Motivation Flashcards

1
Q

What is motivation responsible for

A

activation and direction of behaviour

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2
Q

What is the homeostatic school of thought on motivation

use eating as an example

A

the motivation or drive to feed is a consequence
of a deficit in nutrients that build up across time, after the last meal. Alleviation of that deficit state, by taking in
nutrients, acts to reduce drive and ultimately to stop feeding.

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3
Q

What is the problem with the idea that motivation is purely homeostatic

A

not all behaviours stem from an underlying deficit state.
So sexual behaviour, aggression and many motivated behaviours in humans, e.g. running in a race, do not appear to be alleviating some deficit state.

In these other examples it is more usual to talk about ‘incentive motivation’ – the
pull of behaviour towards goals/incentives, e.g. a gold medal at the Olympics, rather than a push (or drive) from within.

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4
Q

Describe the ‘internal’ and ‘external’ feelings involved with eating a cake when you are full

A

the smell and ‘look’ of the chocolate cake, along with our past experience with it, over-rides any internally driven satiety signals.

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5
Q

Is motivation thought to be based on internal or external factors

A

generally accepted that there can be both internal factors (sensations) and external factors (incentives) that motivate behaviour and these factors can interact. Thus, food can seem much more desirable and attractive when we are hungry than when we are ‘full’.

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6
Q

What are the 2 phases of motivated behaviour

A

1) consummatory, when the animal interacts with the
goal object e.g. ingestive responses and sexual reflexes

2) appetitive, when the animal performs voluntary
behaviour to seek out the goal, e.g. food searching, lever pressing for warm air.

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7
Q

What is a rat decerebrate preparation

A

if a cut is made above the midbrain of a rat to cut off the influence of the forebrain

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8
Q

How does appetitive and consummative behaviours change in a rat decerebrate preparation

A

animal is no longer able to seek out and consume food/water or a sexual partner, but is
able to interact with the goal object if the goal is placed appropriately to allow the activation of somato-motor
reflexes, e.g. swallowing liquid food/water if placed in the mouth. Thus, while the animal shows no appetitive, goal
directed behaviours, it can, nonetheless, perform very simple reflexive responses

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9
Q

Where is the coordination of consummatory reflex behaviours and appetitive behaviours found in the brain

A

neural activity in the forebrain,

including the hypothalamus and amygdala

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10
Q

What borders the hypothalamus rostrally and caudally

A

rostrally by the optic chiasm and

caudally by the mammillary bodies.

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11
Q

How can the hypothalamus be divided

A

grossly into lateral, medial and periventricular regions as well as anterior, middle and posterior regions.

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12
Q

What was the hypothalamus originally identified as ?

Why was this thought to be the case?

A

as a structure that could act as a drive centre.

Stimulation and lesions of neurons within the hypothalamus led, respectively, to the activation and loss of motivated behaviours such as sex, feeding and drinking.

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13
Q

Describe the neural inputs to the hypothalamus from the brainstem

A

(a) somatic afferents, n.b. not somatotopic, no feature detection important in neuroendocrine reflexes e.g. milk ejection (maternal care) and stereotypic behaviour (sex)
(b) visceral afferents from nucleus of the solitary tract (NST) and reticular formation conveying gustatory and olfactory information

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14
Q

Describe the neural inputs from the forebrain to the hypothalamus

A

Afferents from the amygdala (and orbitofrontal cortex) are carrying information about the motivational significance of external stimuli.

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15
Q

Is the hypothalamus directly responsive to hormones

A

yes

Many regions of the hypothalamus are rich in steroid hormone receptors.

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16
Q

How is the hypothalamus directly sensitive to temperature and osmolarity

A

Cells in the preoptic area are sensitive to changes in temperature while osmoreceptors are found in the OVLT, a circumventricular organ.

hypothalamus is well placed to respond to changes in the chemical composition of the blood as many of the hypothalamic capillaries are ‘fenestrated’, like peripheral capillaries and are therefore open to the entry of large molecules from blood to brain.

