Olfactory Cortical Neurons Research Articles

Trans-ACPD induces a slow post-stimulus inward tail current (I ADP) in guinea-pig olfactory cortex neurones in vitro

The metabotropic glutamate receptor agonist trans-(±)-1-amino-1,3-cyclopentanedicarboxylic acid (trans-ACPD) produced a slow, persistent excitation of guinea-pig olfactory cortical neurones in vitro, and the appearance of a prominent post-stimulus afterdepolarization. The corresponding slow inward tail current (I ADP) revealed under voltage clamp was insensitive to tetrodotoxin (or atropine) but was blocked by Cd 2+ or tetrabutylammonium. The I ADP properties resembled those of the slow inward tail current induced by muscarinic agonists in these neurones, suggesting a common intracellular transduction mechanism.

Muscarinic receptor activation induces a prolonged post-stimulus afterdepolarization with a conductance decrease in guinea-pig olfactory cortex neurones in vitro

The persistent excitation of guinea-pig olfactory cortical neurones in vitro by the muscarinic agonist oxotremorine-M (OXO-M) was investigated. In OXO-M (10–20 μM), a slowly-decaying afterdepolarization (sADP) accompanied by sustained repetitive firing was induced following a long depolarizing stimulus. The corresponding slow inward current ( I ADP) revealed under voltage clamp behaved like a K +-mediated tail current, but was associated with a decreased membrane conductance. I ADP was insensitive to tetrodotoxin (TTX), Ba 2+, Cs +, or 4-aminopyridine (4-AP), but was blocked by 500 μM TEA or TBA (tetrabutylammonium). The OXO-M response and I ADP were also reduced by Cd 2+ or Ca 2+-free solution, suggesting a dependence on Ca 2+-entry. We propose that OXO-M induces a novel outward K + current that can be slowly de-activated by Ca 2+-entry during a depolarizing stimulus. Summation of I ADP tail currents could contribute to the sustained muscarinic excitation of mammalian cortical neurones.

Muscarinic receptors mediating suppression of the M-current in guinea-pig olfactory cortex neurones may be of the M2-subtype.

Guinea-pig olfactory cortical neurones in vitro were voltage clamped by means of a single intracellular microelectrode technique. Hyperpolarizing voltage commands from holding potentials between -40 to -50 mV produced slow inward current relaxations reflecting deactivation of the M-current (IM). IM was reversibly suppressed by 30 microM muscarine or carbachol; this suppression was insensitive to pirenzepine (up to 300 nM) but was inhibited by gallamine (10-20 microM) or 4-diphenyl-acetoxy-N-methylpiperidine (100, 500 nM), suggesting the involvement of the M2-type muscarinic receptor.

Age-dependent cell death in the olfactory cortex: lack of transneuronal degeneration in neonates.

Adult olfactory cortical neurons in layer IIa undergo fulminant transneuronal degeneration after removal of afferent olfactory bulb fibers (Price, '76, Neurosci Abst. 2:161; Heimer and Kalil, '78, J. Comp. Neurol. 178:559-609). This provides an unusual example of dependence of a mature population of neurons on axonal input. In order to investigate whether similar transneuronal degeneration occurs in immature animals, a series of rats were subjected to unilateral olfactory bulb removal at various ages during the first 3 postnatal weeks. The brains were examined for degeneration after short survivals by use of the de Olmos cupric silver method, which selectively stains degenerating neurons. In addition, animals with long survivals were examined with the HRP retrograde tracing method, in order to determine if cells that survive the acute effects of deafferentation develop normal patterns of connections. Young neurons are more resistant to the effects of olfactory bulb removal than more mature neurons. There was little degeneration of cortical neurons after bulb ablation during the first 2 postnatal weeks. Although layer IIa does not become distinct from layer IIb in these experimental animals, cells that have connections normally characteristic of the cells of layer IIa, and are situated at the superficial edge of layer II, were identified with the HRP method. The severity of transneuronal degeneration increases and becomes adultlike between the second and third postnatal weeks. This increase in transneuronal degeneration is temporally associated with a progressive reduction in axonal sprouting following deafferentation during the first 3 postnatal weeks, as described in the companion paper (Friedman and Price, '86). Thus, axon sprouting may "protect" the immature IIa neurons from the effects of removal of the fibers from the olfactory bulb. A period of normal cell death has also been identified in olfactory cortex by the use of the de Olmos cupric silver method. This cellular degeneration is much less severe and has a different time course and laminar distribution than the transneuronal degeneration produced by olfactory bulb ablation in adults. Although normal cell death appears to be potentiated by removal of the olfactory bulb on postnatal day 1, it is clearly a different process from the transneuronal reaction.

Effects of cooling on guinea pig olfactory cortex maintained in vitro

Electrical activities from brain slices of guinea pig olfactory cortex were studied during gradual cooling without a temperature gradient. At normal temperature the potential evoked by stimulation of the lateral olfactory tract consists of an initial spike (IS), a negative (N), and a positive (P) potentials. The IS potential has been considered to be presynaptic in origin and the latter two postsynaptic. During cooling from 37 to 15°C, the amplitude of both the IS and the N potentials increased to attain the maximum value (10—36% increase) at about 32°C, then decreased gradually and disappeared at around 15°C. On the other hand, the durations of the IS and the N potentials were prolonged gradually on cooling from 37 to 17°C. Most of the olfactory cortical neurons responded with one or two firings to the tract stimulation. The firing numbers increased on cooling down to about 32°C and declined on further cooling, which corresponds with the behavior of the N potential. All these effects were reversible on rewarming. Augmentation of the N potential might depend primarily on the increase in amplitude of the IS potential and secondarily on the increase of amount of liberated transmitter substance and/or the delayed inactivation process of the transmitter action.