS) neurons in halothane-anesthetized rats revealed that microinfusions of morphine into the ventral tegmental area (VTA) primarily inhibited spontaneously active NAS units. These inhibitory effects were reversed by alpha-flupenthixol (s.c.), suggesting a role for dopamine (DA) in the observed opiate-induced effect. VTA opiate microinfusions also inhibited the evoked (driven) responses of silent cells (spontaneously inactive) in the NAS elicited by stimulation of hippocampal afferents to the NAS. In addition, this inhibition of driven response was reversed by naloxone (s.c.) but not by alpha-flupenthixol, implying a VTA-mediated non-DA mechanism. Morphine applied iontophoretically to cells within the NAS inhibited spontaneous activity but not fimbria-driven cellular activity, suggesting that the systemic effects of opiates on NAS activity can be mediated directly in the NAS as well as through VTA afferents. Moreover, since VTA-induced inhibition of fimbria-driven activity was reversed by systemic opiates, opiates also can exert effects through other, as yet unidentified NAS afferent systems.
The nucleus accumbens septi (NAS) receives afferent input from the amygdala via the stria terminalis and from the hippocampus via the fimbria. Extracellular recordings from 196 NAS neurons in halothane-anesthetized rats revealed heterogeneous response patterns following stimulation of the amygdala. The observation that 30% of anterior NAS units but only 16% of posterior NAS units were responsive to amygdala stimulation suggested a topographical arrangement of amygdala efferents. Comparing the effects of amygdala and fimbria stimulation revealed that the two afferent pathways converge onto individual NAS neurons, but that the two sites of stimulation can differentially influence other neurons. The present results clarify the topographical distribution of amygdala input to the NAS, confirm that inputs from two limbic structures are integrated within the NAS, and further illustrate the electrophysiological heterogeneity of NAS neurons.
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