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17
Q

What are the different kinds of input to the hypothalamus (4)

A

neural inputs from the brainstem and forebrain

neurons directly responsive to hormones, temperature and osmolarity

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18
Q

What are the 3 ways types of output from the hypothalamus

A

endocrine via the pituitary
behavioural responses
autonomic responses via the descending projections

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19
Q

How can endocrine responses from the hypothalamus via the pituitary occur (2)

A

r (i) directly via a neural signal to the posterior pituitary resulting in the secretion of neuroendocrine
products into the general circulation

(ii) indirectly by secreting hormones into the local portal plexus (within the median eminence) which drains into the
blood vessels of the anterior pituitary. These in turn control the synthesis and release of anterior pituitary hormones into the general circulation involved in the control of reproduction, maternal care, etc.

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20
Q

What kind of behavioural responses can the hypothalamus control

A

can control simple stereotyped movements e.g. biting, shivering, gnawing, drinking and sexual mounting via reflex motor circuits in the brainstem

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21
Q

How can the hypothalamus affect the ANS

What is the other ANS coordinating centre in the brain? How does this work?

A

both neurally and humorally

NTS in the brainstem
acts upon other brainstem nuclei and neurons in the spinal cord to control preganglionic autonomic neurons

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22
Q

What ANS coordinating centres do elaborate homeostatic adjustments involve?

A

reciprocal connections between the NST and higher centres
including the amygdala and paraventricular nucleus of the
hypothalamus.

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23
Q

Where are the temperature sensitive areas in hypothalamus

A

preoptic area

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24
Q

What happens if you change the temperature of the preoptic area

A

elicits thermoregulatory behaviour, including reflexive shivering, panting and grooming as well as learning to perform an action to cause a brief lowering of hypothalamic temperature

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25
Q

What do lesions of the preoptic region result in

A

impairs thermoregulatory behaviour in

response to changes in ambient temperature

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26
Q

Cooling or warming of the preoptic area elicits thermoregulatory behaviour, including reflexive shivering, panting and grooming as well as learning to perform an action to cause a brief lowering of hypothalamic temperature Conversely, lesions of the preoptic region impair thermoregulatory behaviour in response to changes in ambient temperature. What does this suggest

A

changes in the internal environment can be sensed by the hypothalamus and, via negative feedback loops, the appropriate behaviours can be generated to restore the balance

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27
Q

What happens to a rat with a preoptic lesion if the temperature changes

A

don’t shiver or pant but can still learn to press a lever for hot or cool air and thus can achieve thermal regulation!

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28
Q

Which area of the hypothalamus increases activity upon presentation of food?

What is this activity dependent upon

A

lateral hypothalamus

the motivational state of the animal. They do
not fire if the monkey is satiated

the hypothalamus is in a position to match behaviour to current needs

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29
Q

What did early lesion studies suggest about the lateral hypothalamus

What was the evidence

Which area is suggested to serve an opposite function? What was a problem with this study?

A

it was a feeding centre

Electrolytic lesions of the LH produced profound aphagia and stimulation of the same region induced eating in sated rats

lesions of the ventromedial hypothalamus (VMH) caused over-eating and obesity

the overeating seen following VMH lesions was found to be due, in part, to disruption of axons between the arcuate nucleus and other hypothalamic and brainstem nuclei.

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30
Q

What are the LH and VMH sensitive to according to early lesion studies

A

LH- hunger

VMH - satiety

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31
Q

What was the problem with the early lesion studies of the LH

A

only looked at very selective
behaviours and LH lesions actually resulted in the loss of
MOST motivated behaviours, not just eating. Subsequently it
became clear that these electrolytic lesions not only destroyed
intrinsic cell bodies within the LH but also fibres passing
through the LH which included monoamine axons within the
medial forebrain bundle (mfb)

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32
Q

How does selective lesions of LH neurons differ to the original results which didn’t spare mfb fibres

A

more restricted feeding deficits were seen. There is considerable recovery of function across time but there remain residual deficits in the ability to respond appropriately to
homeostatic/physiological challenges that mimic dehydration (injection of NaCl) and starvation (2-DG treatment).

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33
Q

What is the mPOA

What receptors are abundant here? What can they detect

A

medial preoptic area

steriod receptors to detect changes in circulating testosterone and oestrogen/progesterone levels

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34
Q

What happened to male rats with mPOA lesions

A

loss of copulatory behaviour in the presence of a female rat BUT the male rat would still show intense excitement in the presence of a female rat in heat.

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35
Q

What are the environmental cues that initiate feeding

A

include the sight, smell and taste of food as well as conditioned stimuli associated with food such as McDonalds and Costa Coffee signs.

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36
Q

What are some physiological cues that initiate feeding

A

declining levels of blood glucose and fatty acids, i.e. gluco- and lipo-privation.

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37
Q

What are the short term satiety mechanisms

A

feedback from tasting, smelling and swallowing food as well as distension of the stomach following ingestion

Humoral factors e.g. CCK released by the duodenum when it receives food rich in fats acts on receptors in the pylorus that are transmitted to brainstem, via the vagus, to reduce feeding.

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38
Q

What are long term satiety mechanisms

A

signals arising from nutrient reservoirs can affect food intake.

eg Leptin, a peptide secreted by well nourished adipose tissue increases metabolic rate and decreases food intake. It also increases brain’s sensitivity to short term satiety signals such as CCK

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39
Q

What are 2 neuropeptides are in involved in stimulating eating

A

melanin concentrating hormone (MCH) and orexin in the LH

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40
Q

What are orexin and MCH activated by

A

NPY from neurons in the arcuate nucleus

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41
Q

What NPY neurons affected by

A

contain leptin receptors, that when stimulated act to inhibit NPY neuronal activity.

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42
Q

What happens to NPY neurons when we become hungry

A

leptin levels decrease and this releases NPY neurons in the arcuate nucleus from their inhibition by leptin. Also, other cues, such as the release of ghrelin from the stomach when it empties, activate NPY neurons directly. The resulting increase in NPY release in the LH, causes voracious eating and, in the paraventricular nucleus (PVN), a decrease in metabolic rate and a decrease in insulin

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43
Q

How does NPY integrate a variety of physiological mechanisms that promote feeding and preserve the body’s energy supplies

A

increase in NPY release in the LH, causes voracious eating and, in the paraventricular nucleus (PVN), a decrease in metabolic rate and a decrease in insulin

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44
Q

What happens to NPY when the body becomes well nourished

A

leptin levels increase, causing a reduction in NPY activity and as a consequence, a reduction in LH orexin and MCH neuronal activity.

The latter results in
decreased feeding and, via a loss of NPY release in the PVN, an increase in metabolic activity (via ACTH release from the pituitary and increase of tone in the SNS).

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45
Q

How do lesions in the hypothalamus affect sexual reflexes

What can give the same result

A

lesions of the mPOA abolish sexual copulatory behaviour in male rats while lesions of VMH impair female sexual behaviours including lordosis and solicitation.

even with an intact POA, a loss of steroids, brought about by castration, will abolish, as effectively, male sexual behaviour

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46
Q

What is the role of circulating steroid levels in sexual motivation

A

permissive role

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47
Q

How do we know circulating sex hormones play a permissive role in female sexual behviour

A

Ovariectomy in females reduces female sexual behaviour in the presence of an intact VMH

behaviours can be reinstated with oestradiol, followed by progesterone

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48
Q

How do sex hormones act to stimulate sexual behaviour normally

How was this shown

A

Androgen receptors are especially concentrated in the mPOA and oestradiol receptors and oestrogen
inducible progesterone receptors are found within the VMH.
sex hormones act on the steroid dependent neurons in these areas

implanting testosterone directly into the mPOA of castrated male rats and oestrogen/progesterone into the VMH of ovariectomised female rats restores their sexual behaviour

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49
Q

How do lesions of the mPOA affect the sexuality and motivation for access to a female

How does that compare to castration

A

impaired copulatory behaviour in the rat, as expected, but did not affect the rat’s motivation to lever press to obtain access to the female

castration did disrupt lever pressing as well as copulatory behaviour demonstrating that sex hormones are essential more generally in motivated sexual behaviou

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50
Q

How are the effects of lesions in the POA similar for temperature and sex in males

A

Rats with preoptic lesions didn’t display usual panting and vascular dilation in response to warming but did press a lever to obtain a cold puff of air.

lesions of the medial preoptic area impaired copulatory behaviour in the rat, as expected, but did not effect the rats motivation to lever press to obtain access to the female

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51
Q

Generally which motivational responses survive hypothalamic lesion

What is the hypothalamus therefore more preoccupied

A

incentive motivational responses/ instrumental responses

primarily to subserve the integration and expression of more reflexive and consummatory responses

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52
Q

Give a brief overview of the hypothalamus in motivation and homeostasis (3)

A
  1. The hypothalamus controls the internal environment via efferent systems which co-ordinate endocrine, autonomic and
    behavioural responses.
  2. The expression of motivated behaviours fulfill the primary needs of the organism - food, shelter, sexual and social interactions. By monitoring the internal state, the hypothalamus performs a key role in signalling biological priorities.
  3. Lesions of the hypothalamus that interfere with this information flow disrupt the expression of stereotyped motivated
    behaviours
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53
Q

Where is the amygdala

A

lies in the anterior temporal lobe rostral to the hippocampus in the end wall of the inferior
horn of the lateral ventricle, adjacent to olfactory cortex.

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54
Q

What are the 3 subdivisions of the amygdala

A
cortico-medial division (Co+M)
central nucleus (C)
basolateral amygdala (BL)
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55
Q

What are the 2 principal efferent pathways from the amygdala

Give a brief description

A

i) ventral amygdalofugal pathway - diffuse pathway, coursing directly across the temporal stem
ii) stria terminalis - fibre bundle running around lateral ventricle in groove between caudate tail and thalamus

56
Q

Describe the Co+M of the amygdala

A

receives olfactory information and amongst other things, is the route via which pheromones (secretions from urogenital tract) come to elicit social and sexual behaviour.

Important cues in non-human animals. Looking for sex attractant hormones in humans have so far been fruitless.

57
Q

What are pheromones’

A

secretions from the urogenital tract

58
Q

What does the central nucleus of the amygdala control?

what are its afferents and efferents

A

controls the ANS, the endocrine system and simple motor reflexes. It has afferents from the solitary tract; efferents to the hypothalamus and brain stem

59
Q

What is the in/ouput of the basolateral amygdala

A

receives input from higher-order sensory regions

projects to regions
involved in planning and action including the prefrontal cortex and the ventral striatum.

60
Q

How do lesions of the AMYGX affect male rats sexually

How does this affect rats for feeding

A

will not press lever to receive a female
can still mount and intromit

will not press lever for food but can eat

61
Q

How does a male rat act sexually if it is castrated but has an intact amygdala

Why is this

A

even with an intact amygdala, castration abolishes lever pressing to get a female

contains steroid receptors and testosterone may well act here to promote appetitive behaviours.

62
Q

What human study reinforces amygdala lesion studies on its role in feeding

A

Consistent with the importance of the amygdala in rats in responding to incentive food cues, the human amygdala is activated whilst we look and select items from high incentive menus in a PET scanner

63
Q

What is the amygdala necessary for

give examples for rats and humans

A

appetitive behaviour elicited by cues in the environment predictive of primary rewards.

These incentive motivational cues may be the light that the rat has learned is associated with a sexually receptive female or food reward. Equally, in humans they are the McDonalds and Costa signs.

64
Q

What is the role of the amygdala (4)

A
  1. The amygdala is important in the assessment of the motivational significance of stimuli in our environment.
  2. Via its connections with the hypothalamus and the brainstem it can co-ordinate the output of a variety of response systems,
    autonomic, endocrine and simple reflex behaviours.

3.Voluntary action, which is an important component of motivational expression may be controlled by the amygdala’s
connections with the ventral striatum and prefrontal cortex.

  1. The amygdala also plays a major role in emotion
65
Q

If the Amygdala identifies motivationally significant environmental cues, how does it control voluntary action?

A
  1. Major output to ventral striatum
    This includes the nucleus accumbens and ventral regions of the caudate and putamen. It allows access to the motor systems of the basal ganglia.
  2. Ventral striatum receives a specific dopaminergic input from the A10 group of dopamine neurons in the Ventral Tegmental Area (VTA), adjacent to the A9 substantia nigra
66
Q

What might have been the reasons the original LH lesion studies which also damaged ]

give further evidence for this

A

e dopamine projections to the striatum (caudate-putamen and nucleus accumbens) run in the medial forebrain bundle (mfb) then aspects of the original LH syndrome may be due to damage to these fibres.

LH lesion deficits could be reversed by treatment with dopamine agonists

67
Q

What is 6-OHDA

What is it used for

What does this use lead to

A

a chemical neurotoxin

used to damage DA projections in the mfb

caused profound depletions of dopamine within the striatum, and also aphagia and adipsia as well as akinesia. In particular, the aphagia and adipsia mirrored the LH syndrome

68
Q

What is the nigrostriatal DA system

What does a loss of this system result in

A

DA neurons in the substantia nigra that project to the dorsal striatum: caudate and putamen

akinesia seen
in Parkinson’s disease which includes the inability to perform consummatory ingestive responses,
and aphagia and adipsia seen in the LH syndrome

69
Q

What is the mesolimbic DA pathway

A

DA projections to the ventral striatum, including nucleus accumbens, are involved in appetitive/preparatory responses, thereby mediating incentive motivation

70
Q

Why do we think the mesolimbic DA pathway is involved in appetitive behaviour

A

DA in the nucleus accumbens is released in the presence of primary rewards such as food, a sexual partner, as well as stimuli associated with them, such as a light or noise (McDonalds signs)

lesions of this pathway with 6-
OHDA disrupt the appetitive behaviours that occur in anticipation of the primary reward such as investigative behaviours and locomotor activity but have no effect on the consummatory responses, i.e. copulating or eating.

71
Q

When are appetitive behaviours mediated by the mesolimbic DA pathway activated

A

in the presence of cues that predict primary rewards, promote food or sex seeking behaviours making it more likely that the animal/human will come into contact with the goal object.

72
Q

Why does boring, miserable looking food look ‘tempting’ when hungry

A

orexin neurons activated in the hungry state send projections to the nucleus accumbens and its DA innervation. This may be one route by which hunger can alter incentive motivational processes.

73
Q

How do DA lesions of the ventral striatum compare with lesions of the hypothalamus and amygdala

A

exact opposite of hypothalamic lesions but look similar to that seen following amygdala lesions.

74
Q

What is the final common pathway for many drugs of abuse?

A

mesolimbic DA pathway

75
Q

Describe the location of the brainstem reticular core

A

continuous with intermediate gray of spinal cord caudally and lateral hypothalamus and subthalamic regions rostrally. It is located medially in the brain stem and composed of loosely aggregated cells of different types and sizes intermingled with fibres of differing orientations (hence, net-like appearance).

76
Q

What are the 2 main categories of the functions of the reticular formation

A

integration of basic, stereotyped response patterns

regulation of the level of brain activity

77
Q

What does the reticular formation’s role in integration of basic, stereotyped patterns of responding include (2)

A

• Pattern generation for posture and locomotion:
swallowing; chewing; vomiting; sneezing; eye
movements, etc.
• Regulation of the respiratory cycle and cardiovascular
control.

78
Q

What does electrical stimulation of the reticular formation lead to

A

n induced widespread cortical activation (desynchronisation of the EEG) thought to subserve sleep and wakefulness.

79
Q

What are reticular neurons part of

A

the isodendritic core

80
Q

How do RF neurons project to the cortex

A

direct, via medial forbrain bundle (mfb) that runs through lateral hypothalamus,

indirect, via the intralaminar nuclei of the thalamus which in turn project to the cortex and striatum.

81
Q

How can brainstem RF neurons be categorised

A

into discrete,
chemically defined components:
Populations of neurons contain DOPAMINE, NORADRENALINE,
SEROTONIN and ACETYLCHOLINE

82
Q

What are the components of the isodendritic core (6)

A

RF populations of neurons that contain DOPAMINE, NORADRENALINE,
SEROTONIN and ACETYLCHOLINE

cholinergic neurons of the basal forebrain and the HISTAMINERGIC neurons of the posterior hypothalamus.

83
Q

What is common about the structures of RF neurons

A

While these different chemically defined groups of neurons have very widespread or diffuse projections,
nevertheless have discrete patterns of termination that differ not only from one another but also between one cortical or subcortical region and the next

84
Q

What is the role of RF dopamine neurons briefly

A

Activation of appetitive and

consummatory behaviours

85
Q

Briefly, what is NA thought to play a role in in the RF

A

attention and orienting

86
Q

What does activation of the locus coeruleus during sensory stimulation lead to

Which NT does this involve

A

increase in the signal-to-noise
ratio.

Stimulation not only enhances the inhibitory effect of a ‘meaningless’ tone on hippocampal neurons but also enhances the excitatory effect of a ‘meaningful’ tone on hippocampal neurons

NA

87
Q

When is it thought that noradrenergic control of attentional function may be
particularly important

A

under times of stress, when locus coeruleus neurons are maximally activated and
noradrenaline is released in cortical terminal fields

88
Q

What has manipulation of 5-HT affect

What has this lead to clinically

A

processes concerned with behavioural inhibition, particularly in aversive situations.

impulsive behaviour and obsessive compulsive behaviour
have been linked to reduced 5-HT in the forebrain, whereas, drugs that increase brain 5-HT are used to treat such disorders, as well as anxiety and
depressive states (e.g. Prozac)

89
Q

What have forebrain cholinergic systems been associated with?

What data is this idea based upon?

A

functions related to learning and memory,

based partly on experimental data but also on clinical data relating disorders of learning and memory to degeneration of the forebrain cholinergic neurons, i.e. Alzheimers disease

90
Q

What cholinergic brain systems should you not confuse should you not

A

pedunculopontine
cholinergic neurons in the brainstem involved in sleep and the forebrain cholinergic systems associated with learning and memory

91
Q

What do most drugs currently used to treat psychiatric disorders interact with

A

one or other of the main monoaminergic systems.

92
Q

Define sleep behaviourly

what is another definition

A

by the normal suspension of consciousness

electrophysiologically by specific brain wave activity

93
Q

How does a human’s sleep-wake rhythm different in the absence of day/night cues

A

still show a sleep-wake rhythm but the cycle either lengthens or shortens by about half an hour, - such a rhythm is dependent upon the SCN of the hypothalamus

94
Q

What does an EEG measure

What does it represent

A

fluctuations in electrical activity in the brain from surface scalp electrodes

summed activity of many cortical cells, which are probably synchronised, in part, by thalamic
activity as well as with each other. Most of the activity contributing to the EEG is probably in the form of
slow membrane potentials (EPSP”s & IPSPS’s)

95
Q

what is most of the activity contributing to the EEG in the form of

A
slow membrane potentials (EPSP”s & IPSPS’s); 
action potentials (spikes) in cortical cells are too brief to sum together, except during epileptic seizures.
96
Q

How are the stages of sleep characterised

A

by recording

electrical brain activity across the scalp

97
Q

What are the 2 characteristic EEG patterns during the waking day

A

high frequency (15-60 Hz), low amplitude activity known as Beta activity that occurs when the eyes are open and signals an active cortex;

lower frequency (8-13 Hz) activity called Alpha activity which is associated with quiet waking states.

98
Q

What are the frequencies of alpha and beta activity in the waking day

A
beta = 15-60Hz
alpha = 8-13 Hz
99
Q

What characterises stage 1 and 2 of sleep

A

stage 1: drowsy period; decreasing EEG frequency, 4-8 Hz and increasing amplitudes called theta waves giving way to light

stage 2: further decreases in frequency and increases in amplitude and intermittent high frequency spike clusters or spindles (has K complex)

100
Q

What characterises stages 3 and 4 of sleep

A

Stage 3 sleep represents a
moderate to deep sleep

stage 4 sleep = the deepest sleep with lowest frequencies and highest amplitude waves known as Delta waves.

101
Q

Which stage of sleep has an EEG very similar to the awake state

A

REM (following slow wave sleep)

102
Q

What does a typical 7 hour sleep period comprise

A

several cycles that

alternate between REM and the 4 stages of NON-REM sleep

103
Q

What are the non REM periods of sleep characterised by

A

decreases in muscle tone, heart rate, breathing, blood pressure and metabolic rate

104
Q

What are periods of REM sleep characterised by

A

increases in blood pressure, heart rate and metabolic rate, nearly as high as the awake state. Also accompanied by rapid rolling eye movements and paralysis of large muscles.

105
Q

What are some of the differences between the awake state and the various stages of sleep revealed by functional neuroimaging

A

While some cortical regions were equally active during the awake state and REM sleep, extra-striate cortex and certain limbic structures were significantly more active during REM sleep.

In contrast, prefrontal cortex was less active.

primary visual cortex, as well as some other areas, were significantly less active during REM sleep but extra-striate cortex was more active.

106
Q

What are some of the proposed functions of sleep (3)

A

restoration of bodily and mental functions including removal of toxins produced by active neurons during the day, brain development (in children) and memory consolidation

107
Q

What are the 2 brain structures that mainly contribute to the control of the sleep-wake cycle

A

• The Brainstem modulatory neurotransmitter
systems

• The Thalamus

108
Q

Which part of the brain did Magoun stimulate to find it caused wakefulness

What did Hess find that related to this

A

a group of cholinergic neurons in the brainstem (pedunculopontine)

stimulating the thalamus with low frequency pulses in an awake animal produced a slow wave sleep.

109
Q

What do we think underlies the transition from NON-REM sleep to waking state

A

has been shown that acetylcholine, or noradrenaline, shifts cells in the cortex and thalamus from an intrinsic burst-firing mode to a single spiking mode.

110
Q

What happens in the intrinsic burst firing mode of sleep

What happens in the tonically active state

A

e thalamus becomes synchronised with the cortex, essentially disconnecting the cortex from the outside world. This disconnection is maximal during Delta sleep

thalamo-cortical neurons transmit information to the cortex

111
Q

When is the disconnection of the cortex from the outside world greatest

A

during delta sleep

112
Q

How does thhe activity of differet monoamine neurotransmitter neurons change during REM and non-REM sleep (3)

A

During non-REM sleep the activity of cholinergic, noradrenergic and serotonergic neurons is decreased.

However with the onset of REM sleep, serotonin and noradrenalin neurons decrease their activity even further while pedunculopontine cholinergic neurons become active.

Just before REM offset, the firing rates of serotonin and noradrenaline neurons increase again.

113
Q

What is the VLPA

What is its role in sleep

A

Ventrolateral preoptic area of the Hypothalamus

very important in providing the switch
between the wake and sleeping state.

114
Q

What is the set up of the ‘flip flop’ model

what is the purpose

A

VLPA has an inhibitory innervation onto the ascending arousal system.

Likewise, the ascending arousal pathways have an inhibitory input onto the VLPA.

Such a flip-flop switch is essential to provide sharp and clearly defined boundaries between wakefulness and sleep

115
Q

How do lesions of the VLPA affect sleep

A

reduce total sleep time by more than 50%.

Lesioned animals display a normal circadian pattern but tend to wake up more during the sleep cycle but also fall asleep more during the wake cycle as well.

116
Q

What are other neurochemical systems which feed into the flip flop system

A

orexin containing
neurons (excitatory)

MCH (melanin concentrating hormone) -
containing neurons (inhibitory).
117
Q

Give some causes of acute insomnia

What is longer term insomnia associated with

A

stress, jet lag, drugs

psychiatric disorders eg depression that may well upset the balance of neuromodulatory
transmitter systems

118
Q

What is narcolepsy

A

characterised by frequent REM sleep attacks

during the day and possible cataplexy (temporary loss of muscle control).

119
Q

What is a possible gene associated with narcolepsy

A

Research in dogs, has identified a genetic disorder caused by a mutation of the orexin receptor 2 gene

120
Q

Where are orexin neurons found

When are they most active

A

exclusively in cells of the tuberal region of the hypothalamus, i.e. lateral hypothalamus

most active during wakefulness, in
particular, during locomotor exploration.

121
Q

Where do orexin neurons project to

What do they do

A

send excitatory projections to reticular modulatory systems including noradrenaline and serotonin systems and act to increase activity in the arousal pathways

act to tip the balance of the flip-flop switch in the favor of the waking state

122
Q

What happens to the flip flop switch in the absence of orexin receptors

A

the flip-flop switch is weakened and switching between states becomes more frequent.

123
Q

What is the interesting link between hunger and sleep with orexin neurons

A

Orexin neurons are activated by hunger signals from the arcuate NPY neurons and stimulate eating. Just before a meal animals are usually very active whilst very often, just after a meal, animals go to sleep. Very likely that orexin plays a dominant role in this pattern of sleep-wakefulness related to feeding behaviour.

124
Q

How can food availability affect the the sleep cycle

A

Nocturnal animals can become diurnal if the only available food source can be found in the day.

This links the sleep-wake cycle with the day-night cycle

125
Q

How long is the sleep wake cycle

Is this based off the external world?

A

24 hours

animals tend to be either nocturnal or diurnal

without cues from the external world animals, including humans, still display an approx. 24 hour sleep-wake cycle, give or take half an hour

126
Q

What is the point of animals evolving biological clocks

A

overall successful adaptation to the daily environment necessitates rhythmic behaviour and physiology. This has been provided by the evolution of biological rhythms driven by biological clocks.

127
Q

What is the principal biological clock in mammals

A

suprachiasmatic nucleus (SCN)

128
Q

Describe the SCN

A

principal mammalian body clock

a paired nucleus located in the anterior hypothalamus, lying above the optic chiasm on each side of the third ventricle.

129
Q

What does the SCN do in the absence of light

A

free run with a period slightly below or above 24 hours.

130
Q

How do the fibres of the SCN act as a clock

A

individual SCN neurons are

circadian oscillators that are coupled to make a pacemaker

131
Q

What happens without the SCN

A

biological rhythmicity is lost

132
Q

Where does the SCN receive light dark information from

what does this allow

A

directly from the retina, via the retinohypothalamic tract,

resulting in entrainment of the clock to the 24 hr light-dark cycle

133
Q

What feature of SCN- retina connection allows them to be tuned to light

A

a subset of retinal
ganglion cells contain a light sensitive pigment, melanopsin, which is particularly sensitive to blue wavelength
light. It is these ganglion cells that send their axons to the SCN.

134
Q

What does the SCN control the rhythmicity of? (3)

A

many physiological as well as psychological functions, via its connections to a variety of nuclear groups within the hypothalamus, in particular, the dorsomedial nucleus (DMN), as
well as to other diencephalic sites, including the midline thalamus and the bed nucleus of the stria terminalis.

These include endocrine and autonomic output
as well as mood and emotional state

135
Q

Name one route through which the SCN controls the sleep wake cycle

A

through its regulation of the VLPA, via the DMN.

136
Q

Name some disorders which disrupt the SCN clock (4)

A

a number of mood disorders such as depression and anxiety as well as
neurodegenerative disorders such as Huntington’s and Alzheimers disease.

137
Q

Why is the understanding of the disruption of the SCN clock important for Alzheimer’s patients

A

it is the night-time wanderings that make it extremely difficult for relatives to look after elderly sufferers. If rhythmicity could be restored, these sufferers could be looked after in their home environment, for longer.